Selective enhancement of insulin sensitivity in the mature adipocyte is sufficient for systemic metabolic improvements

Thomas S. Morley, Jonathan Y. Xia, Philipp E. Scherer

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

Dysfunctional adipose tissue represents a hallmark of type 2 diabetes and systemic insulin resistance, characterized by fibrotic deposition of collagens and increased immune cell infiltration within the depots. Here we generate an inducible model of loss of function of the protein phosphatase and tensin homologue (PTEN), a phosphatase critically involved in turning off the insulin signal transduction cascade, to assess the role of enhanced insulin signalling specifically in mature adipocytes. These mice gain more weight on chow diet and short-term as well as long-term high-fat diet exposure. Despite the increase in weight, they retain enhanced insulin sensitivity, show improvements in oral glucose tolerance tests, display reduced adipose tissue inflammation and maintain elevated adiponectin levels. These improvements also lead to reduced hepatic steatosis and enhanced hepatic insulin sensitivity. Prolonging insulin action selectively in the mature adipocyte is therefore sufficient to maintain normal systemic metabolic homeostasis.

Original languageEnglish (US)
Article number7906
JournalNature Communications
Volume6
DOIs
StatePublished - Aug 5 2015

Fingerprint

insulin
Adipocytes
Insulin Resistance
Insulin
Adipose Tissue
augmentation
sensitivity
adipose tissues
diets
phosphatases
Phosphoprotein Phosphatases
Liver
Adiponectin
High Fat Diet
Glucose Tolerance Test
Nutrition
Phosphoric Monoester Hydrolases
Type 2 Diabetes Mellitus
Weight Gain
Signal Transduction

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Chemistry(all)
  • Physics and Astronomy(all)

Cite this

Selective enhancement of insulin sensitivity in the mature adipocyte is sufficient for systemic metabolic improvements. / Morley, Thomas S.; Xia, Jonathan Y.; Scherer, Philipp E.

In: Nature Communications, Vol. 6, 7906, 05.08.2015.

Research output: Contribution to journalArticle

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