Relevance of Screening Subclinical Cushing’s Syndrome in Patients with Type 2 Diabetes Mellitus | Chapter 4| Medical Science: Updates and Prospects Vol. 4

 

Background: Subclinical Cushing’s syndrome (SCS) is defined as autonomous cortisol secretion in patients devoid of specific clinical symptoms of hypercortisolism, as in the classic CS. Subtle cortisol hypersecretion from adrenal incidentalomas is associated with alterations of the hypothalamic-pituitary-adrenal (HPA) axis due to autonomous adrenal function, occurring in the absence of the typical clinical phenotype of hypercortisolism. This condition has been defined as subclinical Cushing’s syndrome (SCS). Despite the absence of overt symptoms, sustained exposure to chronic, slightly elevated cortisol concentrations may result in some classical metabolic complications of CS, such as impaired glucose tolerance and diabetes. Studies reported a higher frequency of SCS in type 2 diabetics, which can be considered an exacerbating factor for diabetes and poor glycemic control. Currently, the frequency of SCS is widely variable.

 

Aim of the Study: This study intends to prospectively evaluate the prevalence of SCS among type 2 diabetic (T2D) patients with poor control, and to determine whether systematic screening for SCS in T2D patients is worthwhile.

 

Methods: It was a cross-sectional study including 221 T2D patients referred to the National Institute of Nutrition of Tunis for poor glycemic control (HbA1c ≥ 8%). Inclusion criteria were age >40 years and poor glycemic control; patients with a history of adrenal mass or pituitary adenoma were excluded. SCS screening was performed in two steps. The first screening step of SCS was the 1-mg overnight dexamethasone suppression test (ODST) using a revised criterion for cortisol suppression. In the second confirmatory step, patients with abnormal ODST underwent a 48-h, 2-mg low-dose dexamethasone suppression test (LDDST) to confirm the diagnosis. The cut-off for cortisol suppression was 50 nmol/L (1.8 µmol/dL) in the two tests.

 

Results: The mean age ± SD of the patients was 58.7 ± 8.78 years. Overweight and obesity were found in 34% and 47%, respectively. Mean duration of diabetes was 10.84 ± 6.55 years, and mean baseline HbA1c ± SD was 10.9±1.8%. Thirteen patients (5.9%) failed to suppress cortisol levels less than the cut-off after ODST. SCS was confirmed by LDDST in one patient among them (0.45%). The autonomous cortisol secretion was related to a pituitary adenoma. This study revealed that the frequency of SCS of 0.45% did not allow for performing an analytical study in order to identify predictive factors of SCS among T2D patients.

 

Conclusion: SCS is rare among T2D patients. Systematic screening of SCS in T2D patients with poor glycemic control is not worthwhile. The screening should be performed only in patients with specific clinical and/or biological indicators. Further multicenter studies with larger sample sizes are needed to explore potential risk factors for SCS in T2D patients.

 

 

Author(s) Details

Manel Jemel Hadiji

Department of Endocrinology, National Institute of Nutrition, Tunis, Tunisia.

 

Imen Ksira
Department of Endocrinology, National Institute of Nutrition, Tunis, Tunisia.

 

Emna Haouat
Department of Endocrinology, National Institute of Nutrition, Tunis, Tunisia.

 

Henda Kammoun Jamoussi
Department of Nutrition, National Institute of Nutrition, Tunis, Tunisia.

 

Hajer Kandara
Department of Endocrinology, National Institute of Nutrition, Tunis, Tunisia.

 

Ines Kammoun
Department of Endocrinology, National Institute of Nutrition, Tunis, Tunisia.

 

Please see the book here :- https://doi.org/10.9734/bpi/msup/v4/6657

Gut Microbiota as a Modulator of Insulin Resistance: A Review | Chapter 7 | Medical Science: Recent Advances and Applications Vol. 12

 

Insulin resistance is the pivotal pathogenic component of many metabolic diseases, including type 2 diabetes mellitus, and is defined as a state of reduced responsiveness of insulin-targeting tissues to physiological levels of insulin. Recent studies have progressively uncovered aspects of the gut microbiota and how it contributes to the metabolism of key nutrients during IR. The purpose of this review is to examine the role of gut microbiota as a modulator of insulin resistance. Growing evidence indicates that dysbiosis, marked by reduced microbial diversity and an imbalance between beneficial and harmful species, contributes to metabolic dysfunction. Key findings show that a higher Firmicutes-to-Bacteroidetes ratio, the inflammatory action of lipopolysaccharide (LPS), and the beneficial effects of short-chain fatty acids (SCFAs) are central to understanding the link between microbiota and host metabolism. Protective taxa such as Akkermansia muciniphila and Faecalibacterium prausnitzii support metabolic stability, while endotoxin elevation worsens inflammation and insulin resistance. Current therapeutic strategies—including diet modification, physical activity, prebiotics, probiotics, and faecal microbiota transplantation (FMT)—demonstrate potential in restoring microbial balance. Despite these advances, challenges such as interindividual variability and the need for standardised, long-term trials remain. In conclusion, gut microbiota should be regarded not as a passive indicator but as an active therapeutic modulator with strong potential in the prevention and management of insulin resistance.

 

Author(s) Details

Noor Ali Hussein
Babylon Education Directorate, Ministry of Education, Hillah, Iraq.

 

Please see the book here :- https://doi.org/10.9734/bpi/msraa/v12/6442

Rising Obesity in India: Challenges in Achieving Nutrition-related SDGs | Chapter 7 | Food Science and Agriculture: Research Highlights Vol. 4

 

India bears a disproportionate share of the world’s malnutrition burden. Alongside continuing undernutrition and micronutrient gaps, a rapidly rising epidemic of overweight and obesity is making progress toward SDG-2 difficult. NFHS-5 (2019–21) reports that 24% of women, 23% of men and 3.4% of children under five are overweight or obese. Once concentrated in high-income countries, obesity is now escalating in low- and middle-income countries as well; globally, the share of 5–19-year-olds with obesity grew from 7% to 16% between 1990 and 2022, while adult obesity rose from 2% to 8% over the same period. Projections suggest that by 2050, India could be among the nations with the largest absolute numbers of people living with obesity, which will intensify the risk of non-communicable disease (NCD) and slow progress toward SDG-3. The consequences of obesity in terms of morbidity, disability and premature mortality contribute substantially to the overall disease burden. This surge reflects an interplay of socio-economic, cultural and environmental forces such as rapid urbanisation; rising incomes and increasingly sedentary, screen-centric work; a dietary shift toward aggressively marketed, ultra-processed, calorie-dense foods; and digital platforms that enable effortless, frequent access to high-calorie meals. Despite flagship efforts such as Poshan Abhiyaan, Fit India, and Eat Right India, the problem of overnutrition remains insufficiently addressed. A comprehensive, multi-sector response is needed. Priority actions include fiscal and regulatory measures (higher taxes on high-fat, high-salt, high-sugar foods and subsidies for fruits, vegetables and whole grains), clear front-of-pack nutrition labels, restrictions on unhealthy food marketing, especially targeting children and healthier food environments in schools, workplaces and public institutions. Urban planning that supports active living, women-centred health initiatives, community nutrition literacy and the revitalisation of diverse traditional food systems can further shift demand toward healthier choices. A coordinated, evidence-led approach is essential to protect India’s demographic dividend, curb the NCD surge and achieve SDG-aligned, sustainable nutrition outcomes.

