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Remission of obesity and insulin resistance is not sufficient to restore mitochondrial homeostasis in visceral adipose tissue. | LitMetric

Remission of obesity and insulin resistance is not sufficient to restore mitochondrial homeostasis in visceral adipose tissue.

Redox Biol

Department of Physiological Sciences, Universitat de Barcelona, 08907, Barcelona, Spain; Nutrition, Metabolism and Gene Therapy Group; Diabetes and Metabolism Program; Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), Barcelona, Spain; Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y la Nutrición (CIBEROBN), Instituto de Salud Carlos III, 28029, Madrid, Spain. Electronic address:

Published: August 2022

AI Article Synopsis

Article Abstract

Metabolic plasticity is the ability of a biological system to adapt its metabolic phenotype to different environmental stressors. We used a whole-body and tissue-specific phenotypic, functional, proteomic, metabolomic and transcriptomic approach to systematically assess metabolic plasticity in diet-induced obese mice after a combined nutritional and exercise intervention. Although most obesity and overnutrition-related pathological features were successfully reverted, we observed a high degree of metabolic dysfunction in visceral white adipose tissue, characterized by abnormal mitochondrial morphology and functionality. Despite two sequential therapeutic interventions and an apparent global healthy phenotype, obesity triggered a cascade of events in visceral adipose tissue progressing from mitochondrial metabolic and proteostatic alterations to widespread cellular stress, which compromises its biosynthetic and recycling capacity. In humans, weight loss after bariatric surgery showed a transcriptional signature in visceral adipose tissue similar to our mouse model of obesity reversion. Overall, our data indicate that obesity prompts a lasting metabolic fingerprint that leads to a progressive breakdown of metabolic plasticity in visceral adipose tissue.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9287736PMC
http://dx.doi.org/10.1016/j.redox.2022.102353DOI Listing

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