HYPOTHALAMIC THERMOSENSITIVITY IN GENETIC OBESITY

遗传性肥胖啮齿动物，广泛用作早发性动物模型 肥胖和糖尿病，都有大量的代谢和内分泌 不足之处。这项提案涉及监管方面的缺陷 能量平衡。肥胖的动物往往体温低，体温低。 代谢率，它们在进餐时产生的热量比瘦小的动物少 在寒冷的环境中。在生热过程中节省的能量被储存为 胖的。这些缺陷被归因于棕色脂肪代谢的缺陷。 本研究的假设是，大脑的中枢控制机制 温度调节可能导致能量平衡失衡。 关于肥胖动物的许多观察结果与以下观点一致 监管机构已被重新设置为较低水平。下丘脑 通过测量耗氧量和干燥度来检测热敏性 和下丘脑加热和冷却过程中的蒸发热损失 不同环境温度的瘦和肥胖的Zucker大鼠。推论 可以从这些关于温度调节装置的测量中得出 点和调整器的增益。

Genetically obese rodents, widely used as animal models of early-onset obesity and diabetes, have a large number of metabolic and endocrine deficiencies. This proposal deals with deficiencies in the regulation of energy balance. Obese animals tend to have a low body temperature and low metabolic rate, and they produce less heat than lean animals during a meal and during cold exposure. The energy saved in thermogenesis is stored as fat. These deficits have been attributed to faulty brown fat metabolism. The hypothesis of the present work is that central control mechanisms of temperature regulation may contribute to energy balance disequilibrium. Many observations regarding obese animals are consistent with the idea that the regulatory has been re-set to a lower level. Hypothalamic thermosensitivity will be examined by measuring oxygen consumption and dry and evaporative heat loss during hypothalamic heating and cooling at different ambient temperatures in lean and obese Zucker rats. Inferences can be drawn from these measurements regarding the thermoregulatory set point and the gain of the regulator.