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Effect of short‐term starvation versus high‐fat diet on intramyocellular triglyceride accumulation and insulin resistance in physically fit men
Author(s) -
Johnson Nathan A.,
Stannard Stephen R.,
Rowlands David S.,
Chapman Phillip G.,
Thompson Campbell H.,
O'Connor Helen,
Sachinwalla Toos,
Thompson Martin W.
Publication year - 2006
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2006.033399
Subject(s) - medicine , endocrinology , insulin resistance , triglyceride , insulin , type 2 diabetes , pancreatic hormone , biology , diabetes mellitus , chemistry , cholesterol
It is currently believed that intramyocellular triglyceride (IMTG) accumulation and insulin resistance are a consequence of dietary fat ingestion and/or the elevated circulating lipid levels associated with chronic fat surplus. The purpose of this study was to compare the effect of short‐term starvation versus low‐carbohydrate (CHO)/high‐fat diet on IMTG accumulation and the development of insulin resistance in physically fit men. Intramyocellular triglyceride content, measured as intramyocellular lipid (IMCL) by proton magnetic resonance spectroscopy ( 1 H‐MRS), and glucose tolerance/insulin sensitivity, assessed by frequently sampled intravenous glucose tolerance test (IVGTT), were determined after 67 h of: (a) water‐only starvation (S); and (b) very low‐CHO/high‐fat diet (LC). These diets had in common significant restriction of CHO availability but large differences in fat content. All results were compared with those measured after a mixed CHO diet (C). Dietary interventions were administered by cross‐over design. The level of dietary‐induced IMTG accumulation ( P = 0.46), insulin resistance ( P = 0.27) and glucose intolerance ( P = 0.29) was not different between S and LC treatments. Intramyocellular triglyceride content and insulin sensitivity were negatively correlated ( r =−0.63, P < 0.01). Therefore, whilst insulin resistance may be due to fat accumulation at a cellular level, in the integrated human organism this outcome is not exclusively a function of dietary fat intake. The comparable level of IMTG accumulation and insulin resistance following S and LC may suggest that these metabolic perturbations are largely a consequence of the increased lipolytic response associated with CHO restriction.