Clore Laboratory, University of Buckingham, Buckingham, UK.
FEBS Lett. 2010 Jun 3;584(11):2381-6. doi: 10.1016/j.febslet.2010.04.027. Epub 2010 Apr 20.
GPR41 is reportedly expressed in murine adipose tissue and mediates short chain fatty acid (SCFA)-stimulated leptin secretion by activating Galpha(i). Here, we agree with a contradictory report in finding no expression of GPR41 in murine adipose tissue. Nevertheless, in the presence of adenosine deaminase to minimise Galpha(i) signalling via the adenosine A1 receptor, SCFA stimulated leptin secretion by adipocytes from wild-type but not GPR41 knockout mice. Expression of GPR43 was reduced in GPR41 knockout mice. Acetate but not butyrate stimulated leptin secretion in wild-type mesenteric adipocytes, consistent with mediation of the response by GPR43 rather than GPR41. Pertussis toxin prevented stimulation of leptin secretion by propionate in epididymal adipocytes, implicating Galpha(i) signalling mediated by GPR43 in SCFA-stimulated leptin secretion.
GPR41 据报道在鼠脂肪组织中表达，并通过激活 Galpha(i) 介导短链脂肪酸 (SCFA) 刺激的瘦素分泌。在这里，我们同意一项相反的报告，即在鼠脂肪组织中未发现 GPR41 的表达。然而，在存在腺苷脱氨酶以最小化通过腺苷 A1 受体的 Galpha(i) 信号传导的情况下，SCFA 刺激来自野生型但不是 GPR41 敲除小鼠的脂肪细胞中的瘦素分泌。GPR43 的表达在 GPR41 敲除小鼠中减少。乙酸盐而不是丁酸盐刺激野生型肠系膜脂肪细胞中的瘦素分泌，这与通过 GPR43 而不是 GPR41 介导该反应一致。百日咳毒素可防止霍乱毒素在附睾脂肪细胞中刺激丙酸盐刺激的瘦素分泌，这表明 GPR43 介导的 Galpha(i) 信号传导参与了 SCFA 刺激的瘦素分泌。