 

 

Author(s) Details

Rekha Sharma
Sri Guru Gobind Singh College of Commerce, University of Delhi, Delhi, India.

 

Deepali Sharma
Sri Guru Tegh Bahadur Khalsa College, University of Delhi, Delhi, India.

 

Please see the book here :- https://doi.org/10.9734/bpi/fsarh/v4/6373

The Role of Leptin in Pathology of Polycystic Ovary Syndrome (PCOS) | Chapter 5 | An Overview of Disease and Health Research Vol. 6

 

Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder with significant impacts on women’s health. This intricate condition affects the endocrine and metabolic systems, characterised by features such as anovulation, infertility, obesity, insulin resistance, and the presence of polycystic ovaries. The aim of this review is to investigate the diagnostic potential of leptin in PCOS. The objective is to contribute to the existing body of knowledge by examining the relationship between leptin, the leptin receptor gene, obesity, and the various metabolic and hormonal irregularities associated with PCOS. In this regard, a comprehensive review of the literature from the past decade was conducted using databases such as Google Scholar, PubMed, and Scopus. The search strategy was aimed at gathering relevant studies on the relationship between leptin and PCOS, including genetic aspects. All the reviewed studies unanimously confirm the diagnostic potential of leptin in PCOS, emphasising its relevance in metabolic disorders associated with PCOS. Leptin is a fat cell-derived hormone that promotes a shift from carbohydrate to fat oxidation and regulates glucose homeostasis. Leptin, classified within the “tumour necrosis factor” family as a cell factor, is an amino peptide consisting of 167 amino acids. Leptin plays a crucial role in relaying metabolic signals to the brain and modulating the hypothalamic-pituitary-ovarian axis. PCOS involves hyperandrogenism, inappropriate luteinizing hormone secretion, insulin resistance, and hyperinsulinemia. The relationship between leptin and key factors in PCOS, such as gonadotropins, androgens, and insulin, remains a subject of ongoing research and discussions. The evidence gathered highlights elevated leptin levels, particularly in obesity, as a consistent characteristic of PCOS. The positive correlation between leptin and fat cell quantity underscores its potential role in PCOS pathogenesis. Leptin extends its impact beyond weight regulation, influencing oocyte maturation and activating ovarian enzymes involved in steroid production. Genetic studies on Leptin Receptor Gene (LEPR) polymorphisms indicate associations between specific genetic variants and PCOS susceptibility. Combining leptin with markers like Anti-Mullerian Hormone (AMH) shows high diagnostic accuracy, offering potential utility in clinical assessments. The multifaceted impact of leptin on both reproductive and metabolic aspects is evident. The findings support the integration of leptin with other markers for enhanced diagnostic accuracy, providing a promising avenue for future clinical applications in PCOS assessments.

 

 

Author(s) Details

Sushitha ES
Srinivas Institute of Medical Sciences and Research Center, India.

 

Prajna P Shetty
Srinivas Institute of Medical Sciences and Research Center, India.

 

Sasikala Kathiresan
AIIMS-Madurai, India.

 

Sauvit S Patil
Ramnarain Ruia Autonomous College, Affiliated to University of Mumbai, Mumbai, India.

 

Deepa M
AIIMS-Madurai, India.

 

Emil Phinehas
AIIMS-Madurai, India.

 

Bhavit Bansal
Sant Hirdaram Medical College of Naturopathy and Yogic Sciences for Women, India.

 

Delna NS
EMS Memorial Co-operative Hospital and Research Centre- College of Paramedical Sciences, India.

 

Please see the book here:- https://doi.org/10.9734/bpi/aodhr/v6/6253

Interrelation between Diabetes Mellitus and Periodontal Disease | Chapter 7| Medical Research and Its Applications Vol. 9

 The purpose of this chapter is to present scientific evidence for the links between Periodontitis and diabetes with a focus on potential common pathophysiologic pathways including those associated with inflammation, altered host responses and insulin resistance. The pathogenesis of periodontal disease is complex because it reflects a combination of the initiation and maintenance of the chronic inflammatory process by a diverse microbial flora and its numerous bacterial products. The interrelation between diabetes mellitus and inflammatory periodontal disease has been intensively studied for more than 50 years. It seems that there is a reciprocal relationship between these two illnesses: one tends to exacerbate the other, and treating one with care can help treat the other. This relationship is largely mediated by inflammation, which is responsible for the pathogeny and consequences of diabetes mellitus as well as periodontal disease. Conversely, periodontal infection can seriously impair the metabolic control of some diabetic patients. Moreover, treatment of periodontal disease and reduction of oral signs of inflammation may have a beneficial effect on diabetes. Further research is needed to clarify how inflammatory periodontal diseases may affect insulin resistance, glycemic control and the risk of developing other diabetic complications.

 

 

Author(s) Details

A. R. Gharat

Department of Periodontics, Nair Hospital Dental College, Floor no 2, Room no:202, Dr A L Nair Road, Opposite Maratha Mandir, Mumbai Central Pin: 400008, Maharashtra, India.

 

Please see the book here:- https://doi.org/10.9734/bpi/mria/v9/12567F

The Interplay of Leptin, Inflammation, and Obesity: A Comprehensive Review | Chapter 4 | Medicine and Medical Research: New Perspectives Vol. 5

Obesity has become a global health concern, with its prevalence rising dramatically in recent decades. This book chapter examines the complex relationship between leptin, inflammation, and obesity, synthesizing current research to provide a comprehensive understanding of their interconnected roles in metabolic health. Leptin's crucial function in regulating energy balance and metabolism was first explored, highlighting its connection to adipose tissue mass and its impact on appetite control and energy expenditure. This book chapter delves into the inflammatory aspects of obesity, discussing how excess adipose tissue contributes to a chronic low-grade inflammatory state, which in turn leads to various metabolic dysfunctions and related health complications. A key focus is placed on the dual role of leptin as both a metabolic regulator and a pro-inflammatory cytokine, elucidating how leptin dysregulation links obesity to inflammation and subsequent metabolic disorders. The chapter also considers the implications of leptin resistance in obesity and its contribution to sustained inflammation. Finally, potential therapeutic targets emerging from this intricate interplay were discussed, offering perspectives on managing obesity-related complications through interventions targeting leptin signaling and inflammatory pathways. This comprehensive analysis aims to enhance our understanding of the leptin-inflammation-obesity axis and its significance in developing effective strategies for obesity management and prevention of associated metabolic disorders.

