Johnson Nathan A, Stannard Stephen R, Rowlands David S, Chapman Phillip G, Thompson Campbell H, O'Connor Helen, Sachinwalla Toos, Thompson Martin W
The School of Exercise and Sport Science, The University of Sydney, Lidcombe 1825, Australia.
Exp Physiol. 2006 Jul;91(4):693-703. doi: 10.1113/expphysiol.2006.033399. Epub 2006 Apr 20.
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 (1H-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.
目前认为，肌内甘油三酯（IMTG）蓄积和胰岛素抵抗是膳食脂肪摄入和/或与慢性脂肪过剩相关的循环脂质水平升高的结果。本研究的目的是比较短期饥饿与低碳水化合物（CHO）/高脂肪饮食对身体健康男性IMTG蓄积和胰岛素抵抗发展的影响。通过质子磁共振波谱（1H-MRS）测量肌内甘油三酯含量，以肌内脂质（IMCL）表示，并通过频繁采样静脉葡萄糖耐量试验（IVGTT）评估葡萄糖耐量/胰岛素敏感性，在67小时后测定：（a）仅饮水饥饿（S）；（b）极低CHO/高脂肪饮食（LC）。这些饮食的共同之处在于CHO可利用性受到显著限制，但脂肪含量差异很大。所有结果均与混合CHO饮食（C）后测得的结果进行比较。饮食干预采用交叉设计。S组和LC组治疗之间，饮食诱导的IMTG蓄积水平（P = 0.46）、胰岛素抵抗（P = 0.27）和葡萄糖不耐受（P = 0.29）无差异。肌内甘油三酯含量与胰岛素敏感性呈负相关（r = -0.63，P < 0.01）。因此，虽然胰岛素抵抗可能是由于细胞水平的脂肪蓄积，但在完整的人体中，这一结果并非完全取决于膳食脂肪摄入。S组和LC组后IMTG蓄积和胰岛素抵抗水平相当，这可能表明这些代谢紊乱在很大程度上是与CHO限制相关的脂解反应增加的结果。
