Assessment of Insulin, GLUT2 and inflammatory cytokines genes expression in pancreatic ß-Cells in zebrafish (Danio rario) with overfeeding diabetes induction w/o glucose.

ABSTRACT: In recent years, zebrafish have been proposed as a model for rapid analysis of gene function and biological activity due to high genetic similarities with humans. The aim of this study was to determine the effects of overfeeding-induced diabetes w/o glucose on inflammatory cytokine as well as insulin and glucose transporter-2 genes (GLUT2) genes expression in the pancreas in zebrafish. MATERIALS AND METHODS: The experiment was performed on 120 zebrafish (duplicated sample) with a specific genetic mapping (AB-Wild type). A total of 8 tanks, each containing 15 fish per 2-liter water, were used and divided into four groups: (1) Control group, (2) regular diet with glucose,3) Only Artemia overfeeding and 4) Combined Artemia with glucose. We induced T2DM zebrafish using glucose monohydrate solution in water and repeated daily Artemia feeding. In this model, fasting blood glucose increase is preceded by obesity and glucose intolerance. The experiment lasted for two months. Blood glucose and fish biometrics were measured in two steps. The expression of TNFα, IFNγ, GLUT2 and Insulin genes were quantified by a Real-Time qPCR System (Applied Biosystems, USA) using a set of specific primers. RESULTS: The highest mortality rate was observed in combined Artemia and glucose (p < 0.05). We showed significantly higher expression of IL-1B and TNF-α as well as inhibitory cytokines such as IFNγ genes in overfeeding induced diabetes(OID) which was highest in the combined Artemia and glucose group.(p < 0.05)The GLUT2 gene expression was higher in the pure artemia group which decreased to a lower level by adding glucose to Artemia in the diet. (p < 0.05). Also, the lowest insulin gene expression was observed in the combined group (p < 0.05). CONCLUSIONS: In zebrafish, diabetes induction with overfeeding and supraphysiological glucose in diet accompanied with higher expression of inflammatory cytokines genes in the pancreas as well as lower insulin and GLU2 genes. These epigenetic factors appeared to initiate pancreatic beta dysfunction alongside insulin resistance and could have a crucial role in the pathogenesis of overfeeding-induced diabetes using primitive animal models.

Assessment of Arterial Stiffness in Metabolic Syndrome Related to Insulin Resistance in Apparently Healthy Men.

BACKGROUND: Assessment of subclinical atherosclerosis in metabolic syndrome is one of the global health targets' priorities. This study aimed to evaluate the subclinical atherosclerosis in metabolic syndrome related to insulin resistance in healthy and physically active men. METHODS: A consecutive group of 68 healthy men, 30-55 years of age, was studied. Anthropometric parameters, proinflammatory factors, and insulin level were measured, and pulse wave analysis (PWA) was performed by applanation tonometry and then processed with dedicated software (SphygmoCor®). The metabolic syndrome was defined according to International Diabetes Federation (IDF) and metabolic health as ≤1 component of metabolic syndrome according to the Joint Interim Statement criteria. RESULTS: The odds ratio of insulin resistance for metabolic syndrome was 5.16 (95% confidence interval: 1.44-18.5), P = 0.008. In PWA, metabolically healthy subjects had lower aortic systolic and diastolic, and cardiac end-systolic pressures (103.5 ± 9.9 vs. 108.8 ± 11.0), P = 0.03, (76.2 ± 8.8 vs. 80.6 ± 7.8), P = 0.04, and (96.5 ± 9.2 vs. 101 ± 10.1), P = 0.05, respectively. Furthermore, metabolic syndrome was accompanied by higher ejection duration% (38.8 ± 3.5 vs. 36.9 ± 2.8), P = 0.04, and lower subendocardial viability ratio (SEVR) (139.8 ± 17.7 vs. 150.9 ± 17.6), P = 0.05. Insulin resistance was associated with higher cardiac end-systolic pressure (103.0 ± 6.9 vs. 96.7 ± 10.4), P = 0.015. CONCLUSION: Metabolic risk factors had incremental correlations with central arterial pressures and cardiac end-systolic pressure. Furthermore, the composite of metabolic syndrome components imposed additional load on cardiac muscle by higher cardiac ejection duration and impairment in perfusion with lower Buckberg SEVR. Likewise, insulin resistance could be an early marker of arterial stiffness in healthy and active young to middle-age men.

Menopause is an independent predictor of metabolic syndrome in Iranian women.

BACKGROUND: Gender differences in prevalence and consequences of the metabolic syndrome as a strong predictor of cardiovascular disease (CVD), are challenging problems. Postmenopausal status may explain in part the cause of acceleration of CVD with aging. The purpose of this study was to investigate the relation of menopause and metabolic syndrome independent of aging among Iranian women. METHODS: On the basis of consecutive recruitment, 940 women between 20 and 76 years old participated in the study. Anthropometric indices, fasting blood glucose, lipid profile were measured, Framingham risk score and homeostasis model assessment (HOMA-IR) were calculated for all participants. The metabolic syndrome (MetS) was defined according to the National Cholesterol Education Program Adult Treatment Panel III. We used IDF definition for metabolic syndrome modified by our recent local data as an alternative measurements. RESULTS: The overall prevalence of metabolic syndrome was 26.4%. Its prevalence was 53.5% in postmenopausal versus 18.3% in premenopausal women. On binary logistic regression analysis, HOMA index, body mass index, waist to hip ratio, family history of diabetes and hypertension had an independent and significant effect on metabolic syndrome. Age-adjusted odds ratio (OR) of postmenopausal status for metabolic syndrome was 2.85 (95%CI: 1.31-6.20) (P<0.008). Framingham risk score was 8.3+/-7.7 in MetS+ve cases versus 1.9+/-2.1 in MetS-ve cases (P<0.001). There were significant differences between Framingham risk score in postmenopause 9.1+/-6.4 versus premenopause 1.6+/-1.6 (P<0.001). A significant correlation was found between Framingham risk score and body mass index, waist to hip ratio, HOMA-IR and components of metabolic syndrome (P<0.001). Forty percent of participants with premature menopause had metabolic syndrome versus 24% in age-matched group and Framingham risk score was significantly higher than normal cases 5.4+/-4.9 versus 2.0+/-2.3 (P<0.001). CONCLUSION: Menopausal status can be a predictor of metabolic syndrome independent of age in Iranian women. Menopause is a process closely related to insulin resistance and cardiovascular risk factors.