Pankov Iu A
Mol Biol (Mosk). 2013 Jan-Feb;47(1):38-49. doi: 10.7868/s0026898413010138.
Obesity and diabetes mellitus are associated with low or elevated serum leptin and insulin levels (U-like relation). Mutations in LEP and INS are linked to leptin and insulin decrease while mutations in LEPR and INSR to their increase. Homozygous LEP mutations are associated with the early onset of severe obesity and diverse impairment of physiological functions. Recessive LEPR mutations are associated with similar pathology in homozygous state. Missense mutations of INS are dominant. They induce synthesis of chimeric pro-insulin that may interfere folding and processing of active insulin molecules. In the heterozygous state they cause insulin deficiency and PND. Recessive INS mutations do not induce synthesis of anomalous pro-insulin, and they are associated with PND only in homozygous state. Mutations of INSR induce insulin resistance, lipodystrophy, other pathology, and suggest an important role of insulin in glucose level regulation and in stimulation of fat accumulation as well.
肥胖症和糖尿病与血清瘦素和胰岛素水平降低或升高相关(呈U型关系)。LEP和INS的突变与瘦素和胰岛素减少有关,而LEPR和INSR的突变则与它们的增加有关。纯合子LEP突变与严重肥胖症的早发及多种生理功能损害相关。隐性LEPR突变在纯合状态下与类似病理相关。INS的错义突变是显性的。它们诱导嵌合胰岛素原的合成,这可能会干扰活性胰岛素分子的折叠和加工。在杂合状态下,它们会导致胰岛素缺乏和永久性新生儿糖尿病(PND)。隐性INS突变不会诱导异常胰岛素原的合成,且仅在纯合状态下与PND相关。INSR的突变会诱导胰岛素抵抗、脂肪营养不良及其他病理状况,并表明胰岛素在血糖水平调节以及脂肪堆积刺激中也起着重要作用。