Open AccessA Diet High in Fat and Fructose Induces Early Hepatic Mitochondrial Aging
Author(s) -
Bramlage Kristin S.,
Bhattacharjee Jashdeep,
Kirby Michelle,
Myronovych Andriy,
Gupta Rohun,
Gonzalez RosaMaria Salazar,
Xanthakos Stavra,
Bove Kevin,
Kohli Rohit
Publication year - 2021
Publication title -
journal of pediatric gastroenterology and nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 131
eISSN - 1536-4801
pISSN - 0277-2116
DOI - 10.1097/mpg.0000000000003068
Subject(s) - steatosis , medicine , endocrinology , fructose , steatohepatitis , triglyceride , endoplasmic reticulum , mitochondrion , oxidative stress , chop , fatty liver , biology , biochemistry , cholesterol , chemotherapy , disease
To investigate the effect of high fructose diet on ultrastructure and content of hepatic mitochondria, we randomized 6–8 weeks old male C57Bl6/J mice to ad lib chow or high‐fat‐high‐fructose (HF2) diet for 32 weeks. HF2‐fed mice gained more weight, had higher plasma alanine aminotransferase, and fasting glucose levels and increased hepatic triglyceride content at all time points compared to chow‐fed mice. HF2‐fed mice had lower mitochondrial to nuclear DNA ratio compared to chow‐fed mice. HF2‐fed mice had lower average mitochondrial surface area and the number of mitochondria compared to chow‐fed mice. HF2‐fed mice had higher expression of the hepatic endoplasmic reticulum stress marker Chop , compared to chow‐fed mice. A diet high in fat and fructose leads to enhanced hepatic mitochondrial aging, depletion, and dysfunction, which may be important determinants of nonalcoholic steatohepatitis pathogenesis.