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首页> 外文期刊>Cell metabolism >SH2B regulation of growth, metabolism, and longevity in both insects and mammals.
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SH2B regulation of growth, metabolism, and longevity in both insects and mammals.

机译：SH2B调节昆虫和哺乳动物的生长，代谢和寿命。

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摘要

SH2B1 is a key regulator of body weight in mammals. Here, we identified dSH2B as the Drosophila homolog of SH2B1. dSH2B bound to Chico and directly promoted insulin-like signaling. Disruption of dSH2B decreased insulin-like signaling and somatic growth in flies. dSH2B deficiency also increased hemolymph carbohydrate levels, whole-body lipid levels, life span, and resistance to starvation and oxidative stress. Systemic overexpression of dSH2B resulted in opposite phenotypes. dSH2B overexpression in fat body decreased lipid and glucose levels, whereas neuron-specific overexpression of dSH2B decreased oxidative resistance and life span. Genetic deletion of SH2B1 also resulted in growth retardation, obesity, and type 2 diabetes in mice; surprisingly, life span and oxidative resistance were reduced in SH2B1 null mice. These data suggest that dSH2B regulation of insulin-like signaling, growth, and metabolism is conserved in SH2B1, whereas dSH2B regulation of oxidative stress and longevity may be conserved in other SH2B family members.
机译：SH2B1是哺乳动物体重的关键调节剂。在这里，我们确定dSH2B是SH2B1的果蝇同源物。 dSH2B与Chico结合并直接促进胰岛素样信号传导。 dSH2B的破坏减少了果蝇中的胰岛素样信号传导和体细胞生长。 dSH2B缺乏症还会增加血淋巴碳水化合物水平，全身脂质水平，寿命以及对饥饿和氧化应激的抵抗力。 dSH2B的系统过度表达导致相反的表型。脂肪体内dSH2B的过表达降低了脂质和葡萄糖水平，而神经元特异性的dSH2B的过表达降低了抗氧化性和寿命。 SH2B1的基因缺失还导致小鼠生长发育迟缓，肥胖和2型糖尿病。令人惊讶地，SH2B1无效小鼠的寿命和抗氧化性降低。这些数据表明，SH2B1保留了胰岛素样信号传导，生长和代谢的dSH2B调控，而其他SH2B家族成员可能保持了氧化应激和长寿的dSH2B调控。

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