No abstract

High-protein diets have been shown to alleviate detrimental effects of high-fat diets and this effect can be partially mimicked by dietary L-leucine supplementation. Here, we aimed to elucidate the early mechanisms and the specificity of leucine effects. We performed a 1-week trial with male C57BL/6 mice fed ad libitum with semisynthetic high-fat diets containing an adequate (10 % w/w, AP) or high (50 % w/w, HP) amount of whey protein, or supplemented with L-leucine corresponding to the leucine content within the HP diet (Leu) or supplemented with equimolar L-alanine (Ala). Food and water intake were monitored continuously using a computer-controlled monitor system and body composition changes were assessed using quantitative NMR. HP completely prevented the AP-induced accumulation of body fat. Leu and Ala resulted in a similar reduction of body fat accumulation which was intermediate between AP and HP. There were no significant effects on plasma glucose or insulin. Triacylglycerol content and gene expression of lipogenesis enzymes in liver as well as plasma cholesterol were reduced by HP compared to AP with Leu and Ala again showing intermediate effects. Body fat gain and liver triacylglycerols were strongly correlated with total energy intake. Water intake was rapidly increased by HP feeding and total water intake correlated strongly with total amino nitrogen intake. We concluded that the positive effects of high-protein diets on metabolic syndrome associated traits are acutely due to effects on satiety possibly linked to amino nitrogen intake and on the subsequent suppression of liver lipogenesis without evidence for a specific leucine effect.

High-protein diets have been shown to prevent the development of diet-induced obesity and can improve associated metabolic disorders in mice. Dietary leucine supplementation can partially mimic this effect. However, the molecular mechanisms triggering these preventive effects remain to be satisfactorily explained. Here we review studies showing a connection between high protein or total amino nitrogen intake and obligatory water intake. High amino nitrogen intake may possibly lower lipid storage, and prevent insulin resistance. Suggestions are made for further systematical studies to explore the relationship between water consumption, satiety, and energy expenditure. Moreover, these examinations should better distinguish between leucine-specific and unspecific effects. Research in this field can provide important information to justify dietary recommendations and strategies in promoting long-term weight loss and may help to reduce health problems associated with the comorbidities of obesity.

High protein diets can alleviate detrimental effects of high fat diets as discussed to be partially due to Leu. C57BL/6 male mice were fed ad libitum for 1 wk with high‐fat diets (20% of fat) containing an adequate (10%, APD) or high (50%, HPD) amount of whey protein, or supplemented with Leu corresponding to the Leu content within the HP diet (LD) or supplemented equimolar with Ala (AD) in order to clarify the specificity of Leu effects. Food and water intake were monitored (computer controlled system). Body composition was assessed (QMR). HP completely prevented the AP induced accumulation of body fat. LD and AD resulted in similar reductions of body fat accumulation which was intermediate between AP and HP. Triacylglycerol concentrations and gene expression of lipogenic enzymes in liver as well as plasma cholesterol were lower by HP compared to AP, both LD and AD showed intermediate effects. Body fat gains correlated with total energy intake (P<0.0001). Water intake rapidly increased by HP feeding and correlated with total nitrogen intake (P<0.0001). Feed energy efficiency correlated with energy intake (P<0.0001). We concluded that the positive effects of high protein diets on metabolic syndrome associated traits are mainly due to effects on satiety linked to amino‐N intake. There is no specific metabolic effect of Leu at least in the short term. Grants PE643/7‐1, PE643/10‐1, Deutsche Forschungsgemeinschaft, Germany.