Pathogenesis of pre-diabetes: Mechanisms of fasting and postprandial hyperglycemia in people with impaired fasting glucose and/or impaired glucose tolerance

Gerlies Bock, Chiara Dalla Man, Marco Campioni, Elizabeth Chittilapilly, Rita Basu, Gianna Toffolo, Claudio Cobelli, Robert Rizza

Research output: Contribution to journalArticle

144 Scopus citations

Abstract

Thirty-two subjects with impaired fasting glucose (IFG) and 28 subjects with normal fasting glucose (NFG) ingested a labeled meal and 75 g glucose (oral glucose tolerance test) on separate occasions. Fasting glucose, insulin, and C-peptide were higher (P < 0.05) in subjects with IFG than in those with NFG, whereas endogenous glucose production (EGP) did not differ, indicating hepatic insulin resistance. EGP was promptly suppressed, and meal glucose appearance comparably increased following meal ingestion in both groups. In contrast, glucose disappearance (Rd) immediately after meal ingestion was lower (P < 0.001) in subjects with IFG/impaired glucose tolerance (IGT) and IFG/diabetes but did not differ in subjects with IFG/normal glucose tolerance (NGT) or NFG/NGT. Net insulin action (Si) and insulin-stimulated glucose disposal (Si*) were reduced (P < 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in subjects with NFG/NGT or IFG/NGT. Defective insulin secretion also contributed to lower postprandial Rd since disposition indexes were lower (P < 0.001, ANOVA) in subjects with NFG/IGT, IFG/IGT, and IFG/diabetes but did not differ in subjects with NFG/NGT and IFG/NGT. We conclude that postprandial hyperglycemia in individuals with early diabetes is due to lower rates of glucose disappearance rather than increased meal appearance or impaired suppression of EGP, regardless of their fasting glucose. In contrast, insulin secretion, action, and the pattern of postprandial turnover are essentially normal in individuals with isolated IFG.

Original languageEnglish (US)
Pages (from-to)3536-3549
Number of pages14
JournalDiabetes
Volume55
Issue number12
DOIs
StatePublished - Dec 1 2006

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism

Fingerprint Dive into the research topics of 'Pathogenesis of pre-diabetes: Mechanisms of fasting and postprandial hyperglycemia in people with impaired fasting glucose and/or impaired glucose tolerance'. Together they form a unique fingerprint.

  • Cite this

    Bock, G., Man, C. D., Campioni, M., Chittilapilly, E., Basu, R., Toffolo, G., Cobelli, C., & Rizza, R. (2006). Pathogenesis of pre-diabetes: Mechanisms of fasting and postprandial hyperglycemia in people with impaired fasting glucose and/or impaired glucose tolerance. Diabetes, 55(12), 3536-3549. https://doi.org/10.2337/db06-0319