Substantial evidence has linked dehydroepiandrosterone (DHEA) levels to the anti-obesity and anti-diabetic effects of exercise. While 5′-adenosine monophosphate-activated protein kinase (AMPK) is a negative regulator of adipocyte differentiation and lipid accumulation, activation of mammalian target of rapamycin complex 1 (mTORC1), which is inhibited by AMPK, is required for adipocyte differentiation and positively regulates lipid accumulation. DHEA treatment activates the AMPK pathway in C2C12 myotubes. Hence, DHEA addition to preadipocytes and adipocytes might activate AMPK and inhibit mTORC1, resulting in the inhibition of adipogenesis and lipid accumulation. Therefore, we investigated the effect of DHEA on the AMPK pathway, mTORC1 activity, adipocyte differentiation, and lipid accumulation in 3T3-L1 cells. DHEA suppressed lipid accumulation and adipogenic marker expression during differentiation. It also activated AMPK signaling in preadipocytes and adipocytes and suppressed mTORC1 activity during differentiation. These results suggest that the activation of the AMPK pathway and inhibition of mTORC1 activity may mediate the anti-obesity effect of DHEA, providing novel molecular-level insights into its physiological functions.

大量证据表明脱氢表雄酮（DHEA）水平与运动的抗肥胖和抗糖尿病作用有关。5'-腺苷单磷酸激活蛋白激酶（AMPK）是脂肪细胞分化和脂质蓄积的负调节剂，而受AMPK抑制的雷帕霉素复合物1（mTORC1）哺乳动物靶标的激活是脂肪细胞分化和正向调节所必需的。脂质堆积。DHEA治疗激活C2C12肌管中的AMPK途径。因此，DHEA添加到前脂肪细胞和脂肪细胞中可能会激活AMPK并抑制mTORC1，从而抑制脂肪生成和脂质蓄积。因此，我们调查了DHEA对3T3-L1细胞中AMPK途径，mTORC1活性，脂肪细胞分化和脂质蓄积的影响。DHEA抑制分化过程中脂质积累和成脂标记物的表达。它还激活前脂肪细胞和脂肪细胞中的AMPK信号，并抑制分化过程中的mTORC1活性。这些结果表明，AMPK途径的激活和mTORC1活性的抑制可能介导DHEA的抗肥胖作用，从而提供了对其生理功能的新的分子水平见解。