Effects of Methylmercury and Theaflavin Digallate on Adipokines in Mature 3T3-L1 Adipocytes: A Recent Study | Chapter 3 | Current Advances in Chemistry and Biochemistry Vol. 6

 Diabetes is a leading cause of morbidity around the world, and it is frequently associated with obesity, metabolic syndrome, and other inflammatory diseases associated with aging. Environmental factors such as metals and persistent organic pollutants, in addition to genetic and lifestyle factors, may increase the severity or lower the threshold of these conditions. Methylmercury is toxic to adipocytes in cell culture and may affect adipokine secretion. The effects of different concentrations of theaflavin digallate on methylmercury-exposed 3T3-L1 adipocytes in cell culture were investigated in this study. Resistin, adiponectin, and the lipid peroxidation product 4-hydroxynonenal (4-HNE) were all secreted. Lipid (Oil Red O) staining was used to evaluate the treatment of adipocytes. When compared to control cells, methylmercury exposure increased the levels of resistin, adiponectin, and 4-HNE. Cells treated with methylmercury had fewer adipocytes and clumped lipid droplets. These findings suggest that methylmercury causes reactive oxygen species to be produced, resulting in the development of an inflammatory response. Methylmercury was reduced by theaflavin-3,3′-digallate. maintaining adipocyte morphology and adiponectin, resistin, and 4-hydroxynonenal secretion patterns Other anti-inflammatory and signaling agents could be tested at the biochemical level using this experimental model system before being studied in animal models. To gain a better understanding of the anti-oxidative effects of polyphenolic compounds, different TF-3 concentrations can be used.

Authoor (S) Details

Shubhangi Chauhan
Department of Chemistry and Biochemistry, University of Alaska Fairbanks, Fairbanks, AK 99775-6160, USA and Institute of Arctic Biology, University of Alaska Fairbanks, Fairbanks, AK 99775-7000, USA.

Kriya Dunlap
Department of Chemistry and Biochemistry, University of Alaska Fairbanks, Fairbanks, AK 99775-6160, USA and Institute of Arctic Biology, University of Alaska Fairbanks, Fairbanks, AK 99775-7000, USA.

Lawrence K. Duffy
Department of Chemistry and Biochemistry, University of Alaska Fairbanks, Fairbanks, AK 99775-6160, USA and Institute of Arctic Biology, University of Alaska Fairbanks, Fairbanks, AK 99775-7000, USA.

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A Comparative Cross-Sectional Study on Interplay of Adipokines in the Pathogenesis of Essential Hypertension in Ghana | Chapter 5 | Research Trends and Challenges in Medical Science Vol. 6

 Background: Mechanistic risk factors for hypertension are the renin-angiotensin-system (RAS), endothelial dysfunction and the sympathetic nervous system. The research sought to elucidate the interplay of adipokines in essential hypertension pathogenesis. Methodology: 200 confirmed hypertensive KATH patients and 50 age-matched normotensive patients were recruited in this comparative cross-sectional study. Blood pressure, anthropometric and socio-demographic data of the participants were obtained voluntarily. The participants' serum levels of adiponectin, leptin and resistin were quantified using ELISA. It also analysed the renal function, lipid profile and glycemic status of all subjects. Results: A significantly higher anthropometric adiposity index was observed for hypertensive patients compared to normotensive patients, CI (p<0.0001), BAI (p<0.0001) and AVI (p=0.002). In hypertensive patients, adiponectin (p < 0.0001) levels were significantly lower than in normotensive patients. In addition, significantly higher serum leptin concentrations (p = 0.016) and leptinadiponectin ratio (p = 0.001) were observed in the hypertensive population compared to the normotensive group. In addition , the study found a direct association between serum leptin and weight (r = 0.111, p = 0.022), BMI (r = 0.129, p = 0.009) and WHtR (r = 0.098, p = 0.045), but an inverse relationship between hypertensive height (r = 0.134, p = 0.006). Serum leptin among hypertensive patients has a significant negative correlation with HDL-C (r = 0.174, p = 0.013). As predicted by resistin and adiponectin, the total aOR for hypertension was 1.12 (95% Cl, 1.02–1.25); p = 0.019) and 0.93 (95% Cl, 0.91–0.95); p = 0.0001) respectively. Conclusion: In the pathogenesis of essential hypertension, we found that elevations in serum levels of leptin and resistin and low levels of adiponectin may play a role. Therefore, as potential indicators for early and accurate detection of high blood pressure, adipokines may offer themselves. At the same time, the conclusions regarding the correlation between leptin and obesity are also confirmed by our current results. To investigate the physiological and pathological functions of adipokines in hypertension, further longitudinal studies in a larger population are warranted.

Author(s) Details

Dr. Osei Asibey
Department of Molecular Medicine, School of Medical Science, Kwame Nkrumah University of Science and Technology (KNUST), Kumasi, Ghana and Department of Clinical Biochemistry, Komfo Anokye Teaching Hospital (KATH), Kumasi, Ghana.

Francis Agyemang Yeboah
Department of Molecular Medicine, School of Medical Science, Kwame Nkrumah University of Science and Technology (KNUST), Kumasi, Ghana.

W. K. B. A. Owiredu
Department of Molecular Medicine, School of Medical Science, Kwame Nkrumah University of Science and Technology (KNUST), Kumasi, Ghana.

Emmanuel Acheampong
Department of Molecular Medicine, School of Medical Science, Kwame Nkrumah University of Science and Technology (KNUST), Kumasi, Ghana and School of Medical and Health Sciences, Edith Cowan University, Western Australia, Australia.

Enoch Odame Anto
Department of Molecular Medicine, School of Medical Science, Kwame Nkrumah University of Science and Technology (KNUST), Kumasi, Ghana and School of Medical and Health Sciences, Edith Cowan University, Western Australia, Australia.

Isaac K. Owusu
Department of Medicine, Komfo Anokye Teaching Hospital (KATH), Kumasi, Ghana.

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