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

Insulin Resistance Contributes to Neuroinflammation, Cognitive Decline and Brain Senescence in Congenic Obese LA/Ntul//-cp Rats | Chapter 9 | Advancement and New Understanding in Medical Science Vol. 7

Search for a suitable an animal model may prove to be more productive to determine if insulin resistance and its direct metabolic sequelae might be significant co-contributors to the neuronal declines that occur in NIDDM, obesity, and progression of dementia conditions. The burgeoning prevalence of obesity and overweight conditions from the age of adolescence and throughout the lifespan has reached epidemic proportions in industrialized nations throughout the globe. One of the most prevalent findings in obesity is the emergence of insulin resistance, which is linked to both a persistent inflammatory state and systemic hypoxia in adipose tissue. Insulin resistance impacts several aspects of substrate oxidation and oxidative free radical production in brain and somatic tissues, and it is likely that adipose tissue depots are the source of cytokine-linked chronic inflammation. In studies with aging congenic lean and obese rats chronic hyperinsulinemia and brain shrinkage has now been reported, albeit it in the absence of Type 2 diabetes (NIDDM), hypertension (HTN) or other comorbidities, thereby suggesting that aspects of disordered substrate metabolism including insulin resistance as commonly observed in obesity may be a key contributory factor in the development of a neuroinflammatory linked brain shrinkage with accompanying decreases in brain mass, protein and DNA content, and which were further compromised when fed an isocaloric high vs. a low glycemic insulinogenic diet containing sucrose vs. cornstarch respectively. These findings imply that in this strain of obese rats, chronic insulin resistance due to obesity, which is at least partially caused by dietary variables, is a plausible independent risk factor in the development of neuroinflammation, DNA damage, brain shrinkage, and neural senescence.

Author(s) Details:

Orien L. Tulp,
Colleges of Medicine and Graduate Studies, University of Science Arts and Technology, Montserrat, British West Indies, MSR1110 and the Einstein Medical Institute, North Palm Beach, FL 33409, USA.

Please see the link here: https://stm.bookpi.org/ANUMS-V7/article/view/13427

Determining the Effect of High Carbohydrate Diets on Brain Composition and Senescence in Aging Hyperinsulinemic Obese LA/Ntul//-cp Rats | Chapter 12 | Novel Research Aspects in Medicine and Medical Science Vol. 2

 This division determine the effect of corpulent phenotype and the carbohydrate type resulted in alterations in intellect composition in the corpulent phenotype of the congenic LA/Ntul//-cp rat, groups (n= 8 rats/group) of male littermate lean and corpulent rats were fed standardized isocaloric diets holding 54% (w/w) cornstarch (ST diet) or 54% (w/w) sucrose (SUC diet) from 1 just before 10.5 ± 0.5 months of age. Malnutrition is a extensive global public health issue that donates to several able to be consumed-related non-able to be contracted illnesses. In reduced-income nations, adult food is frequently missed. In low- and middle-proceeds nations, both two-fold malnutrition (over and undernutrition) and food transition survive. The current popular emphasis on liquid produced by mammals diets has resulted in an upwards shift in abstinence from food carbohydrate use. The strain's obese phenotype exhibits hypertrophic-hyperplastic obesity all along early postweaning development and early beginning chronic hyperinsulinemia outside NIDDM. The total fat, protein, and DNA of typical aliquots of dissected brain tissues were resolved. When fed the SUC meat as opposed to the ST diet, frame weights of obese >> lean mammals were higher in both genotypes. In rats augment the SUC diet compared to the ST diet, intellect mass was a little smaller in lean individuals distinguished to fat individuals. Brain total Protein and DNA content of lean rats were > corpulent rats and were modestly Lower in SUC than ST augment rats in both phenotypes, but the percent of lipid content was equivalent to brain bulk. The decreased intelligence mass was characterized by balanced decreases in total lipid, brain protein and intellect DNA content and were further impaired when augment the insulinogenic sucrose diet. Total body fat bulk of obese was considerably greater than happen in lean littermates and was only modestly better in SUC than ST fed rats in both phenotypes. These results signify that brain development and cellular growth is impaired in the aging, hyperinsulinemia-likely obese phenotype concerning this strain, were further impaired when augment SUC than ST diets, and the decreased brain limits were likely associated with happening of a chronic neuronal angering syndrome common to overdone fat accretion and corpulence, resulting in impulsive brain senescence.

Author(s) Details:

Orien L. Tulp,
Colleges of Medicine and Graduate Studies, University of Science Arts and Technology, Montserrat, MSR1110, British West Indies and The Einstein Medical Institute, NPB, Florida-34040, USA.

Please see the link here: https://stm.bookpi.org/NRAMMS-V2/article/view/11843

Combined Intranasal Insulin/Saxagliptin/Metformin Therapies Ameliorates the Effect of Combined Oral Contraceptives (Cos)-Induced Metabolic Syndrome (MetS) with a Major Target on Glucose Metabolism in Adult Female Wistar Rats: A Recent Study | Chapter 10 | New Horizons in Medicine and Medical Research Vol. 12

This study's goal is to assess the impact of long-term usage of combination oral contraceptives (COC; ethinyl estradiol and levonorgestrel) on metabolic syndrome indicators in adult female wistar rats, as well as any potential therapeutic treatment.

64 female Wistar rats were given either distilled water, Norethindrone, COC, Intranasal Insulin, Saxagliptin, Metformin, or INI+MET or INI+SAX in this study. After 8 weeks of COC exposure, the mice were separated into therapeutic groups. Indicators such as changes in body weight, insulin levels, inflammatory cytokines, glycated haemoglobin (Hb1Ac), and fasting blood glucose (FBG) levels were assessed. Treatment with INI+SAX and INI+MET considerably decreased FBG and Hb1Ac levels, while also significantly raising insulin levels in the INI+MET groups (p (leq) 0.05). Analysis of the serum lipid profile showed a statistically significant decrease in HDL levels, which were significantly increased in the INI+SAX group. In the INI+MET group, the decreased catalase activity shown in the COC group was reversed (p (leq) 0.05). The effects of COC therapy on the level of TNF-(alpha) were not significantly increased, while the effects of INI and INI + MET were. It has been proven that using MET, SAX, and INI together can reverse a number of MetS indices. This project will include a clinical phase to support and validate the preclinical findings.

Author(s) Details:

Saheed Olanrewaju Afolabi,

Department of Pharmacology and Therapeutics, University of Ilorin, Ilorin, Nigeria.

Joy Folahan,

Department of Pharmacology and Therapeutics, University of Ilorin, Ilorin, Nigeria.

Olalekan Agede,

Department of Pharmacology and Therapeutics, University of Ilorin, Ilorin, Nigeria.

Olufunke Olorundare,

Department of Pharmacology and Therapeutics, University of Ilorin, Ilorin, Nigeria.

Please see the link here: https://stm.bookpi.org/NHMMR-V12/article/view/7279