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CD47 differentially regulates white and brown fat function.

Heather Norman-Burgdolf1,2, Dong Li1,3, Patrick Sullivan4,3

  • 1Department of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY 40536, USA.

Biology Open
|December 17, 2020
PubMed
Summary
This summary is machine-generated.

Mice lacking CD47 show enhanced energy expenditure and are protected against obesity. This is due to increased fat breakdown in white adipose tissue and improved mitochondrial function in brown adipose tissue.

Keywords:
Brown fatCD47LipolysisMitochondriaWhite fat

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Area of Science:

  • Metabolic research
  • Obesity mechanisms
  • Adipose tissue biology

Background:

  • Mechanisms to increase energy expenditure are key therapeutic targets for obesity.
  • Previous studies showed that mice lacking CD47 (Cluster of Differentiation 47) are leaner and protected from diet-induced obesity.

Purpose of the Study:

  • To investigate the physiological role of CD47 deficiency in regulating mitochondrial function and energy expenditure in white and brown adipose tissue.
  • To elucidate the mechanisms underlying the lean phenotype in CD47-deficient mice.

Main Methods:

  • Comparative analysis of white and brown adipose tissue morphology and function in CD47-deficient and wild-type mice.
  • Ex vivo and in vitro studies assessing lipolysis, lipogenesis, and mitochondrial respiration.
  • Measurement of free fatty acid-mediated uncoupling in brown adipose tissue mitochondria.

Main Results:

  • CD47-deficient mice exhibited comparable white fat mass but smaller adipocytes, indicating enhanced lipolysis.
  • Mitochondria from brown adipose tissue of CD47-deficient mice showed significantly higher rates of free fatty acid-mediated uncoupling.
  • No significant morphological differences were observed in brown adipose tissue between groups.

Conclusions:

  • CD47 deficiency enhances lipolysis in white adipose tissue, increasing fuel availability.
  • Elevated brown adipose tissue mitochondrial uncoupling, fueled by increased lipolysis, contributes to the lean phenotype and increased energy expenditure in CD47-deficient mice.