Dietary Medium-Chain Triglycerides Attenuate Hepatic Lipid Deposition in Growing Rats with Protein Malnutrition

Abstract

SummaryThe objective of this study was to investigate the effects of dietary mediumchain triglycerides (MCT) on hepatic lipid accumulation in growing rats with protein malnutrition. Weaning rats were fed either a low-protein diet (3%, LP) or control protein diet (20%, CP), in combination with or without MCT. The four groups were as follows: CP-MCT, CP ϩ MCT, LP Ϫ MCT, and LP ϩ MCT. Rats in the CP Ϫ MCT, CP ϩ MCT and LP ϩ MCT groups were pair-fed their respective diets based on the amount of diet consumed by the LP Ϫ MCT group. Rats were fed each experimental diet for 30 d. Four weeks later, the respiratory quotient was higher in the LP Ϫ MCT group than those in the other groups during the fasting period. Hepatic triglyceride content increased in the LP groups compared with the CP groups. Hepatic triglyceride content in the LP ϩ MCT group, however, was significantly decreased compared with that in the LP Ϫ MCT group. Levels of carnitine palmitoyltransferase (CPT) 1a mRNA and CPT2 mRNA were significantly decreased in the livers of the LP Ϫ MCT group, as compared with corresponding mRNA levels of the other groups. These results suggest that ingestion of a low-protein diet caused fatty liver in growing rats. However, when rats were fed the low-protein diet with MCT, hepatic triglyceride deposition was attenuated, and mRNA levels encoding CPT1a and CPT2 were preserved at the levels of rats fed control protein diets.

Dietary protein insufficiency: an important consideration in fatty liver disease?

“…It has been suggested that decreasing protein and replacing energy loss with a higher proportion of sucrose may be the driving force of the emerging high incidence of fatty liver disease in developing countries. In the studies we have explored here, protein was substituted by sucrose in two studies (27,50) and by a variety of starches in four other studies (9,40,49,55) demonstrating that replacing protein with a specific source of simple sugars was not solely responsible for the effects of low-protein diets observed. Is the development of fatty liver in this model due to low protein or high carbohydrate or a combination of both?…”

“…An inner mitochondrial membrane CPT2 then converts the long-chain acylcarnitine to acyl-CoA for β-oxidation. It has been reported that a low-protein diet (3 %) in weanling rodents impaired hepatic expression of CPT1 and CPT2 genes and promoted fatty liver development (27) . Fatty liver induced by this 3 % protein diet was attenuated when the rat diets were supplemented with dietary medium-chain TAG (27) .…”

“…It has been reported that a low-protein diet (3 %) in weanling rodents impaired hepatic expression of CPT1 and CPT2 genes and promoted fatty liver development (27) . Fatty liver induced by this 3 % protein diet was attenuated when the rat diets were supplemented with dietary medium-chain TAG (27) . While the evidence from low protein dietary studies so far is limited, existing data suggest a role of PPARα regulation and mitochondria in mediating the effect of paternal protein malnutrition on offspring hepatic metabolism (28) .…”

“…In animal models, feeding a 5 % of low-protein diet to Wistar rats for 4 weeks resulted in increased hepatic TAG accumulation (27) . Similarly, feeding Sprague-Dawley male rats with a low-protein diet for 4 weeks also led to hepatic TAG accumulation which was associated with down-regulation of hepatic microsomal TAG transfer protein and increased expression of acetyl CoA carboxylase (49) .…”

Regulation of odd chain fatty acid metabolism in the development of metabolic diseases in mice fed a low protein diet

“…NAFLD, which is a precursor for the development of T2DM and MS, is highly prevalent in the developing world particularly in the Middle East, South America and Africa. Studies in rodents and humans have shown that a low-protein diet (generally defined as < 9 % of total energy) causes several metabolic disturbances including increased oxidative stress, hepatic steatosis, glucose intolerance as well as elevated adiposity Kuwahata et al (2011), Kang et al (2011), Jahan-Mihan et al (2015) .…”