Insufficient islet compensation to insulin resistance vs. reduced glucose effectiveness in glucose-intolerant mice

Bo Ahrén, G Pacini

Research output: Contribution to journalArticlepeer-review

78 Citations (SciVal)

Abstract

This study evaluated the relative contribution of insulin-dependent mechanisms vs. mechanisms independent on dynamic insulin for glucose intolerance induced by high-fat diet. C57BL/6J mice underwent a frequently sampled intravenous glucose tolerance test (1 g/kg glucose) at 1 wk and 1, 3, and 10 mo after initiation of a high-fat diet (58% fat; control diet 11% fat) to measure glucose effectiveness (S-G) and disposition index (DI), i.e., insulin sensitivity (SI) times early or total insulin secretion. Glucose disappearance (KG) and SI were reduced in high-fat-fed mice at all time points. Total (50 min) insulin secretion was sufficiently increased at all time points to compensate for the reduced SI, as judged by normal DI50 min. In contrast, early (10 min) insulin secretion was not sufficiently increased; DI10 min was reduced after 1, 3, and 10 mo. SG was reduced after 1 wk; the reduction persisted throughout the study period. Thus glucose intolerance induced by high-fat diet is, in early phases, solely explained by reduced glucose effectiveness, whereas insufficient early insulin secretion is of importance after long-term feeding.
Original languageEnglish
Pages (from-to)E738-E744
JournalAmerican Journal of Physiology: Endocrinology and Metabolism
Volume283
Issue number4
DOIs
Publication statusPublished - 2002

Subject classification (UKÄ)

  • Physiology

Keywords

  • glucose intolerance
  • insulin secretion
  • glucose tolerance
  • high-fat diet

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