Low-fat diet, and medium-fat diets containing coconut oil and soybean oil exert different metabolic effects in untrained and treadmill-trained mice

Abstract

BackgroundDiets containing fats of different proportions and types have been demonstrated to influence metabolism. These fats differ in long chain fatty acids (LCFAs) or medium chain fatty acids (MCFAs) content. In our laboratory using swimming as the training modality, MCFAs increased endurance attributed to increased activities of oxidative enzymes. How it affects whole-body metabolism remains unexplored. The present study investigated the metabolic, biochemical and genetic adaptations with treadmill running as the training modality.MethodsC57BL/6N mice were divided into untrained and trained groups and provided with low-fat (10% kcal from soybean oil), coconut oil (10% kcal from soybean oil, 20% kcal from coconut oil) or soybean oil (30% kcal from soybean oil) diet. Training was performed on a treadmill for 30 days. After recovery, whole-body metabolism at rest and during exercise, endurance, substrate metabolism, mitochondrial enzyme activities, and gene expression of training-adaptive genes in the muscle and liver were measured.ResultsAt rest, medium-fat diets decreased respiratory exchange ratio (RER) (p < 0.05). Training increased RER in all diet groups without affecting oxygen consumption (p < 0.05). During exercise, diets had no overt effects on metabolism while training decreased oxygen consumption indicating decreased energy expenditure (p < 0.05). Coconut oil without training improved endurance based on work (p < 0.05). Training improved all endurance parameters without overt effects of diet (p < 0.05). Moreover, training increased the activities of mitochondrial enzymes likely related to the increased expression of estrogen related receptor (ERR) α and ERRβ (p < 0.05). Coconut oil inhibited peroxisome proliferator-activated receptor (PPAR) β/δ activation and glycogen accumulation in the muscle but activated PPARα in the liver in the trained state (p < 0.05). Substrate utilization data suggested that coconut oil and/or resulting ketone bodies spared glycogen utilization in the trained muscle during exercise thereby preserving endurance.ConclusionOur data demonstrated the various roles of diet and fat types in training adaptation. Diets exerted different roles in PPAR activation and substrate handling in the context of endurance exercise training. However, the role of fat types in training adaptations is limited as training overwhelms and normalizes the effects of diet in the untrained state particularly on endurance performance, mitochondrial biogenesis, and ERR expression.

Low-intensity exercise induces acute shifts in liver and skeletal muscle substrate metabolism but not chronic adaptations in tissue oxidative capacity

“…Mice are more reliant on glucose at a given exercise intensity than humans; however, a goal of this study was to use protocols that emphasized lipid utilization. In this regard, untrained C57BL/6 mice exercising at the speeds and incline used in the present study have a respiratory quotient slightly below 0.8 (39), lending credence to the notion that lipid was likely a primary fuel utilized herein. All exercise bouts were performed during the light cycle (6 -10 AM) and were designed to recapitulate a low-exercise intensity, which induced a mild increase in blood lactate postexercise (Fig.…”

Coordinated Modulation of Energy Metabolism and Inflammation by Branched-Chain Amino Acids and Fatty Acids

“…Long-chain, medium-chain, and short-chain fatty acids regulate the expression of PGC-1α through different molecular mechanisms ( Supplementary Table 1 ). PGC-1α interplays with peroxisome proliferators-activated receptor γ (PPARγ) as PPARγ coactivator, and some medium-chain fatty acids (MCFAs) and short-chain fatty acids (SCFAs) could activate PPARγ and promote PGC-1α transcription to modulate mitochondrial biogenesis ( 53 – 57 ). Acetate treatment activated G-protein-coupled receptor 43 (GPR43), and GPR43 further activated ERK1/2 and cAMP response element-binding protein (CREB) in differentiated brown adipocytes, significantly increasing the mRNA expression levels of PGC-1α ( 57 , 58 ).…”

In silico identification of natural compounds from virgin coconut oil as potential ligand peroxisome proliferator-activated receptor-gamma as preventive food leads against colitis

“…[ 15 ] Other studies have also mentioned that VCO inhibits PPAR-β/δ in muscle and activates PPAR-a in the liver. [ 16 ] Hence, it is likely that VCO also influences colonic PPAR-γ, maintains the balance of intestinal immunity, and provides anti-inflammatory effects. The fact that PUFA contributes to the PPAR signaling pathway and makes VCO an anti-inflammatory makes it a candidate for preventing UC.…”