A Diet High in Fat and Fructose Induces Early Hepatic Mitochondrial Aging. Issue 1 (July 2021)

• Record Type: Journal Article
• Authors: Bramlage, Kristin S.; Bhattacharjee, Jashdeep; Kirby, Michelle; Myronovych, Andriy; Gupta, Rohun; Gonzalez, Rosa-Maria Salazar; Xanthakos, Stavra; Bove, Kevin; Kohli, Rohit
• Is Part Of: Journal of pediatric gastroenterology and nutrition. Volume 73:Issue 1(2021)
• Publication Date: 2021-07
• Subjects: fatty liver -- NAFLD -- NASH -- obesity -- steatohepatitis; Children -- Nutrition -- Periodicals; Pediatric gastroenterology -- Periodicals; Infants -- Nutrition -- Periodicals; Nutrition disorders in children -- Periodicals; Child Nutrition -- Periodicals; Digestive System -- growth & development -- Periodicals; Gastrointestinal Diseases -- Periodicals; Infant Nutrition -- Periodicals; Nutrition Disorders -- Periodicals; Child; 618.923
• DOI: 10.1097/MPG.0000000000003068
• Languages: English
• ISSNs: 0277-2116

Abstract

Abstract : ABSTRACT: 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.