Display Settings:

Format

Send to:

Choose Destination
Annu Rev Nutr. 2005;25:391-406.

The insulin resistance syndrome: definition and dietary approaches to treatment.

Author information

  • Division of Cardiovascular Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA. greaven@cvmed.stanford.edu

Abstract

The ability of insulin to stimulate glucose disposal varies at least sixfold in apparently healthy individuals, and approximately one-third of the population that is most resistant to this action of insulin is at greatly increased risk to develop a number of adverse clinical outcomes. Type 2 diabetes occurs when insulin resistant individuals are unable to secrete enough insulin to compensate for the defect in insulin action, and this was the first clinical syndrome identified as being related to insulin resistance. Although the majority of insulin-resistant individuals are able to maintain the level of compensatory hyperinsulinemia needed to prevent the development of a significant degree of hyperglycemia, the combination of insulin resistance and hyperinsulinemia greatly increases the likelihood of developing a cluster of closely related abnormalities and the resultant clinical diagnoses that can be considered to make up the insulin resistance syndrome (IRS). Since being overweight/obese and sedentary decreases insulin sensitivity, it is not surprising that the prevalence of the manifestations of the IRS is increasing at a rapid rate. From a dietary standpoint, there are two approaches to attenuating the manifestations of the IRS: (a) weight loss to enhance insulin sensitivity in those overweight/obese individuals who are insulin resistant/hyperinsulinemic; and (b) changes in macronutrient content of diets to avoid the adverse effects of the compensatory hyperinsulinemia. This chapter will focus on defining the abnormalities and clinical syndromes that compose the IRS and evaluating the dietary changes that can ameliorate its adverse consequences.

PMID:
16011472
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Atypon
    Loading ...
    Write to the Help Desk