Induction of Fructose Mediated De Novo Lipogenesis Coexists with the Upregulation of Mitochondrial Oxidative Function in Mice Livers.

ABSTRACT:

Background

Dysfunctional mitochondrial metabolism and sustained de novo lipogenesis (DNL) are characteristics of metabolic dysfunction-associated steatotic liver disease (MASLD), a comorbidity of obesity and type 2 diabetes. Fructose, a common sweetener and a potent inducer of lipogenesis, contributes to the etiology of MASLD.

Objectives

Our goal was to determine whether higher rates of DNL, through its biochemical relationships with mitochondria, can contribute to dysfunctional induction of oxidative networks in the liver.

Methods

Male C57BL/6JN mice were given a low-fat (10% fat kcal, 49.9% corn starch kcal), high-fat (HF; 60% fat kcal), or HF/high-fructose diet (HF/HFr; 25% fat kcal, 34.9% fructose kcal) for 24 wk. In a follow-up study, mice on normal feed pellets

SUBMITTER: Bhattacharjee P 

PROVIDER: S-EPMC12264563 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature