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Mild Suppression of Hyperinsulinemia to Treat Obesity and Insulin Resistance

Page, Melissa M.; Johnson, James D.

Trends in endocrinology and metabolism. Volume 29:Number 6 (2018, June); pp 389-399 -- Elsevier Science Pub. Co -- Elsevier

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  • Title:
    Mild Suppression of Hyperinsulinemia to Treat Obesity and Insulin Resistance
  • Author: Page, Melissa M.;
    Johnson, James D.
  • Found In: Trends in endocrinology and metabolism. Volume 29:Number 6 (2018, June); pp 389-399
  • Journal Title: Trends in endocrinology and metabolism
  • Subjects: Endocrinology--Periodicals; Metabolism--Periodicals; Metabolism; insulin--hyperinsulinemia--obesity--insulin resistance--glucose homeostasis; Dewey: 616.4
  • Rights: legaldeposit
  • Publication Details: Elsevier Science Pub. Co
    Elsevier
  • Abstract: Abstract :

    Insulin plays roles in lipid uptake, lipolysis, and lipogenesis, in addition to controlling blood glucose levels. Excessive circulating insulin is associated with adipose tissue expansion and obesity, yet a causal role for hyperinsulinemia in the development of mammalian obesity has proven controversial, with many researchers suggesting it as a consequence of insulin resistance. Recently, evidence that specifically reducing hyperinsulinemia can prevent and reverse obesity in animal models has been presented. Our experiments, and others in this field, question the current dogma that hyperinsulinemia is a response to obesity and/or insulin resistance. In this review, we discuss preclinical evidence in the context of the broader literature and speculate on the possibility of clinical translation of alternative approaches for treating obesity.

    Highlights:

    Insulin acts on multiple tissues to stimulate the synthesis and storage of carbohydrates, lipids, and proteins.

    Hypersecretion of insulin is a physiological contributor to diet-induced obesity in animal models.

    Obesity can be treated in adult mice following an acute reduction in insulin secretion.

    The results of clinical studies are mixed, and additional, more specific manipulations are needed to translate the preclinical knowledge for humans.


  • Identifier: System Number: LDEAvdc_100065561795.0x000001; Journal ISSN: 1043-2760; 10.1016/j.tem.2018.03.018
  • Publication Date: 2018
  • Physical Description: Electronic
  • Shelfmark(s): ELD Digital store

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