No Indices of Increased Type 2 Diabetes Risk in Individuals with Reactive Postprandial Hypoglycemia.
Špela VolčanšekUrška Rahne PercMojca LunderDrazenka Pongrac BarlovicPublished in: Metabolites (2022)
Reactive postprandial hypoglycemia (RPH) is an understudied condition that lacks clinical definition, knowledge of future health implications, and an understanding of precise underlying mechanisms. Therefore, our study aimed to assess the glycemic response after glucose ingestion in individuals several years after the initial evaluation of RPH and to compare glucose regulation in individuals with RPH vs. healthy volunteers. We assessed the inter- and intra-individual differences in glucose, insulin, and C-peptide concentrations during 5-h oral glucose tolerance tests (OGTTs); the surrogate markers of insulin resistance (HOMA-IR and Matsuda index); and beta-cell function (distribution index and insulinogenic index). The study included 29 subjects with RPH (all females, aged 39 (28, 46) years) and 11 sex-, age-, and body mass index (BMI)-matched controls. No biochemical deterioration of beta-cell secretory capacity and no progression to dysglycemia after 6.4 ± 4.2 years of follow-up were detected. RPH subjects were not insulin resistant, and their insulin sensitivity did not deteriorate. RPH subjects exhibited no differences in concentrations or in the shape of the glucose-insulin curves during the 5-h OGTTs compared to age- and BMI-matched controls. No increased incident type 2 diabetes risk indices were evident in individuals with RPH. This dictates the need for further research to investigate the magnitude of future diabetes risk in individuals experiencing RPH.
Keyphrases
- type diabetes
- glycemic control
- blood glucose
- body mass index
- insulin resistance
- cardiovascular disease
- healthcare
- public health
- weight gain
- metabolic syndrome
- weight loss
- mental health
- stem cells
- single cell
- polycystic ovary syndrome
- mesenchymal stem cells
- social media
- adipose tissue
- risk assessment
- breast cancer risk
- cell therapy
- high fat diet induced