(07-09-06) Dietary glycemic index and liver steatosis.

Valtuena S, Pellegrini N, Ardigo D, Del Rio D, Numeroso F, Scazzina F, Monti L, Zavaroni I, Brighenti F.

Internal Medicine and Biomedical Sciences, University of Parma, Parma, Italy.

BACKGROUND: Insulin resistance (IR) and liver steatosis (LS) are interlinked metabolic derangements whose prevalence is rapidly increasing, but the effect of dietary carbohydrate quality on LS is unknown. OBJECTIVE: The objective was to describe the relation of IR and LS to total carbohydrate, total dietary fiber, and the glycemic index (GI) and glycemic load of the diet. DESIGN: The study was a cross-sectional evaluation of 247 apparently healthy subjects who had no evidence of viral, toxic, or autoimmune hepatitis and who were unselected for alcohol intake. The homeostasis model assessment index was used as a surrogate measure of IR, and a liver echography was used as a proxy for LS grading. Dietary data were collected by using 3-d food records. Total carbohydrate intake, total dietary fiber, GI, and glycemic load were calculated by using a semiquantitative food-frequency questionnaire concerning the dietary sources of carbohydrates. RESULTS: The prevalence of high-grade LS (HG-LS) increased significantly across quartiles of dietary GI (P for trend < 0.034): HG-LS in the 4th quartile (high GI) was twice that in the first 3 quartiles (low to medium GIs), whereas no relation was observed with total carbohydrates, total dietary fiber, or glycemic load. In insulin-sensitive subjects (first 3 quartiles of homeostasis model assessment index of IR), the prevalence of HG-LS did not differ significantly between GI groups, but, in insulin-resistant subjects (4th quartile of homeostasis model assessment index of IR), it was twice as high in those with high GI as in those with low to medium GIs (P = 0.005). CONCLUSIONS: High-GI dietary habits are associated with HG-LS, particularly in insulin-resistant subjects. Dietary advice on the quality of carbohydrate sources therefore may be a complementary tool for preventing or treating LS of metabolic origin.

PMID: 16825687 [PubMed - in process]
Am J Clin Nutr. 2006 Jul;84(1):136-42; quiz 268-9.

Source: www.pubmed.com

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