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三碘甲状腺原氨酸（T3）通过抑制 PI3K/AKT 信号通路促进白色脂肪褐变。

Triiodothyronine (T3) promotes browning of white adipose through inhibition of the PI3K/AKT signalling pathway.

机构信息

Department of Endocrinology, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, 362000, Fujian, China.

Department of Respiratory Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, 362000, Fujian, China.

出版信息

Sci Rep. 2024 Sep 2;14(1):20370. doi: 10.1038/s41598-024-71591-0.

DOI:10.1038/s41598-024-71591-0
PMID:39223267
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11369215/
Abstract

Obesity arises from an imbalance between energy consumption and energy expenditure, and thyroid hormone levels serve as a determinant of energy expenditure. We conducted experiments at the animal and cellular levels and combined those findings with clinical data to elucidate the role of triiodothyronine (T3) in facilitating the browning of white adipose tissue (WAT) and its underlying mechanism. The results showed (i) the impaired metabolic function of local WAT and the compensatory elevation of systemic thermogenesis in obesity; (ii) T3 treatment of white adipocytes in vitro and local WAT in vivo induced a shift towards a morphologically "brown" phenotype, accompanied by upregulation of mRNA and protein expression of browning-related and mitochondrial function markers, which suggest that T3 intervention promotes the browning of WAT; and (iii) the aforementioned processes could be modulated through inhibition of the PI3K/AKT signalling pathway; however, whether T3 affects the PI3K/AKT signalling pathway by affecting insulin signalling remains to be studied and clarified. The results of our study indicate that T3 treatment promotes browning of WAT through inhibition of the PI3K/AKT signalling pathway; these findings offer novel perspectives regarding the potential of localised therapies for addressing WAT volume in individuals with obesity.

摘要

肥胖是由能量消耗和能量支出之间的失衡引起的，而甲状腺激素水平是能量支出的决定因素。我们在动物和细胞水平上进行了实验，并将这些发现与临床数据相结合，阐明了三碘甲状腺原氨酸（T3）在促进白色脂肪组织（WAT）褐变及其潜在机制中的作用。结果表明：（i）肥胖时局部 WAT 的代谢功能受损和全身产热的代偿性升高；（ii）T3 处理体外白色脂肪细胞和体内局部 WAT 诱导向形态上“棕色”表型的转变，伴随着褐变相关和线粒体功能标志物的 mRNA 和蛋白表达上调，表明 T3 干预促进了 WAT 的褐变；（iii）上述过程可以通过抑制 PI3K/AKT 信号通路来调节；然而，T3 是否通过影响胰岛素信号来影响 PI3K/AKT 信号通路仍有待研究和阐明。我们的研究结果表明，T3 治疗通过抑制 PI3K/AKT 信号通路促进 WAT 的褐变；这些发现为针对肥胖个体 WAT 体积的局部治疗提供了新的视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0399/11369215/0edcd94d43be/41598_2024_71591_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0399/11369215/a16edfa7fdb3/41598_2024_71591_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0399/11369215/a990b420aaee/41598_2024_71591_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0399/11369215/0fe92e9ac4a4/41598_2024_71591_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0399/11369215/1fa07d2a1607/41598_2024_71591_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0399/11369215/0edcd94d43be/41598_2024_71591_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0399/11369215/a16edfa7fdb3/41598_2024_71591_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0399/11369215/a990b420aaee/41598_2024_71591_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0399/11369215/0fe92e9ac4a4/41598_2024_71591_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0399/11369215/1fa07d2a1607/41598_2024_71591_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0399/11369215/0edcd94d43be/41598_2024_71591_Fig5_HTML.jpg

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