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Review
. 2021 Feb;22(2):e13131.
doi: 10.1111/obr.13131. Epub 2020 Aug 19.

Pathophysiological role of metabolic flexibility on metabolic health

Jose E Galgani  1   2 , Rodrigo Fernández-Verdejo  1
Affiliations
Review

Pathophysiological role of metabolic flexibility on metabolic health

Jose E Galgani et al. Obes Rev. 2021 Feb.

Abstract

Glucose, fatty acids, and amino acids among others are oxidized to generate adenosine triphosphate (ATP). These fuels are supplied from the environment (through food intake) and internal depots (through lipolysis, glycogenolysis, and proteolysis) at different rates throughout the day. Complex adaptive systems permit to accommodate fuel oxidation according to fuel availability. This capacity of a cell, tissue, or organism to adapt fuel oxidation to fuel availability is defined as metabolic flexibility (MetF). There are conditions, such as insulin resistance, diabetes, and obesity, in which MetF seems to be impaired. The observation that those conditions are accompanied by mitochondrial dysfunction has set the basis to propose a link between mitochondrial dysfunction, metabolic inflexibility, and metabolic health. We here highlight the evidence about the notion that MetF influences metabolic health.

Keywords: Insulin resistance; Insulin sensitivity; Lipotoxicity; Obesity.

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References

REFERENCES

    1. Czech MP. Insulin action and resistance in obesity and type 2 diabetes. Nat Med. 2017;23(7):804-814.
    1. Befroy DE, Petersen KF, Dufour S, et al. Impaired mitochondrial substrate oxidation in muscle of insulin-resistant offspring of type 2 diabetic patients. Diabetes. 2007;56(5):1376-1381.
    1. Girousse A, Virtue S, Hart D, et al. Surplus fat rapidly increases fat oxidation and insulin resistance in lipodystrophic mice. Mol Metab. 2018;13:24-29.
    1. Keenan SN, Meex RC, Lo JCY, et al. Perilipin 5 deletion in hepatocytes remodels lipid metabolism and causes hepatic insulin resistance in mice. Diabetes. 2019;68(3):543-555.
    1. Fabbrini E, Yoshino J, Yoshino M, et al. Metabolically normal obese people are protected from adverse effects following weight gain. J Clin Invest. 2015;125(2):787-795.

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