Conjugated linoleic acid regulates adipocyte fatty acid binding protein expression via peroxisome proliferator-activated receptor α signaling pathway and increases intramuscular fat content

The liver plays a key role in lipid metabolism. Depending on species it is, more or less, the hub of fatty acid synthesis and lipid circulation through lipoprotein synthesis. Eventually the accumulation of lipid droplets into the hepatocytes results in hepatic steatosis, which may develop as a consequence of multiple dysfunctions such as alterations in beta-oxidation, very low density lipoprotein secretion, and pathways involved in the synthesis of fatty acids. In addition an increased circulating pool of non-esterified fatty acid may also to be a major determinant in the pathogenesis fatty liver disease. This review also focuses on transcription factors such as sterol-regulatory-element-binding protein-1c and peroxisome proliferator-activated receptor alpha, which promote either hepatic fatty acid synthesis or oxidation. Show more

CD36 (cluster of differentiation 36) is a scavenger receptor that functions in high-affinity tissue uptake of long-chain fatty acids (FAs) and contributes under excessive fat supply to lipid accumulation and metabolic dysfunction. This review describes recent evidence regarding the CD36 FA binding site and a potential mechanism for FA transfer. It also presents the view that CD36 and FA signaling coordinate fat utilization, a view that is based on newly identified CD36 actions that involve oral fat perception, intestinal fat absorption, secretion of the peptides cholecystokinin and secretin, regulation of hepatic lipoprotein output, activation of beta oxidation by muscle, and regulation of the production of the FA-derived bioactive eicosanoids. Thus abnormalities of fat metabolism and the associated pathology might involve dysfunction of CD36-mediated signal transduction in addition to the changes in FA uptake. Show more

Intramuscular fat (IMF) content plays a key role in various quality traits of meat. IMF content varies between species, between breeds and between muscle types in the same breed. Other factors are involved in the variation of IMF content in animals, including gender, age and feeding. Variability in IMF content is mainly linked to the number and size of intramuscular adipocytes. The accretion rate of IMF depends on the muscle growth rate. For instance, animals having a high muscularity with a high glycolytic activity display a reduced development of IMF. This suggests that muscle cells and adipocytes interplay during growth. In addition, early events that influence adipogenesis inside the muscle (i.e proliferation and differentiation of adipose cells, the connective structure embedding adipocytes) might be involved in interindividual differences in IMF content. Increasing muscularity will also dilute the final fat content of muscle. At the metabolic level, IMF content results from the balance between uptake, synthesis and degradation of triacylglycerols, which involve many metabolic pathways in both adipocytes and myofibres. Various experiments revealed an association between IMF level and the muscle content in adipocyte-type fatty acid-binding protein, the activities of oxidative enzymes, or the delta-6-desaturase level; however, other studies failed to confirm such relationships. This might be due to the importance of fatty acid fluxes that is likely to be responsible for variability in IMF content during the postnatal period rather than the control of one single pathway. This is evident in the muscle of most fish species in which triacylglycerol synthesis is almost zero. Genetic approaches for increasing IMF have been focused on live animal ultrasound to derive estimated breeding values. More recently, efforts have concentrated on discovering DNA markers that change the distribution of fat in the body (i.e. towards IMF at the expense of the carcass fatness). Thanks to the exhaustive nature of genomics (transcriptomics and proteomics), our knowledge on fat accumulation in muscles is now being underpinned. Metabolic specificities of intramuscular adipocytes have also been demonstrated, as compared to other depots. Nutritional manipulation of IMF independently from body fat depots has proved to be more difficult to achieve than genetic strategies to have lipid deposition dependent of adipose tissue location. In addition, the biological mechanisms that explain the variability of IMF content differ between genetic and nutritional factors. The nutritional regulation of IMF also differs between ruminants, monogastrics and fish due to their digestive and nutritional particularities. Show more