Dicarboxylic acids counteract the metabolic effects of a Western diet by boosting energy expenditure
Lidia Castagneto-Gissey, … , Stefan R. Bornstein, Geltrude Mingrone
Lidia Castagneto-Gissey, … , Stefan R. Bornstein, Geltrude Mingrone
Published June 17, 2024
Citation Information: J Clin Invest. 2024;134(12):e181978. https://doi.org/10.1172/JCI181978.
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Commentary

Dicarboxylic acids counteract the metabolic effects of a Western diet by boosting energy expenditure

Abstract

Obesity has reached pandemic proportion not only in the West but also in other countries around the world; it is now one of the leading causes of death worldwide. A Western diet is rich in saturated fats and provides more calories than necessary, contributing to the rise of the obesity rate. It also promotes the development of liver steatosis, insulin resistance, hyperglycemia, and hyperlipidemia. In this issue of the JCI, Goetzman and colleagues describe the effects of consuming dicarboxylic acids (DAs) as an alternative source of dietary fat. The 12-carbon dicarboxylic acid (DC12) was administered to mice at 20% of their daily caloric intake for nine weeks in place of triglycerides. Notably, the change in diet increased the metabolic rate, reduced body fat, reduced liver fat, and improved glucose tolerance. These findings highlight DAs as useful energy nutrients for combatting obesity and treating various metabolic disorders.

Authors

Lidia Castagneto-Gissey, Stefan R. Bornstein, Geltrude Mingrone

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Figure 1

DC12 serves as an alternative source of dietary fat.

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DC12 serves as an alternative source of dietary fat. (A) Mice fed a high...
(A) Mice fed a high-fat diet very rich in saturated fatty acids develop obesity and hepatic steatosis and show enhanced circulated levels of glucose and insulin after intraperitoneal glucose administration. In contrast, the addition of 10% DC12 prevents such metabolic disorders. (B) DC12 undergoes β-oxidation in the mitochondria and peroxisomes to form the end products acetyl-CoA and succinyl-CoA. While DC12 is completely oxidized to CO2 and H2O in the mitochondria, acetyl-CoA produced in peroxisomes is transported into the mitochondria where it is completely oxidized.