 

Author (s) Details

Hemali Jha
Department of Internal Medicine, Integral Institute of Medical Sciences and Research, Lucknow, Uttar Pradesh, India.

 

Ishaan Tyagi
 Y Patil Medical College, Pune, Maharashtra, India.

 

Sylvester Noeldoss Lazarus
American University of Barbados, Wildey, Barbados (Caricom).

 

Anamika Chakraborty Samant
Chaitanya Hospital and Obesity Centre, Virar, Palghar, Maharashtra, India.

 

Jitendra Patel

Department of Physiology, GMERS Medical College, Vadnagar, Gujarat, India.

 

Please see the book here:- https://doi.org/10.9734/bpi/mmrnp/v5/1989

The Silent Drivers of Obesity: Pharmaceuticals and Microbes| Chapter 11 | Disease and Health Research: New Insights Vol. 5

 

Abstract: The present study discusses the role of microbiota in the metabolism of psychotropic drugs as well as the dysbiosis associated with the antimicrobial properties of these agents. Psychotropic drugs are endowed with antimicrobial properties and are known to alter the gut microbiome, selectively depleting the Bacteroidetes phylum, and leading to obesity.

 

It is well-established that obesity has reached epidemic proportions throughout the world, however, it is less known that its rates are two to three times higher in mentally ill patients compared to the general population. Both psychotropic drugs-induced dysmetabolism and high fat diet-related weight gain present with a common enteric microbial pattern, and depletion of the Bacteroidetes phylum, suggesting an overlapping pathology. Others have opined that the loss of Bacteroidetes-generated metabolites is the common denominator of weight gain induced either by an unhealthy diet or psychotropic drugs.

 

Since germ-free animals exposed to psychotropics have not demonstrated weight gain, altered commensal flora composition is believed to be necessary and sufficient to induce dysmetabolism. Conversely, not only do psychotropics disrupt the composition of gut microbiota but the latter alter the metabolism of the former. For example, drug metabolism starts in the gut, rather than the liver as it was construed in the past.

 

The potential biomarkers reflecting the status of the Bacteroidetes phylum have been discussed and a closer look at nutritional interventions, fecal microbiota transplantation, and transcranial magnetic stimulation strategies has been taken that may lower obesity rates in chronic psychiatric patients. Obesity is a modifiable risk factor of general morbidity, therefore restoring the physiological levels of Bacteroidetes phylum by various strategies may attenuate or reverse the excess weight in chronic psychiatric patients. If validated, the biological markers described here may offer the clinician additional feedback to estimate the imminence of weight-related complications.

Author (s) Details

Adonis Sfera
Department of Psychiatry, Loma Linda University, Loma Linda, CA, United States and Department of Psychiatry, Patton State Hospital, San Bernardino, CA, United States.

 

Carolina Osorio
Department of Psychiatry, Loma Linda University, Loma Linda, CA, United States.

 

Eddie Lee Diaz
Department of Psychiatry, Patton State Hospital, San Bernardino, CA, United States.

 

Gerald Maguire
Department of Psychiatry, University of California, Riverside, Riverside, CA, United States.

 

Michael Cummings
Department of Psychiatry, Patton State Hospital, San Bernardino, CA, United States.

 

Please see the book here:- https://doi.org/10.9734/bpi/dhrni/v5/2250

Determining the Effect of a High Fructose Diet on Interscapular Brown Adipose Tissue LPL, Cellularity and Lipid Deposition in Aging Congenic Obese-T2DM Rats | Chapter 10 | Contemporary Research and Perspectives in Biological Science Vol. 2

 

The present study aimed to determine the effect of a high fructose diet on brown adipose tissue development in aging congenic obese T2DM rats. The physiological merits of brown adipose tissue (BAT) metabolism as an efficient potential energy buffer that when deficient, may be a contributor to excess fat accretion and to the development of obesity in man and animals.  As such, it offers to be a potential target for therapies that could be developed for its treatment. To determine the effects of dietary fructose consumption on development and cellularity of brown adipose tissue in T2DM, groups of lean and obese SHR/Ntul//-cp rats demonstrating insulin resistance (IR) and heritable T2DM were fed diets containing 54% (w/w) carbohydrate as cornstarch (CS diet) or equal parts CS plus fructose (CSF diet) plus essential proteins, fats, vitamins, minerals, and dietary fiber from one to nine months of age.  The SHR/Ntul//-cp rat is a congenic animal model in which the only genetic difference between the phenotypes is the epigenetic inheritance and natural expression of the obese (-cp) trait, which is distinct from dietary, toxicologic, or pharmacologic factors and is accompanied by the development of chronic insulin resistance (IR) and non-insulin-dependent diabetes (T2DM) shortly after weaning in the obese phenotype.

 

The effects of this study indicate that final weight gain and Interscapular brown adipose tissue mass and cellularity are significantly greater in the obese than in the lean phenotype. In addition, the effects of a high fructose diet resulted in only modest increases in body weight gain, and in differential effects on IBAT cellularity and cell lipid content. Weight gain of obese >> lean and was greater when fed the CSF than the CS diet in both phenotypes; Interscapular brown adipose tissue (IBAT) mass of obese >> Lean and was similar in both phenotypes.  IBAT Mass: Body weight of Obese >> lean, and trended greater in lean CSF vs CS but less in Obese CSF vs CS. IBAT cell size and lipid content of obese >> lean, and the CS vs CSF diet was similar in lean but decreased in the obese phenotype. IBAT cell number of obese >>> lean, while IBAT cell number of lean CSF > lean CS, but IBAT cell number of obese was similar with both diets.  Lipoprotein lipase activity (LPL) of lean >> obese and trended to be greater with the CSF than the CS diet in both phenotypes and IBAT tissue lipid content of obese >> lean with a trend toward CSF > CS in both phenotypes. These results indicate that IBAT development occurs via hyperplasia and hypertrophy in the Obese phenotype of this strain and that long term consumption of the high Fructose diet enhances IBAT cellularity in the lean phenotype while the IBAT cellularity was maximally enhanced by both diets in the obese phenotype.

 

These results further indicate that the impact of long-term consumption of a high fructose diet throughout much of the natural lifespan impacts the development of IBAT mass and cellularity differentially in the lean and obese+T2DM phenotype, likely at least in part due to contributions of longstanding IR in the obese+T2DM animals. Because IR is known to impede cellular glucose uptake in isolated brown adipocytes as an essential process in the expression of cellular thermogenic responses, any potential mechanisms to override or bypass the process or decrease the magnitude of IR would be presumed to exert a beneficial effect. Fructose may increase the potential for the expression of IBAT development and the expression of non-shivering thermogenesis in response to changes in food and environment because it can enter tissues independently of insulin activities, for example, through the GLUT1 and GLUT5 transporters. Nevertheless, in the current investigation, it was discovered that overall fructose consumption was neither significantly advantageous nor ameliorative in resolving crucial parameters of brown adipose tissue expression as contributors to the development of obesity in the obese+T2DM phenotype.

