SIRT3 rs11246020 Polymorphism Associated Postprandial Triglyceride Dysmetabolism

• Published in: Diabetes, metabolic syndrome and obesity Vol. 17; pp. 1279 - 1288
• Main Authors: Yang, Liqun, Zhang, Zhimei, Zhen, Yunfeng, Feng, Jing, Chen, Jinhu, Song, Guangyao
• Format: Journal Article
• Language: English
• Published: New Zealand Dove Medical Press Limited 01.01.2024; Dove Medical Press
• Subjects: Dextrose; Genes; Genetic aspects; genetics; Glucose; Glucose metabolism; Insulin; Insulin resistance; Physiological aspects; postprandial hypertriglyceridemia; Risk factors; sirtuin; Triglycerides; Type 2 diabetes; China; genetics; postprandial hypertriglyceridemia; sirtuin; insulin resistance
• ISSN: 1178-7007; 1178-7007
• DOI: 10.2147/DMSO.S450962

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. 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. 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). 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.