Ghanshyam B Jadhav

Fructose consumption from sucrose and high-fructose corn syrup have Increased both plasma insulin and leptin act in the central nervous system in the long-term regulation of energy homeostasis. Because fructose does not stimulate insulin secretion from pancreatic β cells, the consumption of foods and beverages containing fructose produces smaller postprandial insulin excursions than does consumption of glucose-containing carbohydrate. Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae. In addition, fructose, compared with glucose, is preferentially metabolized to lipid in the liver. Fructose consumption induces insulin resistance, impaired glucose tolerance, hyper insulinemia, hyper triacylglycerolemia, and hypertension in animal models. The data in humans are less clear. Although there are existing data on the metabolic and endocrine effects of dietary fructose that suggest that increased consumption of fructose may be detrimental in terms of body weight and adiposity and the metabolic indexes associated with the insulin resistance syndrome, much more research is needed to fully understand the metabolic effect of dietary fructose in humans. We investigated the effects of NCE-9 on fructose-induced hypertriglyceridemia and liver steatosis in rats. NCE-9 reduced serum TG and VLDL levels and also improve glucose intolerance in fructose-fed rats. This PTP1B inhibitory property may be a promising therapeutic strategy for NCE-9 to treat fructose-induced hepatic steatosis.