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Insulin: The Receptor and Signaling Pathways01:28

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Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
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The Polycomb protein, Bmi1, regulates insulin sensitivity.

Corey E Cannon1, Paul M Titchenell1, David N Groff1

  • 1Institute for Diabetes, Obesity and Metabolism and the Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA.

Molecular Metabolism
|November 8, 2014
PubMed
Summary

Bmi1 (Polycomb Repressive Complex 1 component) loss enhances insulin sensitivity in adult mice by improving glucose uptake and hepatic glucose production. This suggests a novel role for Bmi1 in metabolic regulation.

Keywords:
Hepatic glucose productionInsulin signalingMuscle glucose uptakePolycomb Repressive Complex

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Area of Science:

  • Epigenetics and Gene Regulation
  • Metabolic Physiology
  • Molecular Endocrinology

Background:

  • Polycomb Repressive Complexes (PRC) 1 and 2 epigenetically regulate gene expression.
  • Bmi1, a PRC1 component, is vital for glucose homeostasis and beta cell mass by repressing the Ink4a/Arf locus.
  • The role of Bmi1 in adult glucose homeostasis remained unexplored due to early mortality in Bmi1 knockout models.

Purpose of the Study:

  • To investigate the function of Bmi1 in regulating glucose homeostasis and insulin sensitivity in adult mice.
  • To characterize the metabolic phenotype of mice with heterozygous Bmi1 deficiency.

Main Methods:

  • Metabolic phenotyping of Bmi1 (+/-) mice using in vivo and ex vivo analyses.
  • Performance of glucose and insulin tolerance tests and hyperinsulinemic-euglycemic clamps.
  • Assessment of the insulin signaling pathway at both protein and transcript levels.

Main Results:

  • A negative correlation was observed between Bmi1 levels and insulin sensitivity in aging and liver-specific insulin receptor deficiency models.
  • Heterozygous Bmi1 loss (Bmi1 (+/-)) significantly increased insulin sensitivity in adult mice without altering body weight or composition.
  • Hyperinsulinemic-euglycemic clamps demonstrated reduced hepatic glucose production and enhanced glucose disposal in Bmi1 (+/-) mice, indicating increased peripheral glucose uptake.
  • Elevated Akt phosphorylation in liver and muscle suggested improved insulin signaling.

Conclusions:

  • Bmi1 plays a previously unrecognized role in regulating insulin sensitivity.
  • Enhanced insulin sensitivity in Bmi1 (+/-) mice is mediated by improved Akt phosphorylation.
  • These findings establish Bmi1 as a potential therapeutic target for metabolic disorders.