Abstract

Fasting and then refeeding on a high-carbohydrate diet increases serum and hepatic triacylglycerol (TAG) concentrations compared to standard diets. Fructose is a lipogenic monosaccharide which stimulates de novo fatty acid synthesis. Omega-3 (n-3) fatty acids stimulate hepatic β-oxidation, partitioning fatty acids away from TAG synthesis. This study investigated whether dietary n-3 fatty acids from fish oil (FO) improve the hepatic lipid metabolic response seen in rats fasted and then refed on a high-fructose diet. During the post-prandial (fed) period, rats fed a FO rich diet showed an increase in hepatic peroxisome proliferator-activated receptor α (PPAR-α) gene expression and decreased expression of carbohydrate responsive element binding protein (ChREBP), fatty acid synthase (FAS) and microsomal triglyceride transfer protein (MTTP). Feeding a FO rich diet for 7 days prior to 48 h of fasting resulted in lower hepatic TAG, lower PPAR-α expression and maintenance of hepatic n-3 fatty acid content. Refeeding on a high fructose diet promoted an increase in hepatic and serum TAG and in hepatic PPAR-α, ChREBP and MTTP expression. FO did not prevent the increase in serum and hepatic TAG after fructose refeeding, but did decrease hepatic expression of lipogenic genes and increased the n-3 fatty acid content of the liver. n-3 Fatty acids can modify some components of the hepatic lipid metabolic response to later feeding with a high fructose diet.

Highlights

  • Fasting increases the rate of triacylglycerol (TAG) lipolysis in adipose tissue, resulting in release of non-esterified fatty acids (NEFA) into the bloodstream

  • In the post-prandial state, lipid metabolism is dominated by secretion of TAG-rich lipoproteins from the enterocytes into the circulation from where the TAG fatty acids are cleared by adipose tissue for storage, with remnant lipoprotein particles being cleared by the liver

  • We examined the effect of including fish oil (FO) in the diet of rats on hepatic metabolic responses to feeding, to fasting for 48 h, and to refeeding on a control or high fructose diet following a period of fasting

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Summary

Introduction

Fasting increases the rate of triacylglycerol (TAG) lipolysis in adipose tissue, resulting in release of non-esterified fatty acids (NEFA) into the bloodstream These are used by various tissues as energy substrates. In the post-prandial (fed) state, lipid metabolism is dominated by secretion of TAG-rich lipoproteins from the enterocytes into the circulation from where the TAG fatty acids are cleared by adipose tissue for storage, with remnant lipoprotein particles being cleared by the liver. Components of these may be assembled into very-low density lipoproteins which are released from the liver again, delivering TAG to the circulation

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