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SIRT3基因rs11246020多态性与餐后甘油三酯代谢异常相关。

SIRT3 rs11246020 Polymorphism Associated Postprandial Triglyceride Dysmetabolism.

作者信息

Yang Liqun, Zhang Zhimei, Zhen Yunfeng, Feng Jing, Chen Jinhu, Song Guangyao

机构信息

Department of Internal Medicine, Hebei Medical University, Shijiazhuang, Hebei Province, People's Republic of China.

Hebei Key Laboratory of Metabolic Disease, Shijiazhuang, Hebei Province, People's Republic of China.

出版信息

Diabetes Metab Syndr Obes. 2024 Mar 12;17:1279-1288. doi: 10.2147/DMSO.S450962. eCollection 2024.

Abstract

PURPOSE

Energy metabolism is regulated by SIRT3, no research has been done on the connection between lipid metabolism in the oral fat test and SIRT3 polymorphism. Thus, we conducted a case-control study to investigate the connection between postprandial lipid and SIRT3 polymorphism.

PATIENTS AND METHODS

402 non-obese Chinese subjects were enrolled and their postprandial lipid response to oral fat tolerance test (OFTT) was observed to understand the relationship between rs11246020 gene and postprandial triglyceride metabolism.

RESULTS

In a binary logic regression model, a protective effect of the T allele of the rs11246020 SIRT3 for postprandial hypertriglyceridemia was shown (OR=0.417, 95% CI = 0.219-0.794, p=0.008). Compared to the CC genotype, individuals with the TT+CT variant of the rs11246020 SIRT3 gene demonstrated significantly lower levels of homeostasis model assessment of insulin resistance (HOMA-IR) (p=0.04), postprandial plasma glucose (PPG) (p=0.037), fasting plasma glucose (FPG) (p=0.02), and 4-hour triglyceridemia (Tg) (p=0.032).

CONCLUSION

The C allele of rs11246020 SIRT3 gene may be a risk factor to increased possibility of postprandial triglyceridemia after an oral fat test, which involved in the mechanism of glucose and insulin metabolism.

摘要

目的

能量代谢受SIRT3调节,关于口腔脂肪试验中脂质代谢与SIRT3多态性之间的联系尚未有研究。因此,我们进行了一项病例对照研究,以探讨餐后脂质与SIRT3多态性之间的联系。

患者与方法

纳入402名非肥胖中国受试者,观察他们对口服脂肪耐量试验(OFTT)的餐后脂质反应,以了解rs11246020基因与餐后甘油三酯代谢之间的关系。

结果

在二元逻辑回归模型中,显示rs11246020 SIRT3的T等位基因对餐后高甘油三酯血症有保护作用(OR = 0.417,95% CI = 0.219 - 0.794,p = 0.008)。与CC基因型相比,rs11246020 SIRT3基因的TT + CT变异个体的胰岛素抵抗稳态模型评估(HOMA-IR)水平显著降低(p = 0.04),餐后血糖(PPG)(p = 0.037)、空腹血糖(FPG)(p = 0.02)和4小时甘油三酯血症(Tg)(p = 0.032)。

结论

rs11246020 SIRT3基因的C等位基因可能是口服脂肪试验后餐后甘油三酯血症可能性增加的危险因素,其参与了葡萄糖和胰岛素代谢机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b20e/10944304/ad73adb51a0e/DMSO-17-1279-g0001.jpg

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