Abstract
Understanding human physiological responses to high‐fat energy excess (HFEE) may help combat the development of metabolic disease. We aimed to investigate the impact of manipulating the n‐3PUFA content of HFEE diets on whole‐body and skeletal muscle markers of insulin sensitivity. Twenty healthy males were overfed (150% energy, 60% fat, 25% carbohydrate, 15% protein) for 6 d. One group (n = 10) received 10% of fat intake as n‐3PUFA rich fish oil (HF‐FO), and the other group consumed a mix of fats (HF‐C). Oral glucose tolerance tests with stable isotope tracer infusions were conducted before, and following, HFEE, with muscle biopsies obtained in basal and insulin‐stimulated states for measurement of membrane phospholipids, ceramides, mitochondrial enzyme activities, and PKB and AMPKα2 activity. Insulin sensitivity and glucose disposal did not change following HFEE, irrespective of group. Skeletal muscle ceramide content increased following HFEE (8.5 ± 1.2 to 12.1 ± 1.7 nmol/mg, p = .03), irrespective of group. No change in mitochondrial enzyme activity was observed following HFEE, but citrate synthase activity was inversely associated with the increase in the ceramide content (r=−0.52, p = .048). A time by group interaction was observed for PKB activity (p = .003), with increased activity following HFEE in HF‐C (4.5 ± 13.0mU/mg) and decreased activity in HF‐FO (−10.1 ± 20.7 mU/mg) following HFEE. Basal AMPKα2 activity increased in HF‐FO (4.1 ± 0.6 to 5.3 ± 0.7mU/mg, p = .049), but did not change in HF‐C (4.6 ± 0.7 to 3.8 ± 0.9mU/mg) following HFEE. We conclude that early skeletal muscle signaling responses to HFEE appear to be modified by dietary n‐3PUFA content, but the potential impact on future development of metabolic disease needs exploring.
Highlights
Dietary energy and fat overconsumption leading to body mass gain is associated with the development of obesity and insulin resistance (Chan et al, 1994; Colditz et al, 1995)
The present data confirm previous observations that subcellular events resulting from high-fat energy excess (HFEE) precede the clear development of whole-body insulin resistance
Six days of HFEE led to increased skeletal muscle ceramide content, the longer chain ceramide species
Summary
Dietary energy and fat overconsumption leading to body mass gain is associated with the development of obesity and insulin resistance (Chan et al, 1994; Colditz et al, 1995). Investigation of the early physiological responses of humans to dietary fat and energy excess is important to improve our understanding of the chronic (mal) adaptations that lead to obesity, insulin resistance, and T2D, and to inform the development of targeted preventative strategies to address these early responses. Studies using equal proportions of the three main classes of fats (SFA, monounsaturated (MUFA), and polyunsaturated (PUFA)) have failed to demonstrate an influence of overfeeding on whole-body measures of insulin sensitivity (Adochio et al, 2009; Brøns et al, 2009; Cornier et al, 2006). There is clear rationale that the fat composition of HFEE diets could modulate the metabolic consequences of overfeeding
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