It was assumed initially the efficacy of bariatric procedures in treating diabetes was mainly

Given the physiological role of ghrelin, these heterogeneous findings are understandable, as ghrelin release and gene expression are regulated by the nutrient flux or the nutritional state of the body. Some studies reported that ghrelin level was low in the obese, because it decreased as intake increased. In contrast, ghrelin level was found to be high in conditions of malnutrition or anorexia nervosa, which suggested the possible existence of ghrelin resistance. In the present study, n-STZ diabetic rats developed polyphagia, polydipsia and polyuria after adulthood, and collective findings demonstrated that significantly increased ghrelin level in STZ-induced diabetic rats accounted for the diabetic polyphagia. These have led us to speculate that in the present work, SG-induced body weight loss and food intake reduction are partly, if not totally, due to the ghrelin level change, and furthermore, have reminded us of the ‘‘hypoinsulinemia’’ in type 1 diabetes and Toltrazuril ‘‘hyperinsulinemia and insulin resistance’’ in type 2 diabetes, in which both represent the morbid situation deserving appropriate therapies to make them go back to normal. Recently, substantial evidence has emerged demonstrating the effectiveness of SG in improving or resolving type 2 diabetes. However, the mechanism for type 2 diabetes resolution after SG is yet to be determined. In fact, not just SG, but other forms of bariatric surgery have been highlighted for their potential to ameliorate hyperglycemia and tackle type 2 diabetes during recent years. There are two general types of bariatric surgery: restrictive procedures including gastric banding and SG, which physically limit the size of the stomach, and gastrointestinal bypass procedures such as Roux-en-Y gastric bypass, which promote the malabsorption of calories. It was assumed initially, that the efficacy of bariatric procedures in treating type 2 diabetes was mainly because of their capacities to promote excess body weight loss. However, some reports later claimed that glycemic control often occurred long before significant weight loss in gastrointestinal bypass procedures such as RYGB, which suggested the mechanisms beyond weight loss and calorie restriction. Nevertheless, despite all the promising results obtained up to now, Tirofiban enthusiasm must remain guarded, as most clinical studies were not randomized and thus are suspect with regard to selection and observational bias. In this research, our results showed that SG failed to attenuate hyperglycemia in n-STZ diabetic rats. Supporting this finding, there were no significant changes in the hormones which were closely associated with glucose metabolism, including insulin, GLP-1 and GIP. The reason of the discrepancy may lie in the difference of the model or species. Herein the nature and characteristics of this n-STZ diabetic rat model needs to be considered. STZ is a substance specifically toxic to pancreatic b cells, and the damage STZ causes to b cells leads directly to the dysfunction of b cells which can not be easily reversed. The n-STZ diabetic rats have reduced b-cell mass, decreased pancreatic insulin reserves, and an impaired secretion of insulin to a glucose stimulus. Therefore, it is possible that in these diabetic rats a point of ‘‘no return’’ exists in reversing pancreatic failure. Besides, n-STZ diabetic rats in this study have an uncontrolled disease duration roughly equivalent to 6 human years, which is relatively long. In addition, Pereferrer FS investigated the influence of SG on four experimental models, including non-obesity model, exogenous obesity caused by excessive calorie intake, genetically determined obesity and genetically determined obesity and type 2 diabetes mellitus. Interestingly, it was found that normalization of weight and metabolic parameters were only observed in exogenous obesity model, and effect was slight in Zucker rats or ZDF rats.