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Background: Ventromedial hypothalamus (VMH) plays a major role in food intake, obesity and energy homeostasis. There is a report of gender difference in energy balance with increased vulnerability of males to cardiac disease. Purpose: Body metabolism is greatly influenced by the diet we eat and some of the blood parameters like plasma glucose, insulin, lipid profile and thyroid profile depict a picture of energy homeostasis of the body. Objective: The present study was conducted to assess the effect of VMH in high fat diet (HFD) induced obesity and its link with insulin, glucose, thyroid and lipid profile of male Wistar rats. Methods: The male rats (n = 12) were given HFD for a period of 10 weeks to induce obesity. After obtaining a basal recording of food intake, body weight, glucose, insulin, thyroid and lipid profile, animals were divided into control and experimental group (n = 6 male in each). Experimental rats underwent electrolytic ablation of VMH whereas control rats underwent sham lesion. A post-lesion recording was taken at the end of four weeks. Results: The rats had a greater food intake and more body weight gain after HFD schedule in both the groups. After VMH lesion, food intake increased further, only in experimental group. Plasma glucose, Insulin, HOMA - IR, total cholesterol (TC) and triglycerides (TG) were significantly increased compared to the pre-lesion values in experimental group (P<0.001). Conclusions: Ten week of HFD resulted in obesity. VMH appears to prevent the development of insulin resistance and hypercholesterolemia which influences the energy homeostasis in male rats after high fat diet. [ABSTRACT FROM AUTHOR]

BACKGROUND Although cardiovascular (CV) risks are reported in first-degree relatives (FDRs) of type 2 diabetics, effects of gender on sympathovagal imbalance (SVI) and CV risks in these subjects have not been investigated. METHODS Body mass index (BMI), blood pressure variability parameters including baroreflex sensitivity (BRS), spectral indices of heart rate variability, autonomic function tests, insulin resistance, lipid profile, inflammatory markers (interleukin 6, high-sensitivity C-reactive protein, tumor necrosis factor α) and oxidative stress (OS) marker were measured and analyzed in control group (without family history of diabetes; 65 women, 60 men) and study group (FDRs of type 2 diabetics; 52 women, 49 men) subjects. RESULTS BMI, heart rate, blood pressure, rate–pressure product, stroke volume, left-ventricular ejection time, cardiac output, total peripheral resistance, homeostatic model of insulin resistance, lipid profile, inflammatory and OS markers, and ratio of low-frequency to high-frequency power of heart rate variability (LF-HF ratio), a sensitive marker of SVI, were significantly increased, and BRS was significantly decreased in study group men compared with women. SVI was more intense in men and was due to concomitant sympathetic activation and vagal inhibition. There was no SVI in control subjects. Multiple regression analysis demonstrated independent contribution of BMI, homeostatic model of insulin resistance, atherogenic index, inflammatory and OS markers, and BRS to LF-HF ratio. Logistic regression analysis demonstrated significant prediction of prehypertension status and rate–pressure product (markers of CV risk) by LF-HF, which was more prominent in men. CONCLUSIONS SVI is more intense in male FDRs of type 2 diabetics, and SVI is associated with increased CV risk due to insulin resistance, dyslipidemia, inflammation, and oxidative stress in these subjects. [ABSTRACT FROM PUBLISHER]