Author (s) Details

Orien L Tulp
Colleges of Medicine and Graduate Studies, University of Science Arts and Technology, Montserrat, BWI MSR1110 and Einstein Medical Institute, N. Palm Beach, FL, 33408, USA.

 

 

Please see the book here:- https://doi.org/10.9734/bpi/crpbs/v2/2210

Gallstones in Tikrit, Iraq: A Population–based Study on the Roles of Obesity, Gender, and Age | Chapter 1 | An Overview of Disease and Health Research Vol. 1

 

Background: Gallstone disease (Cholelithiasis) is among the most common gastrointestinal diseases across the globe. Its prevalence and the risk factors associated with it, however, vary markedly from one region to another. Although awareness of gallstone disease is rising in Iraq, data regarding its prevalence and associated risk factors are limited.

Aim: This study aimed to carry out an immense investigation into the prevalence of gallstones in Tikrit (Iraq) while trying to highlight sex, age, and body mass index (BMI) as risk factors.

Methods: Cross-sectional study executed on 468 grown individuals in Tikrit, Iraq, during the months spanning May to October in the year 2019. Diagnosis of gallstone prevalence was carried out via abdominal ultrasound, plus calculation of participants' BMIs through their heights and weights. SPSS software is used for data analysis. Chi-square tests coupled with logistic regression models were deployed to check associations between demographic variables and gallstone prevalence.

Results: The total prevalence of gallstones was 20.5%. Females (28.4%) were affected significantly more than males (12.4%). Individuals whose BMI ≥ 25 kg/m² had a significantly higher risk of the formation of gallstones (OR=3.41;95%CI:2.18–5.33). Age was not a significantly associated factor with the formation of gallstones.

Conclusion: Obesity, particularly in females, is the leading cause of gallstone disease in Tikrit, Iraq. Results from this study should prompt public health initiatives that direct efforts toward obesity as a predisposing factor, along with screening the vulnerable population at an early stage.

 

Author (s) Details

Abdulhadi M. Jumaa
Department of Physiology, College of Medicine, Tikrit University, Iraq.

 

Ammar L. Hussein
Department of Biochemistry, College of Medicine, Tikrit University, Iraq.

 

Meqdam A. Khalaf
Department of Surgery, College of Medicine, Tikrit University, Iraq.

 

Please see the book here:- https://doi.org/10.9734/bpi/aodhr/v1/5254

Mechanistic Contributors to Subclinical Hypothyroidism in obesity: Review of Molecular Evidence for Impaired Thyroid Hormone Receptor Affinity and Actions from Rat Studies | Chapter 11 | Medical Science: Trends and Innovations Vol. 13

Obesity and its pathophysiologic sequela have become a burgeoning medical issue not only in Africa but worldwide. Obese and overweight patients may sometimes present with symptoms suggestive of disordered carbohydrate metabolism and thyroidal parameters including hypothyroidism. However, when the usual routine thyroid battery of labs comes back, they may identify markers of insulin resistance but often fail to identify any obvious abnormal findings in their hypothalamic-thyroidal axis. To determine the potential for subclinical thyroidal actions as a contributing factor for hormonal regulation of energy balance and the development of obesity and metabolic syndrome, studies of resting and catecholamine stimulated metabolism, in vivo thyroid hormone half-life, thyroid hormone binding characteristics and weight gain, groups of lean and obese congenic LA/Ntul//-cp rats were offered stock or high energy diets and in vivo and in vitro parameters of thyroid hormone action determined. The obese phenotype demonstrated impaired thermic responses to diet and environment and cold-induced thermoregulation, in association with decreases in plasma T3 but not T4 concentrations. Administration of I-131 T4 and I-131 T3 in the obese phenotype of corpulent rats resulted in clearance rates for T3, but T4 clearance was consistently prolonged by approximately 50% among the obese phenotype. The plasma half-life of T4 was ~50% longer in obese than in lean littermates, while the half-life of T3 was similar in both phenotypes. Measures of nuclear thyroid hormone receptor density were similar in both phenotypes, but receptor affinity for T3 was diminished in the obese phenotype, consistent with impaired thyroidal actions as a contributing factor for subclinical hypothyroidism in the obese phenotype of this strain. In conclusion, the current trends in the increasing prevalence of obese and overweight conditions will in all likelihood become a pressing global priority to identify and more fully characterize at the molecular, tissue and organ system levels of effective resolutions to the critical issues of overweight and obese conditions. A doable solution must be found, as urgency is emerging that signals that a metabolic and global healthcare epidemic is tantamount to a tsunami if left unattended.

 

 

Author (s) Details

Orien L Tulp
Department of Medicine, University of Science, Arts and Technology, Olveston, Montserrat, UK, Department of Medicine, Einstein Medical Institute, North Palm Beach, USA and Department of Natural Medicine, East West College of Natural Medicine, Sarasota FL, USA.

 

O F Obidi
Department of Medicine, University of Lagos, Lagos, Nigeria.

 

 

T C Oyesile
Department of Medicine, University of Lagos, Lagos, Nigeria.

 

Frantz Sainvil
Department of Medicine, University of Science, Arts and Technology, Olveston, Montserrat, UK, Department of Medicine, Einstein Medical Institute, North Palm Beach, USA and Department of Medicine, Broward College, Davie FL, USA.

 

Rolando Branly
Department of Medicine, University of Science, Arts and Technology, Olveston, Montserrat, UK and Department of Medicine, Broward College, Davie FL, USA.

 

A Sciranka
Department of Medicine, University of Science, Arts and Technology, Olveston, Montserrat, UK.

 

Syed AA Rizv
Department of Medicine, University of Science, Arts and Technology, Olveston, Montserrat, UK and Department of Medicine, Larkin Hospital, Miami FL, USA.

 

Aftab Awan
Department of Veterinary Medicine, Cambridge University, Cambridge, UK.

 

Michael Anderson
Department of Medicine, University of Science, Arts and Technology, Olveston, Montserrat, UK.

 

George P Einstein
Department of Medicine, University of Science, Arts and Technology, Olveston, Montserrat, UK and Department of Medicine, Einstein Medical Institute, North Palm Beach, USA.

 

Syed AA Rizvi

Department of Medicine, University of Science, Arts and Technology, Olveston, Montserrat, UK and Department of Medicine, Larkin Hospital, Miami FL, USA.

