Recent studies of obesity show that fat tissue fulfills an endocrine function by producing a variety of secreted proteins, called adipocytokines, that may play key metabolic roles. The present investigators have isolated a newly identified adipocytokine, visfatin, from visceral fat of both mice and humans. Expression of visfatin in the plasma increases as obesity develops. This substance corresponds to a protein identified as preB cell colony-enhancing factor (PBEF), a cytokine expressed in lymphocytes. In a study of 101 human males and females, plasma levels of PBEF correlated closely with the amount of visceral fat as estimated by computed tomography. Correlation with the amount of subcutaneous fat was weak. Significant elevations of PBEF mRNA were also found in KKAy mice, which serve as a model for obesity-related type 2 diabetes. These mice become obese at age 6 to 12 weeks and, at the same time, plasma PBEF levels increase significantly, as do levels of PBEF mRNA in visceral fat. Levels in subcutaneous fat change very little. Mice fed a high-fat diet had higher plasma PBEF concentrations than those fed normal chow. When recombinant visfatin was administered intravenously to c57BL/6J mice, plasma glucose decreased within 30 minutes in a dose-dependent manner. The same effect was noted in insulin-resistant obese KKAy mice, mimicking the effect of insulin injection. Visfatin also had insulin-like effects on cultured cells. In both strains of mice, chronic exposure to visfatin, using adenovirus, significantly lowered plasma levels of both glucose and insulin. Visfatin was found to bind to—and activate—the insulin receptor but in a way different from insulin. These studies indicate that visfatin shares properties of insulin both in vitro and in vivo. In addition to helping to understand glucose and lipid homeostasis and adipocyte proliferation, visfatin may prove to be a useful target when developing drug treatments for diabetes.
About 70% of the total population live in rural areas of South Asia, 70% of whom are landless or marginal farmers. Livestock production fulfills diverse roles in the social and economic development of the rural poor in South Asia. It is difficult for poor people to get expensive milk bovine (mainly, cattle in Bangladesh and buffalo in India) to enter dairy farming. As a potential solution, I focused on the mechanism of consignment rearing of domestic animals and investigated this mechanism in India and Bangladesh. We interviewed 246 rural households in India(141) and Bangladesh(105) about the number of cattle and buffaloes reared and their access routes. Fourteen out of the 246 households were found to rear milk bovines owned by others. These were divided into three types of consignment rearing: traditional, with purchase rights, and commercial dairy. The second and third mechanisms were constructed in each area according to the market specifically faced by livestock-raising households.
(-)-N-(trans-4-Isopropylcyclohexanecarbonyl)-D-phenylalanine (A-4166) is a new nonsulfonylurea hypoglycemic agent that lowers blood glucose by stimulating insulin release. In the present study, we examined the effects of A-4166, voglibose (an α-glucosidase inhibitor), and glibenclamide (a sulfonylurea) on the postprandial glycemic increase in rats with or without diabetes millitus. Oral administration of A-4166 (25-100 mg/kg) dose-dependently decreased blood glucose with a rapid onset and short duration in normal rats. On the other hand, glibenclamide (1-4 mg/kg) showed a slower onset of its hypoglycemic action, and voglibose (0.2 mg/kg) had no effect. In the case of postprandial glucose excursion, the carbohydrate-induced increase in blood glucose was reduced by oral administration of either A-4166 or voglibose without causing sustained hypoglycemia in both normal and neonatal streptozotocin-induced diabetic rats. However, the efficacy of voglibose varied with the type of carbohydrate load. Glibenclamide produced a prolonged decrease in blood glucose without any appreciable effect on the initial glucose excursion. After sucrose loading, plasma insulin levels during the initial 1 h were significantly higher in A-4166-treated rats than in control rats, while voglibose completely inhibited the insulin response to sucrose. In glibenclamide-treated rats, an augmented insulin response was not seen. In conclusion, unlike other hypoglycemic agents, A-4166 suppresses postprandial glucose excursions by stimulating the early phase of insulin secretion.
Fat tissue produces a variety of secreted proteins (adipocytokines) with important roles in metabolism. We isolated a newly identified adipocytokine, visfatin, that is highly enriched in the visceral fat of both humans and mice and whose expression level in plasma increases during the development of obesity. Visfatin corresponds to a protein identified previously as pre-B cell colony-enhancing factor (PBEF), a 52-kilodalton cytokine expressed in lymphocytes. Visfatin exerted insulin-mimetic effects in cultured cells and lowered plasma glucose levels in mice. Mice heterozygous for a targeted mutation in the visfatin gene had modestly higher levels of plasma glucose relative to wild-type littermates. Surprisingly, visfatin binds to and activates the insulin receptor. Further study of visfatin's physiological role may lead to new insights into glucose homeostasis and/or new therapies for metabolic disorders such as diabetes.
