Tissue-Specific Fructose Metabolism in Obesity and Diabetes
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PATHOGENESIS OF TYPE 2 DIABETES AND INSULIN RESISTANCE (M-E PATTI, SECTION EDITOR)
Tissue-Specific Fructose Metabolism in Obesity and Diabetes Robert N. Helsley 1 & Francois Moreau 2 & Manoj K. Gupta 3 & Aurelia Radulescu 4 & Brian DeBosch 5 & Samir Softic 1,2,6 Accepted: 10 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review The objective of this review is to provide up-to-date and comprehensive discussion of tissue-specific fructose metabolism in the context of diabetes, dyslipidemia, and nonalcoholic fatty liver disease (NAFLD). Recent Findings Increased intake of dietary fructose is a risk factor for a myriad of metabolic complications. Tissue-specific fructose metabolism has not been well delineated in terms of its contribution to detrimental health effects associated with fructose intake. Since inhibitors targeting fructose metabolism are being developed for the management of NAFLD and diabetes, it is essential to recognize how inability of one tissue to metabolize fructose may affect metabolism in the other tissues. The primary sites of fructose metabolism are the liver, intestine, and kidney. Skeletal muscle and adipose tissue can also metabolize a large portion of fructose load, especially in the setting of ketohexokinase deficiency, the rate-limiting enzyme of fructose metabolism. Fructose can also be sensed by the pancreas and the brain, where it can influence essential functions involved in energy homeostasis. Lastly, fructose is metabolized by the testes, red blood cells, and lens of the eye where it may contribute to infertility, advanced glycation end products, and cataracts, respectively. Summary An increase in sugar intake, particularly fructose, has been associated with the development of obesity and its complications. Inhibition of fructose utilization in tissues primary responsible for its metabolism alters consumption in other tissues, which have not been traditionally regarded as important depots of fructose metabolism. Keywords Sugar . Fructose . Insulin resistance . Diabetes . NAFLD . Dyslipidemia Robert N. Helsley and Francois Moreau contributed equally to this work. This article is part of the Topical Collection on Pathogenesis of Type 2 Diabetes and Insulin Resistance * Samir Softic [email protected] 1
Division of Pediatric Gastroenterology, Department of Pediatrics, University of Kentucky College of Medicine, Lexington, KY 40506, USA
2
Section on Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA
3
Islet Cell and Regenerative Medicine, Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, MA 02215, USA
4
Department of Pediatrics, University of Kentucky College of Medicine and Kentucky Children’s Hospital, Lexington, KY 40536, USA
5
Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63131, USA
6
Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, 138 Leader Ave
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