Lifestyle impact on meal-induced insulin sensitization in health and prediabetes: a focus on diet, antioxidants, and exercise interventions

Can J Physiol Pharmacol. 2013 Feb;91(2):91-100. doi: 10.1139/cjpp-2012-0228. Epub 2013 Feb 11.


The augmented whole-body glucose uptake response to insulin during the postprandial state is described as meal-induced insulin sensitization (MIS). MIS occurs when the presence of food in the upper gastrointestinal tract activates 2 feeding signals (activation of hepatic parasympathetic nerves and elevation of hepatic glutathione level), and causes insulin to release hepatic insulin sensitizing substance (HISS), which stimulates glucose uptake in skeletal muscle, heart, and kidneys. HISS action results in nutrient storage, primarily as glycogen. Impairment of HISS release results in the absence of meal-induced insulin sensitization (AMIS), which causes postprandial hyperglycemia and hyperinsulinemia, and chronically leads to the progression to a cluster of metabolic, vascular, and cardiac dysfunctions, which we refer to as components of the AMIS syndrome. Manipulation of the MIS process in health and in disease, by pharmacological and nonpharmacological interventions, is outlined in this review. High fat or sugar supplemented diet reduces MIS; exercise elevates MIS; and antioxidants protect MIS against reductions associated with diet and age.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antioxidants / administration & dosage
  • Antioxidants / therapeutic use*
  • Blood Glucose / metabolism
  • Diet
  • Eating* / physiology
  • Exercise / physiology*
  • Humans
  • Insulin Resistance* / physiology
  • Life Style*
  • Liver / metabolism
  • Postprandial Period
  • Prediabetic State / blood
  • Prediabetic State / metabolism
  • Prediabetic State / prevention & control*


  • Antioxidants
  • Blood Glucose