The chronic effects of fish oil with exercise on postprandial lipaemia and chylomicron homeostasis in insulin resistant viscerally obese men

Abstract

BackgroundVisceral obesity and insulin resistance are associated with a postprandial accumulation of atherogenic chylomicron remnants that is difficult to modulate with lipid-lowering therapies. Dietary fish oil and exercise are cardioprotective interventions that can significantly modify the metabolism of TAG-rich lipoproteins. In this study, we investigated whether chronic exercise and fish oil act in combination to affect chylomicron metabolism in obese men with moderate insulin resistance.MethodsThe single blind study tested the effect of fish oil, exercise and the combined treatments on fasting and postprandial chylomicron metabolism. Twenty nine men with metabolic syndrome were randomly assigned to take fish oil or placebo for four weeks, before undertaking an additional 12 week walking program. At baseline and at the end of each treatment, subjects were tested for concentrations of fasting apo B48, plasma lipids and insulin. Postprandial apo B48 and TAG kinetics were also determined following ingestion of a fat enriched meal.ResultsCombining fish oil and exercise resulted in a significant reduction in the fasting apo B48 concentration, concomitant with attenuation of fasting TAG concentrations and the postprandial TAGIAUC response (p < 0.05). Fish oil by itself reduced the postprandial TAG response (p < 0.05) but not postprandial apo B48 kinetics. Individual treatments of fish oil and exercise did not correspond with improvements in fasting plasma TAG and apo B48.ConclusionFish oil was shown to independently improve plasma TAG homeostasis but did not resolve hyper-chylomicronaemia. Instead, combining fish oil with chronic exercise reduced the plasma concentration of pro-atherogenic chylomicron remnants; in addition it reduced the fasting and postprandial TAG response in viscerally obese insulin resistant subjects.

α‐Linolenic acid and exercise training independently, and additively, decrease blood pressure and prevent diastolic dysfunction in obese Zucker rats

“…It has been well established that the consumption of n ‐3 PUFA (Slivkoff‐Clark et al . ; Anderson et al . ; Colussi et al .…”

“…) and the concentration of pro‐atherogenic chylomicron remnants (Slivkoff‐Clark et al . ), occur following a combined n ‐3 PUFA and exercise intervention. In addition, the consumption of flaxseed, which is high in ALA, in combination with exercise training, has been shown to improve plasma lipoprotein levels, oxidative stress and inflammation in a model of myocardial ischaemia (Naounou et al .…”

Postprandial lipemia as a cardiometabolic risk factor

“…In humans, while Tinker et al 133 showed that postprandial TRL apoB reduction is likely caused by omega-3 fatty acid mediated suppression of both hepatic and intestinal apoB secretion/synthesis, Slivkoff-Clark et al 134 showed that fish oil independently improved plasma TG homeostasis but did not resolve hyper-chylomicronemia. Instead, combining fish oil with chronic exercise reduced the plasma concentration of pro-atherogenic CM remnants 134 ; in addition it reduced the fasting and postprandial TG response in viscerally obese insulin resistant subjects 134 . In nonobese subjects a high-fish diet decreased TRL apoB48 concentration by reducing the secretion rate and the fractional catabolic rate of apoB48 135 .…”

Dyslipidemia in Obesity: Mechanisms and Potential Targets

“…The mechanism of exercise-induced LPL activity remains unclear, but it was hypothesized that exercise stimulates especially muscular LPL activity, although this could not be confirmed in a recent study [125]. A 12-week walking program supplemented with fish oil (1000 mg eicosepantenoic acid and 700 mg docosahexaenoic acid daily) in subjects with the MetS resulted in lower fasting TG and decreased the postprandial response of TG and apoB48 [126]. Exercise training for 16 weeks in obese subjects with NAFLD resulted in a small reduction in intra-hepatic TG content, although no changes in VLDL-TG or apoB100 secretion were observed [127].…”