Journal of Diabetes Investigation (Nov 2022)

Oral fat tolerance testing identifies abnormal pancreatic β‐cell function and insulin resistance in individuals with normal glucose tolerance

  • Lifang Liu,
  • Xiaoyu Hou,
  • An Song,
  • Yunpeng Guan,
  • Peipei Tian,
  • Chao Wang,
  • Luping Ren,
  • Yong Tang,
  • Ling Gao,
  • Xiaoping Xing,
  • Guangyao Song

DOI
https://doi.org/10.1111/jdi.13867
Journal volume & issue
Vol. 13, no. 11
pp. 1805 – 1813

Abstract

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Abstract Aims/Introduction Insulin sensitivity and β‐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 β‐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 β‐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 β‐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 LnISIM and LnDI. Conclusions In individuals with normal glucose tolerance, β‐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 β‐cell function and insulin resistance.

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