Journal
JOURNAL OF DIABETES INVESTIGATION
Volume 13, Issue 11, Pages 1805-1813Publisher
WILEY
DOI: 10.1111/jdi.13867
Keywords
Insulin resistance; Insulin secretion; Triglyceridemia
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Funding
- Hebei Provincial Government of China
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This study investigated the impact of lipid metabolism disorders on insulin sensitivity and beta-cell function in individuals with normal glucose tolerance. The results showed that as lipid metabolism deteriorated, insulin sensitivity and beta-cell function gradually decreased, with both fasting and postprandial triglyceride concentrations affecting these functions. Postprandial triglyceride concentrations were identified as independent risk factors for impaired beta-cell function and insulin resistance in individuals with normal glucose tolerance.
Aims/Introduction Insulin sensitivity and beta-cell function are affected by lipid metabolism disorders, even before the onset of type 2 diabetes. People are in the postprandial state most of the time. Therefore, identifying postprandial hyperlipemia is important. This study aimed to assess patients with abnormalities in lipid metabolism, but with normal glucose tolerance, using oral fat tolerance testing (OFTT) to identify defects in insulin sensitivity and beta-cell function. Materials and Methods We included 248 volunteers with normal glucose tolerance who underwent OFTT. They were divided into three groups in accordance with their fasting and 4-h postprandial triglyceride (TG) concentrations. Their lipid concentrations during OFTT were compared. The disposition index (DI) was applied to estimate beta-cell function, and the Matsuda insulin sensitivity index (ISIM) was used to assess insulin sensitivity. We used multiple linear regression analysis to estimate the relationships of fasting and postprandial TG concentrations with beta-cell function and insulin sensitivity . Results The changes in TG concentrations during OFTT were more marked than those in low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol or total cholesterol concentrations. As lipid metabolism deteriorated, the ISIM and the DI gradually decreased. Multiple linear regression analysis showed that fasting and 4-h postprandial TG concentrations affected LnISI(M) and LnDI. Conclusions In individuals with normal glucose tolerance, beta-cell function and insulin sensitivity gradually decrease with a deterioration in the lipid profile. Not only fasting TG, but also postprandial TG concentrations are independent risk factors for impaired beta-cell function and insulin resistance.
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