 

Please see the book here:- https://doi.org/10.9734/bpi/msti/v13/5230

Gastric Emptying Dynamics and Glycemic Responses in Obese and Diabetic SHR/N-cp Rat Models: Implications for Understanding Type II Diabetes | Chapter 13 | Medical Science: Trends and Innovations Vol. 12

Obesity and overweight conditions, separately or in concert with Type II Diabetes mellitus (T2DM), are now occurring globally with an alarming incidence throughout much of industrialized society. Disordered gastric physiology is a common observation in diabetes, including processes of both rapid emptying early in T2DM and in gastroparesis in later stages of both T2DM and Type 1, insulin-dependent diabetes. The purpose of the present study was to characterize the expression of the obese and obese+T2DM traits in the development of T2DM and its impact on gastric emptying and glycemic parameters when reared under identical conditions of diet and environment. To determine the characteristics of gastric emptying in lean, obese, and obese diabetic rats, measures of oral glucose tolerance (OGT) were determined, and glycemic parameters of obesity and type II diabetes (T2DM) were measured. The study was approved by the Institutional Animal Care and Use Committee. Fasting plasma Insulin, amylin, and markers of insulin resistance were greater in obese than in lean littermates and increased further in both young and old obese+T2DM rats. The oral glucose tolerance and glucose areas under the curve (AUCglc) were modestly impaired in obese LA/Ntul//-cp rats, with only a modest increment in the early phase (0 to +30 min post ingestion) of luminal glucose uptake. The OGT in obese+T2DM rats was markedly impaired, with additional progression in aging. The fractional AUCglc from 0 to+30 minutes was significantly increased in the obese+T2DM rats, and the acceleration in initial glycemic response of OGT was increased 6-fold in young T2DM rats and remained greatly elevated thereafter. The initial and late post-absorptive glycemic phase of the OGT in old obese individuals was greater than in younger obese T2DM. These results are consistent with epigenetic expression of obesity and obesity+T2DM and with dysregulation in the kinetics of gastric emptying analogous to Dumping Syndrome or Sirt1 dysregulation in the young obese-T2DM phenotype of the SHR/Ntul//-cp rats and the neurologic onset of gastroparesis in old T2DM SHR/Ntul//-cp rats. The result of this study indicates that the aberrant glycemic responses to a standard OGT in obese and obese-T2DM rats were consistent with accelerated gastric emptying in young obese+T2DM rats, in addition to glycemic responses consistent with the onset of gastroparesis in combination with insulin resistance in older obese+T2DM rats.  Thus, the Obese+T2DM rat is a useful model for the further investigation of the pathophysiology of obesity and T2DM as it occurs in man and animals.

 

Author (s) Details

 

Orien L Tulp
Colleges of Medicine and Graduate Studies, University of Science, Arts and Technology, USA.

 

Please see the book here:- https://doi.org/10.9734/bpi/msti/v12/4872

Ceramide Synthase Isoforms and Insulin Resistance: A Molecular Perspective | Chapter 12 | Achievements and Challenges of Medicine and Medical Science Vol. 2

The review analyzes the literature data that forms the basis for the "ceramide-centric" view of insulin resistance pathogenesis and obesity-associated diabetes mellitus type 2. The results of recent independent studies have shown that normal sphingolipid metabolism is one of the most important conditions for maintaining glucose homeostasis in the body. The lipid analysis of adipose tissue, skeletal muscles and liver in rodents with experimental obesity, as well as biopsic specimens of diabetics, indicate the high pathogenicity of specific ceramide family members. Analysis of the clinical material and the results of model experiments showed that increased expression of the isoenzyme CerS-6 positively correlated with the degree of resistance to insulin. The degree of pathogenicity is determined by the length of the acyl chain included in de novo synthesized ceramide with the involvement of one of the six ceramide synthase isoenzymes. Selective inhibition of the ceramide synthase-6 isoenzyme to reduce the tissue level of the most pathogenic C16:0-ceramide may be a promising approach for correcting insulin resistance. The creation of a specific inhibitor of CerS-6 will allow selectively to reduce the tissue content of C16:0-ceramide, which, apparently, may contribute to the development of a new direction of pathogenetically grounded pharmacological correction of obesity-associated insulin resistance.

 

Author (s) Details

Kuzmenko Dmitry Ivanovich
Department of Biochemistry and Molecular Biology, Clinical Laboratory Diagnostics of the Siberian State Medical University, SSMU, 634055, Tomsk, Moskovsky trakt, 2, Building 2. Russia.

 

Klimentyeva Tatyana Konstantinovna
Department of Biochemistry and Molecular Biology, Clinical Laboratory Diagnostics of the Siberian State Medical University, SSMU, 634055, Tomsk, Moskovsky trakt, 2, Building 2. Russia.

 

Please see the book here:- https://doi.org/10.9734/bpi/acmms/v2/2795

 

Unraveling the Weighty Enigma: Exploring the Intricate Relationship between Obesity and Intracerebral Hemorrhage | Chapter 4 | Achievements and Challenges of Medicine and Medical Science Vol. 2

Introduction: Obesity is a global health concern with significant implications for various medical conditions, including cerebrovascular diseases. Intracerebral hemorrhage (ICH), characterized by bleeding within the brain parenchyma, is a severe form of stroke. While obesity is linked to an increased risk of cardiovascular diseases, its specific relationship with ICH is not well understood. This study aims to explore how obesity influences the incidence, severity, and outcomes of ICH.

Methodology: A retrospective cohort study was conducted at D.Y. Patil Medical College, and Hospital Kolhapur, from 2019-2023. The cohort included 500 ICH patients, with detailed clinical and demographic data collected. Statistical analyses, including logistic regression and survival analysis, assessed the relationship between obesity and ICH incidence, severity, short-term survival, and long-term outcomes.

Results: Obesity was significantly associated with an increased incidence of ICH. Interestingly, obese patients showed a short-term survival advantage, with lower mortality rates in the weeks following ICH. However, this benefit diminished over time, with no significant differences in long-term outcomes across BMI categories. Obese patients did not exhibit greater ICH severity or complications compared to non-obese patients.

Conclusion: Obesity is associated with an increased risk of ICH and a paradoxical short-term survival advantage. However, this benefit fades over time, emphasizing the need for continued monitoring and tailored interventions in obese ICH patients.

 

Author (s) Details

Sagar Goya
D. Y. Patil Medical College, Kolhapur, Maharashtra, India.

 

Gayatri G. Dhavalshankh
Department of Pharmacology, D. Y. Patil Medical College, Kolhapur, Maharashtra, India.

 

Sheetal
Jawaharlal Nehru Medical College, Sawangi (Meghe), Wardha, Maharashtra, India.

 

Ganesh P. Dhavalshank
Department of Dermatology, D. Y. Patil Medical College, Kolhapur, Maharashtra, India.

 

Archana G. Dhavalshankh
Department of Pharmacology, D. Y. Patil Medical College, Kolhapur, Maharashtra, India.

