Abstract：
Recent data suggests that (pre)diabetes onset is preceded by a period of hyperinsulinemia. Consumption of the \"modern\" Western diet, over-nutrition, genetic background, decreased hepatic insulin clearance, and fetal/metabolic programming may increase insulin secretion, thereby causing chronic hyperinsulinemia. Hyperinsulinemia is an important etiological factor in the development of metabolic syndrome, type 2 diabetes, cardiovascular disease, polycystic ovarian syndrome, and Alzheimer\'s disease. Recent data suggests that the onset of prediabetes and diabetes are preceded by a variable period of hyperinsulinemia. Emerging data suggest that chromic hyperinsulinemia is also a driving force for increased activation of the hypothalamic-adrenal-pituitary (HPA) axis in subjects with the metabolic syndrome, leading to a state of \"functional hypercortisolism\". This \"functional hypercortisolism\" by antagonizing insulin actions may prevent hypoglycemia. It also disturbs energy balance by shifting energy fluxes away from muscles toward abdominal fat stores. Synergistic effects of hyperinsulinemia and \"functional hypercortisolism\" promote abdominal visceral obesity and insulin resistance which are core pathophysiological components of the metabolic syndrome. It is hypothesized that hyperinsulinemia-induced increased activation of the HPA axis plays an important etiological role in the development of the metabolic syndrome and its consequences. Numerous studies have demonstrated reversibility of hyperinsulinemia with lifestyle, surgical, and pharmaceutical-based therapies. Longitudinal studies should be performed to investigate whether strategies that reduce hyperinsulinemia at an early stage are successfully in preventing increased activation of the HPA axis and the metabolic syndrome.
摘要：
最近的数据表明，（前期）糖尿病发病之前有一段时间的高胰岛素血症。“现代”西方饮食的消费，营养过剩,遗传背景,肝脏胰岛素清除率降低，胎儿/代谢程序可能会增加胰岛素分泌，从而引起慢性高胰岛素血症。高胰岛素血症是代谢综合征发生发展的重要病因,2型糖尿病,心血管疾病,多囊卵巢综合征,和老年痴呆症。最近的数据表明，糖尿病前期和糖尿病的发作之前是高胰岛素血症的可变时期。新的数据表明，在代谢综合征患者中，高胰岛素血症也是下丘脑-肾上腺-垂体（HPA）轴激活增加的驱动力。导致“功能性皮质醇增多症”的状态。这种通过拮抗胰岛素作用的“功能性皮质醇增多症”可以预防低血糖。它还通过将能量通量从肌肉转移到腹部脂肪储存来扰乱能量平衡。高胰岛素血症和“功能性皮质醇增多症”的协同作用促进腹部内脏肥胖和胰岛素抵抗，这是代谢综合征的核心病理生理成分。假设高胰岛素血症诱导的HPA轴活化增加在代谢综合征的发展及其后果中起重要的病因学作用。许多研究已经证明高胰岛素血症与生活方式的可逆性，外科,和基于药物的疗法。应进行纵向研究，以调查在早期减少高胰岛素血症的策略是否成功地预防了HPA轴激活和代谢综合征的增加。
