ROLE OF LIPOLYSIS IN HUMAN OBESITY AND FASTING

第二次国民健康与营养检查调查发现，26% 在20-75岁的美国成年人中，约有3400万人肥胖 (大于120%理想体重)。然而，尽管有很高的 肥胖症的流行和与之相关的此类疾病风险增加 由于糖尿病和高脂血症，尚不清楚是否存在健康风险 肥胖仅仅是过多脂肪组织或 肥胖者的脂肪组织调节是否也存在缺陷。 假定脂肪的生理作用是提供一种替代燃料。 在卡路里缺乏的时期。导致这些问题的因素 禁食期间加速脂肪分解还不完全清楚，但 它们可能是荷尔蒙、神经和新陈代谢的结合。 影响。初步信息显示，禁食的肥胖者 防止过度刺激脂肪分解和不堪重负 体内消耗游离脂肪酸的能力，可能形成 荷尔蒙环境的改变。 拟议中的实验将检验胰岛素对 瘦肥胖者的脂肪分解、FFA再酯化和脂肪氧化 非糖尿病志愿者，以确定脂肪异常是否 代谢可以解释碳水化合物代谢的胰岛素抵抗。 接下来的一系列实验将评估控制 脂解作用，以及脂解作用与葡萄糖动态平衡和 蛋白质的保存，在隔夜和三天内禁食瘦身和肥胖 非糖尿病志愿者。这些实验将监测 脂肪、葡萄糖和蛋白质周转选择性清除或阻断 荷尔蒙、神经或代谢因素都知道会影响脂肪代谢。 倒数第二个实验将调查是否增强了 肥胖患者禁食期间的脂肪分解功能受损 减少荷尔蒙刺激，如果是的话，是否更换 荷尔蒙缺乏，很可能是生长激素，会加速脂肪分解 而不会产生不良的新陈代谢后果。如果是这样的话，最终 实验将评估慢性生长激素治疗对 摄入A的肥胖者的脂肪、蛋白质和碳水化合物代谢 低热量饮食。

The second National Health and Nutrition Examination survey found that 26% of U.S. adults, or about 34 million people, aged 20-75 years were obese (greater than 120% ideal body weight). However, despite the high prevalence of obesity and the associated increased risk of such conditions as diabetes and hyperlipidemia, it is not known whether the health risks of obesity are simply a function of the excessive amount of adipose tissue or whether regulation of adipose tissue is also defective in obese persons. The presumed physiological role of fat is to provide an alternative fuel during periods of caloric deprivation. The factors responsible for acceleration of lipolysis during fasting are incompletely understood, but they are presumably a combination of hormonal, neural and metabolic influences. Preliminary information suggests that fasted obese persons are protected against excessive stimulation of lipolysis and overwhelming of the bodies capacity to consume free fatty acids, possibly form an alteration in the hormonal milieu. The proposed experiments will examine the regulation by insulin of lipolysis, FFA reesterification and fat oxidation in lean nd obese nondiabetic volunteers, to determine whether abnormalities of fat metabolism could explain the insulin resistance of carbohydrate metabolism. The next series of experiments will evaluate the factors that control lipolysis, and the relationship of lipolysis to glucose homeostasis and protein conservation, in overnight and three day fasted lean and obese nondiabetic volunteers. These experiments will monitor the effect of lipid, glucose and protein turnover of selective removal or blockade of hormonal, neural or metabolic factors know to influence lipid metabolism. The penultimate experiments will investigate whether enhancement of lipolysis during fasting is impaired in obese persons as a result of reduced hormonal stimulation and, if so, whether replacement of the hormonal deficiency, most likely growth hormone, can accelerate lipolysis without untoward metabolic consequences. If this is the case, the final experiment will evaluate the effect of chronic growth hormone treatment on fat, protein and carbohydrate metabolism in obese subjects consuming a hypocaloric diet.