 

Please see the book here:- https://doi.org/10.9734/bpi/acmms/v2/2938

Impact of Obesity Subtypes on Short-Term Weight Loss Following Vertical Sleeve Gastrectomy | Chapter 10 | Achievements and Challenges of Medicine and Medical Science Vol. 4

Background: Temporal prevalence studies of worldwide obesity have confirmed that this epidemic continues to worsen and investigators have suggested that the scope of this problem may indeed be underestimated. The pathogenesis of the condition is multifactorial and complex, and it has been suggested that early life exposure to environmental chemicals (termed obesogens) may be a major cause of this epidemic.

Aims: Vertical sleeve gastrectomy has become the most common surgical intervention for medically-complicated obesity. This study was designed to examine the distribution of clinical subtypes of obesity (e.g. psychosocial factors, genetic risk, or obesogens) and to identify the best candidates for vertical sleeve gastrectomy based on clinical subtype.

Study Design: This is a retrospective cohort study in a large, urban teaching hospital.

Place and Duration of Study: Center for Advanced Laparoscopic & Bariatric Surgery, MedStar Washington Hospital Center Washington, DC between October 2018 and June 2019.

Methodology: Consecutive new individuals (n=225) with medically-complicated obesity were evaluated preoperatively in an outpatient bariatric gastroenterology clinic. Subjects (n=17) were excluded. Eighty-four individuals underwent sleeve gastrectomy with a minimum of 6 months of postoperative follow up.

Results: Among the 3 subtypes, early life obesogen exposure was identified in 14.5% of individuals, genetic risk in 24.5% of individuals, and psychosocial factors in 61% of individuals. Percent excess weight loss (mean+/-SD) at 6 months is different among the three groups (pANOVA=.024). Individuals with genetic risk (38%+/-14) have significantly less weight loss (p=.029) than individuals with psychosocial factors (47%+/-15), while there is no difference compared to the obesogen subtype (41%+/-8.9).

Conclusion: The most common clinical subtype of obesity is psychosocial factors, and there is significantly higher short-term weight loss after sleeve gastrectomy in individuals with psychosocial factors. It was also noted that individuals with genetic risk have significantly less weight loss than individuals with psychosocial factors, while there is no difference compared to the obesogen subtype. Weight loss may be moderated by an individual’s genetic risk and early life obesogen exposure.

 

Author (s) Details

 

Raj A. Shah
Carilion Clinic and Virginia Tech Carilion School of Medicine, Roanoke, VA, USA.

 

Anand Nath
MedStar St. Mary’s Hospital, Leonardtown, MD, USA.

 

Timothy R. Shope
State University of New York Upstate Medical University, Syracuse, NY, USA.

 

Ivanesa L. Pardo Lameda
MedStar Washington Hospital Center and Georgetown University, Washington, DC, USA.

 

John S. Brebbia
MedStar Washington Hospital Center and Georgetown University, Washington, DC, USA.

 

Timothy R. Koch
Salem VA Medical Center and Virginia Tech Carilion School of Medicine, Salem, VA, USA.

 

Please see the book here:- https://doi.org/10.9734/bpi/acmms/v4/3174 

Impact of Obesity Subtypes on Short-Term Weight Loss Following Vertical Sleeve Gastrectomy | Chapter 10 | Achievements and Challenges of Medicine and Medical Science Vol. 4

Background: Temporal prevalence studies of worldwide obesity have confirmed that this epidemic continues to worsen and investigators have suggested that the scope of this problem may indeed be underestimated. The pathogenesis of the condition is multifactorial and complex, and it has been suggested that early life exposure to environmental chemicals (termed obesogens) may be a major cause of this epidemic.

Aims: Vertical sleeve gastrectomy has become the most common surgical intervention for medically-complicated obesity. This study was designed to examine the distribution of clinical subtypes of obesity (e.g. psychosocial factors, genetic risk, or obesogens) and to identify the best candidates for vertical sleeve gastrectomy based on clinical subtype.

Study Design: This is a retrospective cohort study in a large, urban teaching hospital.

Place and Duration of Study: Center for Advanced Laparoscopic & Bariatric Surgery, MedStar Washington Hospital Center Washington, DC between October 2018 and June 2019.

Methodology: Consecutive new individuals (n=225) with medically-complicated obesity were evaluated preoperatively in an outpatient bariatric gastroenterology clinic. Subjects (n=17) were excluded. Eighty-four individuals underwent sleeve gastrectomy with a minimum of 6 months of postoperative follow up.

Results: Among the 3 subtypes, early life obesogen exposure was identified in 14.5% of individuals, genetic risk in 24.5% of individuals, and psychosocial factors in 61% of individuals. Percent excess weight loss (mean+/-SD) at 6 months is different among the three groups (pANOVA=.024). Individuals with genetic risk (38%+/-14) have significantly less weight loss (p=.029) than individuals with psychosocial factors (47%+/-15), while there is no difference compared to the obesogen subtype (41%+/-8.9).

Conclusion: The most common clinical subtype of obesity is psychosocial factors, and there is significantly higher short-term weight loss after sleeve gastrectomy in individuals with psychosocial factors. It was also noted that individuals with genetic risk have significantly less weight loss than individuals with psychosocial factors, while there is no difference compared to the obesogen subtype. Weight loss may be moderated by an individual’s genetic risk and early life obesogen exposure.

 

Author (s) Details

 

Raj A. Shah
Carilion Clinic and Virginia Tech Carilion School of Medicine, Roanoke, VA, USA.

 

Anand Nath
MedStar St. Mary’s Hospital, Leonardtown, MD, USA.

 

Timothy R. Shope
State University of New York Upstate Medical University, Syracuse, NY, USA.

 

Ivanesa L. Pardo Lameda
MedStar Washington Hospital Center and Georgetown University, Washington, DC, USA.

 

John S. Brebbia
MedStar Washington Hospital Center and Georgetown University, Washington, DC, USA.

 

Timothy R. Koch
Salem VA Medical Center and Virginia Tech Carilion School of Medicine, Salem, VA, USA.

 

Please see the book here:- https://doi.org/10.9734/bpi/acmms/v4/3174 

Impact of Luminal α-Glucosidase Inhibition on Lipogenic and Glycaemic Enzymes in Obese Diabetic Rats: Consequences for the Treatment of Type 2 Diabetes | Chapter 5 | Medical Science: Trends and Innovations Vol. 10

