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Low-carbohydrate ketogenic diets, glucose homeostasis, and nonalcoholic fatty liver disease

Schugar, Rebecca C.; Crawford, Peter A.

Current Opinion in Clinical Nutrition and Metabolic Care: July 2012 - Volume 15 - Issue 4 - p 374–380
doi: 10.1097/MCO.0b013e3283547157
CARBOHYDRATES: Edited by Luc Tappy and Bettina Mittendorfer

Purpose of review Obesity-associated nonalcoholic fatty liver disease (NAFLD) is highly prevalent, for which weight loss is the generally recommended clinical management. Low-carbohydrate ketogenic diets have been successful in promoting weight loss, but variations in the range of metabolic responses to these diets indicate that the effects of altering macronutrient content are not completely understood. This review focuses on the most recent findings that reveal the relationship between low-carbohydrate diets and NAFLD in rodent models and humans.

Recent findings Low-carbohydrate diets have been shown to promote weight loss, decrease intrahepatic triglyceride content, and improve metabolic parameters of patients with obesity. These ketogenic diets also provoke weight loss in rodents. However, long-term maintenance on a ketogenic diet stimulates the development of NAFLD and systemic glucose intolerance in mice. The relationship between ketogenic diets and systemic insulin resistance in both humans and rodents remains to be elucidated.

Summary Because low-carbohydrate ketogenic diets are increasingly employed for treatment of obesity, NAFLD, and neurological diseases such as epilepsy, understanding the long-term systemic effects of low-carbohydrate diets is crucial to the development of efficacious and safe dietary interventions.

Department of Medicine, Center for Cardiovascular Research, Washington University School of Medicine, St Louis, Missouri, USA

Correspondence to Peter A. Crawford, MD, PhD, Division of Cardiology, Department of Medicine, Washington University School of Medicine, Campus Box 8086, 660 S. Euclid Ave., St Louis, MO 63110, USA. Tel: +1 314 747 3009; fax: +1 314 219 4589; e-mail:

© 2012 Lippincott Williams & Wilkins, Inc.