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脂毒性通过内质网应激抑制垂体生长激素细胞生长激素的合成。

Lipotoxicity suppresses the synthesis of growth hormone in pituitary somatotrophs via endoplasmic reticulum stress.

机构信息

Department of Endocrinology, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.

Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, China.

出版信息

J Cell Mol Med. 2021 Jun;25(11):5250-5259. doi: 10.1111/jcmm.16532. Epub 2021 May 4.

Abstract

Lipotoxicity has been shown to cause dysfunction of many organs and tissues. However, it is unclear whether lipotoxicity is harmful to the somatotrophs, a kind of cell that synthesize growth hormone (GH) in the pituitary. In this study, we performed an epidemiological study, serum levels of triglyceride (TG) and GH showed a negative correlation, even after adjustment for potential confounders. In an animal study, male Sprague-Dawley rats were fed a high-fat diet (HFD) or a control diet for 28 weeks. HFD rats showed impaired GH synthesis, resulting in a decrease in circulating GH levels. The expression of pituitary Pit-1, a key transcription factor of GH, was inhibited. We found that the inositol-requiring enzyme 1α (IRE1α) pathway of endoplasmic reticulum (ER) stress was triggered in HFD rat pituitary glands and palmitic acid-treated GH3 cells, respectively. On the contrary, applying 4-phenyl butyric acid (4-PBA) to alleviate ER stress or 4µ8c to specifically block the IRE1α pathway attenuated the impairment of both Pit-1 and GH expression. In conclusion, we demonstrated that lipotoxicity directly inhibits the synthesis of GH, probably by reducing Pit-1 expression. The IRE1α signaling pathway of ER stress may play an important role in this process.

摘要

脂毒性已被证明会导致许多器官和组织的功能障碍。然而,脂毒性是否对合成生长激素(GH)的垂体细胞有损害尚不清楚。在这项研究中,我们进行了一项流行病学研究,血清甘油三酯(TG)和 GH 水平呈负相关,即使在调整了潜在混杂因素后也是如此。在一项动物研究中,雄性 Sprague-Dawley 大鼠用高脂肪饮食(HFD)或对照饮食喂养 28 周。HFD 大鼠表现出 GH 合成受损,导致循环 GH 水平下降。GH 的关键转录因子 Pit-1 在垂体中的表达受到抑制。我们发现内质网(ER)应激的肌醇需求酶 1α(IRE1α)途径分别在 HFD 大鼠垂体和棕榈酸处理的 GH3 细胞中被触发。相反,应用 4-苯基丁酸(4-PBA)缓解 ER 应激或 4µ8c 特异性阻断 IRE1α 途径可减轻 Pit-1 和 GH 表达的损害。总之,我们证明了脂毒性直接抑制 GH 的合成,可能是通过降低 Pit-1 的表达。ER 应激的 IRE1α 信号通路可能在这个过程中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/55c3/8178284/f0d21a6337e1/JCMM-25-5250-g002.jpg

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