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Metabolism

Cardiac Autophagy Deficiency Attenuates ANP Production and Disrupts Myocardial-Adipose Cross Talk, Leading to Increased Fat Accumulation and Metabolic Dysfunction

  1. Erfei Song1,2,
  2. Daniel Da Eira3,
  3. Shailee Jani3,
  4. Diane Sepa-Kishi3,
  5. Vivian Vu1,
  6. Howard Hunter4,
  7. Mi Lai5,
  8. Michael B. Wheeler5,6,
  9. Rolando B. Ceddia3 and
  10. Gary Sweeney1⇑
  1. 1Department of Biology, York University, Toronto, Canada
  2. 2The First Affiliated Hospital, Jinan University, Guangzhou, China
  3. 3School of Kinesiology and Health Science, York University, Toronto, Canada
  4. 4Department of Chemistry, York University, Toronto, Canada
  5. 5Department of Physiology, Faculty of Medicine, University of Toronto, Toronto, Canada
  6. 6University Health Network, Toronto, Canada
  1. Corresponding author: Gary Sweeney, gsweeney{at}yorku.ca
Diabetes 2021 Jan; 70(1): 51-61. https://doi.org/10.2337/db19-0762
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Abstract

Increased myocardial autophagy has been established as an important stress-induced cardioprotective response. Three weeks after generating cardiomyocyte-specific autophagy deficiency, via inducible deletion of autophagy-related protein 7 (Atg7), we found that these mice (AKO) had increased body weight and fat mass without altered food intake. Glucose and insulin tolerance tests indicated reduced insulin sensitivity in AKO mice. Metabolic cage analysis showed reduced ambulatory activity and oxygen consumption with a trend of elevated respiratory exchange ratio in AKO mice. Direct analysis of metabolism in subcutaneous and visceral adipocytes showed increased glucose oxidation and reduced ATGL expression and HSL phosphorylation with no change in lipid synthesis or fatty acid oxidation. Importantly, we found AKO mice had reduced myocardial and circulating levels of atrial natriuretic peptide (ANP), an established mediator of myocardial-adipose cross talk. When normal ANP levels were restored to AKO mice with use of osmotic pump, the metabolic dysfunction evident in AKO mice was corrected. We conclude that cardiac autophagy deficiency alters myocardial-adipose cross talk via decreased ANP levels with adverse metabolic consequences.

Footnotes

  • This article contains supplementary material online at https://doi.org/10.2337/figshare.13042601.

  • Received August 6, 2019.
  • Accepted October 1, 2020.
  • © 2020 by the American Diabetes Association
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Diabetes: 70 (1)

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Cardiac Autophagy Deficiency Attenuates ANP Production and Disrupts Myocardial-Adipose Cross Talk, Leading to Increased Fat Accumulation and Metabolic Dysfunction
Erfei Song, Daniel Da Eira, Shailee Jani, Diane Sepa-Kishi, Vivian Vu, Howard Hunter, Mi Lai, Michael B. Wheeler, Rolando B. Ceddia, Gary Sweeney
Diabetes Jan 2021, 70 (1) 51-61; DOI: 10.2337/db19-0762

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Cardiac Autophagy Deficiency Attenuates ANP Production and Disrupts Myocardial-Adipose Cross Talk, Leading to Increased Fat Accumulation and Metabolic Dysfunction
Erfei Song, Daniel Da Eira, Shailee Jani, Diane Sepa-Kishi, Vivian Vu, Howard Hunter, Mi Lai, Michael B. Wheeler, Rolando B. Ceddia, Gary Sweeney
Diabetes Jan 2021, 70 (1) 51-61; DOI: 10.2337/db19-0762
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