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n May 20, 2016, the Food and Drug Administration 1 O(FDA) published a set of new regulations. These new labeling requirements were the result of FDA review of new scientific data “on the associations between nutrients and chronic diseases, health-related conditions, physiological endpoints, and/or maintaining a healthy dietary pattern.” The proposal drew over 500 public comments, the majority of which were related to classifications of fats and carbohydrates, signifying that (1) there is great public interest in the topic of nutrition, (2) there exists great confusion regarding how one categorizes nutrients, and (3) more science is needed to determine definitively which nutrients and what quantity of these nutrients promote health or disease. In this issue of Cellular and Molecular Gastroenterology and Hepatology, the article by Duwaerts et al is, therefore, a timely publication that addresses the relative contribution of total caloric intake versus dietary nutrient content to the nonalcoholic fatty liver disease (NAFLD) epidemic. The authors used an isocaloric, mouse NAFLD model to investigate the effects of common dietary components on hepatic and adipose tissue lipid metabolism and glucose homeostasis. Mice were fed chronically for 6 months with a chow or 1 of 4 high-carbohydrate (sourced from either sucrose or starch), high-fat (sourced from either oleate or palmitate) diets. Although all combinations of the isocaloric diet increased hepatic steatosis compared with chow-fed mice, mice fed the starch-oleate diet exhibited the greatest degree of hepatic steatosis, hepatic inflammation, and glucose intolerance, arguably a surprising finding given the reported cardiovascular health benefits of oleate-rich diets. Based on in vivo metabolic tracer studies and analyses of liver and white adipose tissue depots, the authors concluded that combined high-carbohydrate/high-fat diets increase hepatic triglyceride content because of increased hepatic de novo lipogenesis. The authors observed additionally that white adipose tissue mass was reduced significantly in mice fed the oleate-containing diets compared with chow-fed animals, suggesting that adipocyte lipolysis and subsequent hepatic uptake of circulating free fatty acids may also contribute to the hepatic steatosis they observed. They tested this hypothesis by in vivo measurement of white adipose tissue lipogenesis and ex vivo measurement of lipolysis and concluded that, although adipocyte de novo lipogenesis is reduced in both oleate groups, lipolysis contributes significantly only to mice fed a starch-oleate diet. Moreover, they observed that the starcholeate diet caused the greatest amount of white adipocyte inflammation and necrosis by histology, gene array analysis, and flow cytometry analysis of NK cell infiltration. Notably, these findings were reproduced by mice fed a stereotypical Western diet.

In NAFLD, You Are What You Eat, Not Simply How Much You Eat