The global prevalence of obesity+T2DM is approaching endemic proportions throughout much of Industrializes society, with no easy resolution on the horizon. In these conditions, the activities of certain insulin-linked glycemic and lipogenic enzymes including glucokinase, malic enzyme, and glucose-6-phosphate dehydrogenase typically become elevated, as consistent contributors to the elevations in plasma lipid profiles and relative adiposity that are also typically observed in such individuals. The use of miglitol, an alpha-glucosidase inhibitor, has been shown to cause a dose-related delay in luminal sucrose digestion in the upper regions of the small intestine, and in an attenuated and delayed response in the glycemic excursions that normally follow a carbohydrate meal. This study aims to determine the effect of delayed carbohydrate (sucrose) digestion in type 2 diabetes mellites on the activity of glycemic and lipogenic enzyme parameters. Groups (n=6-8/group, mean BW 264±5g vs 263±4g) of young adult male obese T2DM (diabetic) SHR/Ntul//-cp rats were fed a nutritionally complete USDA-formulated diet containing 54% sucrose (CONTROL) or the same diet with 150 mg of the luminal α-glucosidase inhibitor miglitol (MIG) for up to 8 weeks. Standardized analytical procedures established in our laboratory were utilized to quantify the findings. All the collected data were analyzed via standard statistical procedures including student t-test, ANOVA, and Pages L test for trend analysis. All animals demonstrated profound (4+) glycosuria by 8 weeks of age to confirm T2 DM. Body Weight Gain (BWG), relative adiposity and glycosuria were elevated in control animals but decreased significantly following miglitol. Measures of oral Glucose Tolerance (OGT, 250 mg glucose/kg BW, via gavage), AUC for glucose and insulin response to OGT and glycated hemoglobin (HbA1c) were elevated in controls and decreased by 20% after miglitol treatment. Hepatic Glucokinase (GK), malic enzyme (ME) and glucose-6-phosphate dehydrogenase (G6PD) were elevated in the Controls and decreased toward normalization following miglitol treatment. In conclusion, these observations indicate that an 8-week course of miglitol is an effective agent in improving the magnitude of the elevated glycemic and lipogenic enzymes and their impact on developing adiposity in the SHR/Ntul//-cp genetic rat strain of obesity+T2DM and may be an effective adjunct in clinical management of obesity, hyperlipidemia and T2DM. In future studies, it would be productive to extend the luminal therapeutic options beyond the post-adolescent life stage of this investigation to more fully determine the long-term potential of the physiological benefits of luminal α-glucosidase inhibition health and longevity in an animal model predisposed to early onset obesity, insulin resistance and T2DM.

 

Author (s) Details

Orien Lee Tulp
University of Science, Arts and Technology, USA.

 

Please see the book here:- https://doi.org/10.9734/bpi/msti/v10/4703

Mucosal Immunity and Novel Prophylactic Strategy to Combat COVID-19 | Chapter 1 | Disease and Health Research: New Insights Vol. 9

The study aims to explore the role of mucosal immunity in combating COVID-19 with the objective of developing novel prophylactic and therapeutic strategies. Coronavirus disease 2019 (COVID-19) emerged as an expeditiously growing pandemic, in the human population caused by the highly transmissible RNA virus severe acute respiratory syndrome of coronavirus 2 (SARS-CoV-2). In clinical settings, SARS-CoV-2 infection can be elucidated on the basis of amplification of viral RNA from nasopharyngeal swab samples, and saliva tests (less invasive in nature), but sometimes faeces tests show the presence of SARS-CoV-2 RNA even prior to symptoms appear and also long after a patient has tested negative from a conventional swab. The interplay of SARS-CoV-2 infection predominantly occurs at the angiotensin-converting enzyme 2 receptor and transmembrane protease serine-type 2 positive (ACE2 + TMPRSS2+) epithelial cells of the mucosal surfaces like nasal, oral mucosae, and/or the conjunctival surface of the eye where it interacts with the immune system. The largest integrant of the entire immune system is the mucosal immune system which is augmented to provide a defence mechanism against various environmental pathogens at the mucosae. The primary host response towards the pathogen starts from an immune microenvironment of nasopharynx-associated lymphoid tissue (NALT) and mucosa-associated lymphoid tissue (MALT). The presence of exhausted lymphocytes, lymphopenia, pneumonia, and cytokine storm is the hallmark of COVID-19. The multifaceted nature of co-morbidity factors like obesity and type 2 diabetes and their effects on immunity can alter the pathogenesis of SARS-CoV-2 infection. Adipose tissue is a crucial endocrine organ that secretes a plethora of factors like adipokines, cytokines, and chemokines that have a profound impact on metabolism and augment the expression of mucosal pro-inflammatory cytokines, like tumour necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ), and the interleukin-12 (IL-12)/IL-23. Mucosal immunization could be a superior approach to activate mucosal and systemic immune responses against pathogenic invasion at mucosal surface entry ports. Mucosal vaccines are also able to generate strong systemic humoral immunity—required to neutralize any virus particle that dodges the primary immune response. In the case of various vaccines, the weakening of vaccine-induced immunity is associated with breakthrough infections. On the other hand, several lines of evidence suggest that mucosal immunization via natural infection or vaccination induces a more robust immune response in respiratory mucosa, which is the prime target of SARS-CoV-2 infection. To develop an efficient vaccine against mucosal pathogens, contemplation of the design of the delivery route, immunomodulatory features, and adjuvants are very important. In this article,  evidence was provided to understand the significant role of mucosal immunity, along with secretory and circulating immunoglobulin A (IgA) antibodies in generating a novel mucosal vaccine against COVID-19. Moreover, along with mucosal vaccines, a look must be given to combination treatment strategies with plant bioactive molecules. Glycan-binding lectins against viral proteins for targeted activation of the mucosal immune response are one such example. These may play a promising role in halting this emerging virus. In this review, the different aspect of mucosal immunization and their probable prospect against the COVID-19 pandemic have been summarized. Further study on the formulation of nasal spray or inhaler with such plant bioactive molecules or engineered antibodies will be a potent therapeutic and prophylactic strategy in the prevention of a larger array of SARS-CoV2 with reduced side effects.

 

Author (s) Details

 

Swapan K. Chatterjee
Molecular Pharma Pvt. Ltd., 102A Windsor Palace, 6A, Iron Side Road, Kolkata 700019, West Bengal, India.

 

Snigdha Saha
Molecular Pharma Pvt. Ltd., 102A Windsor Palace, 6A, Iron Side Road, Kolkata 700019, West Bengal, India

 

Maria Nilda M. Munoz
Cagayan State University, Tuguegarao City & De La Salle University, Manila 0900, Philippines.

 

Please see the book here:- https://doi.org/10.9734/bpi/dhrni/v9/2196

The Association of Obesity with Isolated Systolic Hypertension: Evidence from a Nationwide Survey in Mongolia | Chapter 10 | Disease and Health: Research Developments Vol. 2

Purpose: To determine the association of obesity with Isolated systolic hypertension among people aged 15-64 years.

Materials and Methods: The study design is a population-based cross-sectional study. An association of obesity with Isolated systolic hypertension (ISH) using data from the “Mongolian STEPS Survey on the prevalence of non-communicable disease and injury risk factors-2009” was examined. A total of 5456 people participated in this study. ISH was defined as systolic blood pressure≥140 mmHg and diastolic blood pressure<90 mmHg. Body weight, height, waist circumference, body fat content, and blood pressure were measured in all survey participants. One in three survey participants was tested for blood glucose, cholesterol, triglycerides, low-density lipoprotein and high-density lipoprotein in serum.

