Ube2i Deletion in Adipocytes Causes Lipoatrophy in Mice

Authors

Aaron R Cox
Natasha Chernis
Kang Ho Kim
Peter M Masschelin
Pradip K Saha
Shawn M Briley
Robert Sharp
Xin Li
Jessica B Felix
Zheng Sun
David D Moore
Stephanie A Pangas
Sean M Hartig

Publication Date

6-1-2021

Journal

Molecular Metabolism

DOI

10.1016/j.molmet.2021.101221

PMID

33771728

PMCID

PMC8080079

PubMedCentral® Posted Date

3-24-2021

PubMedCentral® Full Text Version

Post-print

Published Open-Access

yes

Keywords

Adipocytes, Brown, Adipocytes, White, Adipokines, Adipose Tissue, Brown, Adipose Tissue, White, Animals, Body Composition, Energy Metabolism, Female, Gene Deletion, Hyperinsulinism, Insulin Resistance, Lipodystrophy, Male, Mice, Mice, Knockout, Non-alcoholic Fatty Liver Disease, Signal Transduction, Ubiquitin-Conjugating Enzymes, Ube2i, Lipodystrophy, Adipose tissue, Lipid metabolism

Abstract

OBJECTIVE: White adipose tissue (WAT) expansion regulates energy balance and overall metabolic homeostasis. The absence or loss of WAT occurring through lipodystrophy and lipoatrophy contributes to the development of hepatic steatosis and insulin resistance. We previously demonstrated that sole small ubiquitin-like modifier (SUMO) E2-conjugating enzyme Ube2i represses human adipocyte differentiation. The role of Ube2i during WAT development remains unknown.

METHODS: To determine how Ube2i impacts body composition and energy balance, we generated adipocyte-specific Ube2i knockout mice (Ube2i

RESULTS: Surprisingly, Ube2i

CONCLUSIONS: Our results demonstrate that Ube2i expression in mature adipocytes allows WAT expansion during postnatal growth. Deletion of Ube2i in fat cells compromises and diminishes adipocyte function that induces WAT inflammation and ectopic lipid accumulation in the liver. Our findings reveal an indispensable role for Ube2i during white adipocyte expansion and endocrine control of energy balance.

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