H₂S is generated in the adipose tissue by cystathionine γ-lyase, cystathionine β-synthase, and 3-mercaptopyruvate sulfurtransferase (3-MST). H₂S plays multiple roles in the regulation of various metabolic processes, including insulin resistance. H₂S biosynthesis also occurs in adipocytes. Aging is known to be associated with a decline in H₂S. Therefore, the question arises whether endogenous H₂S deficiency may affect the process of adipocyte maturation and lipid accumulation. Among the three H₂S-generating enzymes, the role of 3-MST is the least understood in adipocytes. Here we tested the effect of the 3-MST inhibitor 2-[(4-hydroxy-6-methylpyrimidin-2-yl)sulfanyl]-1-(naphthalen-1-yl)ethan-1-one (HMPSNE) and the H₂S donor (GYY4137) on the differentiation and adipogenesis of the adipocyte-like cells 3T3-L1 in vitro. 3T3-L1 cells were differentiated into mature adipocytes in the presence of GYY4137 or HMPSNE. HMPSNE significantly enhanced lipid accumulation into the maturing adipocytes. On the other hand, suppressed lipid accumulation was observed in cells treated with the H₂S donor. 3-MST inhibition increased, while H₂S donation suppressed the expression of various H₂S-producing enzymes during adipocyte differentiation. 3-MST knockdown also facilitated adipocytic differentiation and lipid uptake. The underlying mechanisms may involve impairment of oxidative phosphorylation and fatty acid oxidation as well as the activation of various differentiation-associated transcription factors. Thus, the 3-MST/H₂S system plays a tonic role in suppressing lipid accumulation and limiting the differentiation of adipocytes. Stimulation of 3-MST activity or supplementation of H₂S—which has been recently linked to various experimental therapeutic approaches during aging—may be a potential experimental approach to counteract adipogenesis.

H ₂ S 由胱硫醚 γ-裂解酶、胱硫醚 β-合酶和 3-巯基丙酮酸硫转移酶 (3-MST) 在脂肪组织中生成。H ₂ S 在调节包括胰岛素抵抗在内的各种代谢过程中起着多重作用。H ₂ S 生物合成也发生在脂肪细胞中。已知衰老与 H ₂ S 下降有关。因此，问题是内源性 H ₂ S 缺乏是否会影响脂肪细胞成熟和脂质积累的过程。在三个H ₂S 生成酶，3-MST 的作用在脂肪细胞中了解最少。在这里，我们测试了 3-MST 抑制剂 2-[(4-hydroxy-6-methylpyrimidin-2-yl)sulfanyl]-1-(naphthalen-1-yl)ethan-1-one (HMPSNE) 和 H ₂ S 供体 (GYY4137) 对脂肪细胞样细胞 3T3-L1 体外分化和脂肪形成的影响。3T3-L1 细胞在 GYY4137 或 HMPSNE 存在下分化为成熟脂肪细胞。HMPSNE 显着增强了成熟脂肪细胞中的脂质积累。另一方面，在用H ₂ S供体处理的细胞中观察到抑制的脂质积累。3-MST 抑制增加，而 H ₂ S 捐赠抑制各种 H _2的表达脂肪细胞分化过程中产生 S 的酶。3-MST 敲低也促进脂肪细胞分化和脂质摄取。潜在的机制可能涉及氧化磷酸化和脂肪酸氧化的损害以及各种分化相关转录因子的激活。因此，3-MST/H ₂ S系统在抑制脂质积累和限制脂肪细胞分化方面起着滋补作用。刺激 3-MST 活性或补充 H ₂ S（最近与衰老过程中的各种实验性治疗方法相关联）可能是抵消脂肪生成的潜在实验方法。