Results: Mean body weight, mean body mass index and waist circumference in people with ISH were statistically and significantly higher compared to the people with normal blood pressure. The prevalence of obesity in the group with ISH was 21.3 percent. It was statistically and significantly higher than in the normotensive group (11.6 percent) (p=0.0001). The prevalence of central obesity was 55.0 percent in the group with ISH and 45.0 percent in the normotensive group. In terms of gender, central obesity was 76.3 percent in females with ISH and 42.0 percent in males with ISH (p=0.0001). The findings demonstrate that the prevalence of central obesity is significantly higher among females with ISH than males.  Body fat content was high and very high in 66.6 percent of the people with ISH and in 50.5 percent of the people with normal blood pressure (p=0.0001). Body fat content is higher in the group with ISH compared to the normotensive group without gender difference. (p=0.0001) . The association between obesity and ISH by univariate logistic regression analysis was studied. As the study result, the risk of ISH is 1.5 times more in people with central obesity, 2.3 times more in the obese by BMI, and 2.1 times more in people with increased body fat (p=0.003, p=0.0001). On confirmation of multiple logistic regression analysis, age, gender, central obesity, excessive salt intake and increasing blood glucose were independent risk factors for ISH. Central obesity, excessive salt intake and increasing blood glucose are related to the lifestyle of people and those are modifiable risk factors for ISH. 

Conclusions: It was revealed in our study that among 15-64-year-olds, an increase in body mass index, fat content and waist circumference are risk factors for Isolated systolic hypertension. The prevalence of central obesity is significantly higher among females with ISH than males. The risk for Isolated systolic hypertension is 2 times higher in people with central obesity.

 

Author (s) Details

 

Dechmaa J
Internal Department, Ach Medical University, Mongolia.

 

Bolormaa I
National Center for Public Health, Mongolia.

 

Otgontuya D
Asia Development Bank, Mongolia.

 

Davaalkham D
School of Public Health, Mongolian National University of Medical Sciences, Mongolia.

 

Narantuya D
The Third State Central Hospital, Mongolia.

 

Please see the book here:- https://doi.org/10.9734/bpi/dhrd/v2/3646

Effects of Short-Term Almonds and Walnuts Intake on Serum Fatty Acid Composition, Metabolic Profile and Adiposity on Obese Adults | Chapter 6 | Disease and Health: Research Developments Vol. 2

Background: Obesity has emerged as a serious public health threat in the 21st century. According to the 2016 National Health and Nutrition Survey of the Mexican population, the prevalence of overweight and obesity is 72.5% in adults aged 20 and older.

Purpose: The purpose of the study is to evaluate changes in serum fatty acids, metabolic profile and inflammation markers after a dietary intervention of 15g of walnuts and 15g of almonds for 8 weeks in obese subjects.

Patients and Methods: A total of 48 sedentary obese grade I subjects (13 men and 35 women) of 30 to 50 years old without evidence of chronic degenerative, infectious, or neoplastic diseases, was studied. Anthropometric measures, body composition, serum glucose, lipid profile, insulin, lipocalina-2, high sensitivity C-reactive protein (hsCRP), adiponectin, and fatty acids profile were analyzed at the baseline and after 8 weeks of dietary intervention. Data normality was tested using the Kolmogorov-Smirnov test. The anthropometric and metabolic data were expressed as the mean ± standard deviation. Differences between groups were examined using the paired t-test. Non-parametric variables were transformed into logarithms. In order to examine the size effect of each anthropometric and metabolic parameter, we used the Cohen d. The statistical significance was set at p<0.05.

Results: A significant decrease in all measures of obesity (weight, waist circumference, hip circumference, BMI, and fat mass, p<0.0001) was found. The adiponectin (30.4%, p=0.007), lipocalin-2 concentrations (17.9%, p=0.014), and total polyunsaturated fatty acids (PUFAs) percentage (1.6% p=0.040) significantly increased after intervention, particularly the eicosapentaenoic acid and docosahexaenoic acid percentages were increased marginally. A significant decrease in saturated fatty acids levels (3%, p=0.001), in particular the myristic acid (C:14), and palmitic acid (C:16), in total cholesterol (6.7%, p=0.01), and LDL (11.4%, p=0.002) levels, and in all measures of obesity (weight, waist circumference, hip circumference, BMI and fat mass, p<0.0001) were found. The effect size for the intervention was large for all measures of obesity, and moderate for BMI, adiponectin, palmitic acid, and palmitoleic acid.

Conclusion: In conclusion, a significant increase of 30% in adiponectin and LCN2 (17.9%) concentrations were found. Additionally, a significant decrease in all measures of obesity, total cholesterol, and LDL concentrations after the intervention was observed. The SFA percentage significantly decreased, in particular, the myristic acid (C:14), and palmitic acid (C:16). The total PUFAs percentage significantly increased, and particularly the percentages of the eicosapentaenoic acid (EPA, C:20:5 ω-3) and docosahexaenoic acid (DHA C:22:6 ω-3) marginally increased. The effect size was large for all measures of obesity, except for BMI as well as for adiponectin which was moderate. Only in baseline, significant positive correlations of total saturated fatty acids, lauric and stearic acids with hsCRP concentration, and Myristic acid with triglycerides were found. This study data show that the consumption of almonds and walnuts for a short time may improve the metabolic state and measures of obesity.

 

Author (s) Details

 

Mónica I. Cardona-Alvarado
Department of Medical Science, Division of Health Sciences, Campus Leon, University of Guanajuato, Leon, Mexico.

 

Francisco J. Ortega
Department of Diabetes, Endocrinology and Nutrition (UDEN), Institut d’Investigació Biomédica de Girona (IdIBGi), CIBER de la Fisiopatología de la Obesidad y la Nutrición (CIBERobn, CB06/03) and Instituto de Salud Carlos III (ISCIII), Girona, Spain.

 

Enrique Ramírez-Chávez
Department of Biotechnology and Biochemistry, Cinvestav Unidad Irapuato. Guanajuato, México.

 

María Elizabeth Tejeroa
Laboratory of Nutrigenomics and Nutrigenetics, National Institute of Genomic Medicine, Mexico.

 

Jorge Molina-Torre
Department of Biotechnology and Biochemistry, Cinvestav Unidad Irapuato. Guanajuato, México.

 

José M. Fernández-Real
Department of Diabetes, Endocrinology and Nutrition (UDEN), Institut d’Investigació Biomédica de Girona (IdIBGi), CIBER de la Fisiopatología de la Obesidad y la Nutrición (CIBERobn, CB06/03) and Instituto de Salud Carlos III (ISCIII), Girona, Spain.

 

Elva L. Perez-Luque
Department of Medical Science, Division of Health Sciences, Campus Leon, University of Guanajuato, Leon, Mexico.

 

Please see the book here:- https://doi.org/10.9734/bpi/dhrd/v2/3536