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首页> 外文期刊>Biochemical and Biophysical Research Communications >Expression of adiponectin receptors in mouse adrenal glands and the adrenocortical Y-1 cell line: Adiponectin regulates steroidogenesis.
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Expression of adiponectin receptors in mouse adrenal glands and the adrenocortical Y-1 cell line: Adiponectin regulates steroidogenesis.

机译:脂联素受体在小鼠肾上腺和肾上腺皮质Y-1细胞系中的表达:脂联素调节类固醇生成。

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Obesity is frequently associated with malfunctions of the hypothalamus-pituitary-adrenal (HPA) axis and hyperaldosteronism, but the mechanism underlying this association remains unclear. Since the adrenal glands are embedded in adipose tissue, direct cross-talk between adipose tissue and the adrenal gland has been proposed. A previous study found that adiponectin receptor mRNA was expressed in human adrenal glands and aldosterone-producing adenoma (APA). However, the expression of adiponectin receptors in adrenal glands has not been confirmed at the protein level or in other species. Furthermore, it is unclear whether adiponectin receptors expressed in adrenal cells are functional. We found, for the first time, that adiponectin receptor (AdipoR1 and AdipoR2) mRNA and protein were expressed in mouse adrenal and adrenocortical Y-1 cells. However, adiponectin itself was not expressed in mouse adrenal or Y-1 cells. Furthermore, adiponectin acutely reduced basal levels of corticosterone and aldosterone secretion. ACTH-induced steroid secretion was also inhibited by adiponectin, and this was accompanied by a parallel change in the expression of the key genes involved in steroidogenesis. These findings indicate that adiponectin may take part in the modulation of steroidogenesis. Thus, adiponectin is likely to have physiological and/or pathophysiological significance as an endocrine regulator of adrenocortical function.
机译:肥胖症通常与下丘脑-垂体-肾上腺(HPA)轴功能异常和醛固酮增多症有关,但这种关联的机制尚不清楚。由于肾上腺被包埋在脂肪组织中,已经提出了脂肪组织与肾上腺之间的直接串扰。先前的研究发现,脂联素受体mRNA在人肾上腺和醛固酮生成腺瘤(APA)中表达。然而,在蛋白水平或其他物种中,尚未确认脂联素受体在肾上腺中的表达。此外,尚不清楚在肾上腺细胞中表达的脂联素受体是否具有功能。我们首次发现,脂联素受体(AdipoR1和AdipoR2)mRNA和蛋白在小鼠肾上腺和肾上腺皮质Y-1细胞中表达。但是,脂联素本身未在小鼠肾上腺或Y-1细胞中表达。此外,脂联素可急剧降低皮质酮和醛固酮分泌的基础水平。脂联素也抑制了ACTH诱导的类固醇分泌,并且伴随着类固醇生成相关关键基因表达的平行变化。这些发现表明脂联素可能参与了类固醇生成的调节。因此,脂联素作为肾上腺皮质功能的内分泌调节剂可能具有生理和/或病理生理学意义。

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