The present review will present the recent published results and discuss the main effects of nutrients, mainly fatty acids, on the expression of genes involved in lipid metabolism. In this sense, the review focuses in two phases: prenatal life and finishing phase, showing how nutrients can modulate gene expression affecting marbling and fatty acid profile in meat from ruminants. Adiposity in ruminants starts to be affected by nutrients during prenatal life when maternal nutrition affects the differentiation and proliferation of adipose cells enhancing the marbling potential. Therefore, several fetal programming studies were carried out in the last two decades in order to better understand how nutrients affect long-term expression of genes involved in adipogenesis and lipogenesis. In addition, during the finishing phase, marbling becomes largely dependent on starch digestion and glucose metabolism, being important to create alternatives to increase these metabolic processes, and modulates gene expression. Different lipid sources and their fatty acids may also influence the expression of genes responsible to encode enzymes involved in fat tissue deposition, influencing meat quality. In conclusion, the knowledge shows that gene expression is a metabolic factor affecting marbling and fatty acid profile in ruminant meat and diets and their nutrients have direct effect on how these genes are expressed.

The intestinal absorption of cholesterol and lipid micronutrients such as vitamin E has been shown to share some common pathways. The present study aims to further compare the uptake of cholesterol ([3H]cholesterol v. 22-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-23,24-bisnor-5-cholen-3-ol (NBD-cholesterol)) and tocopherol in Caco-2 TC-7 cells and in mouse intestine, with special focus on the respective roles of scavenger receptor class B type I (SR-BI) and Niemann-Pick C1-like 1 (NPC1L1). Conversely to NBD-cholesterol, the uptakes of [3H]cholesterol and tocopherol by Caco-2 cells were impaired by both block lipid transport-1 and ezetimibe, which inhibit SR-BI and NPC1L1, respectively. These inhibitions occurred only when cholesterol or tocopherol was delivered to cells included in micelles that contained biliary acid and at least oleic acid as a lipid. In vivo, after 2 h of digestion in mice, the uptake of the two cholesterol analogues and of tocopherol all showed distinct patterns along the duodenum–jejunum axis. [3H]Cholesterol uptake, which correlated closely to NPC1L1 mRNA expression in wild-type (wt) mice, was strongly inhibited by ezetimibe. Intestinal SR-BI overexpression did not change NPC1L1 expression and led to a significant increase in [3H]cholesterol uptake in the distal jejunum. Conversely, neither ezetimibe treatment nor SR-BI overexpression had an effect on NBD-cholesterol uptake. However, in contrast with SR-BI mRNA expression, tocopherol absorption increased strongly up to the distal jejunum in wt mice where it was specifically inhibited by ezetimibe, and was increased in the proximal intestine of intestinal SR-BI-overexpressing mice. Thus, cholesterol and tocopherol uptakes share common pathways in cell culture models, but display different in vivo absorption patterns associated with distinct contributions of SR-BI and NPC1L1.