No abstract

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.

BackgroundVentromedial 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.PurposeBody 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.ObjectiveThe 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.MethodsThe 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.ResultsThe 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).ConclusionsTen 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.

BackgroundEstradiol is known to inhibit food intake (FI), water intake (WI) and body weight (BW) across the species including women and it is most evident in rats. Ovariectomy in rats and menopause in women produce hyperphagia and obesity. Estradiol substitution in ovariectomized (OVX) rats and hormone replacement in women reverses these changes suggesting that lack of estradiol causes eating related disorders. However, the neurobiological target/s for estradiol mediating effects remains largely unknown. While lesions of basolateral amygdala (BLA) also produce hyperphagia, polydipsia and obesity in female rats suggesting BLA normally inhibits these behaviors.PurposeSince ovariectomy is a useful model to study postmenopausal obesity in women, we have investigated the role of BLA in ovariectomy induced ingestive behaviors.MethodsOvariectomy and stereotaxic lesions in experimental group (n = 6) whereas sham operations in control group (n = 6) were carried out in female rats. Estradiol was injected subcutaneously (s.c) before and after lesions in experimental group and vehicle was injected in control group.ResultsData from the present study shows that there was an additional increase in FI, WI and BW in OVX animals following BLA lesions, but this additive effect was small compared to sham operated controls. Conversely, OVX rats with lesions have shown small but significant reductions in FI, WI, and lost less BW, following s.c injection of estradiol compared to rats with intact BLA.ConclusionThese findings suggest that ovariectomy and estradiol induced changes on ingestive behaviors and body weight are partly mediated via BLA.