Metabolic Research Laboratories, Wellcome Trust-Medical Research Council Institute of Metabolic Science, University of Cambridge, Cambridge, Cambridgeshire CB2 0QQ, UK.
MRC Metabolic Diseases Unit, University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Genomics and Transcriptomics Core, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK.
Cell Rep. 2021 Mar 9;34(10):108810. doi: 10.1016/j.celrep.2021.108810.
Adipogenin (Adig) is an adipocyte-enriched transmembrane protein. Its expression is induced during adipogenesis in rodent cells, and a recent genome-wide association study associated body mass index (BMI)-adjusted leptin levels with the ADIG locus. In order to begin to understand the biological function of Adig, we studied adipogenesis in Adig-deficient cultured adipocytes and phenotyped Adig null (Adig) mice. Data from Adig-deficient cells suggest that Adig is required for adipogenesis. In vivo, Adig mice are leaner than wild-type mice when fed a high-fat diet and when crossed with Ob/Ob hyperphagic mice. In addition to the impact on fat mass accrual, Adig deficiency also reduces fat-mass-adjusted plasma leptin levels and impairs leptin secretion from adipose explants, suggesting an additional impact on the regulation of leptin secretion.
脂联素（Adig）是一种富含脂肪细胞的跨膜蛋白。其在啮齿类细胞的脂肪生成过程中被诱导表达，最近的全基因组关联研究将体重指数（BMI）调整后的瘦素水平与 ADIG 基因座相关联。为了开始了解 Adig 的生物学功能，我们研究了 Adig 缺陷培养脂肪细胞中的脂肪生成，并对 Adig 基因缺失（Adig）小鼠进行了表型分析。来自 Adig 缺陷细胞的数据表明，Adig 是脂肪生成所必需的。在高脂肪饮食喂养和与 Ob/Ob 过度摄食小鼠杂交时，Adig 小鼠比野生型小鼠更瘦。除了对脂肪量积累的影响外，Adig 缺乏还降低了脂肪量调整后的血浆瘦素水平，并损害了脂肪组织外植体的瘦素分泌，表明对瘦素分泌的调节有额外影响。
