ArticlePloS one2013
Oral leucine supplementation is sensed by the brain but neither reduces food intake nor induces an anorectic pattern of gene expression in the hypothalamus.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 36 citations in OpenAlex.
- Nutrient-Based Appetite Regulation.Journal of obesity & metabolic syndrome · 2022Review
- Purinergic signaling in tanycytes and its contribution to nutritional sensing.Purinergic signalling · 2021Review
- Consumption of High-Leucine-Containing Protein Bar Following Breakfast Impacts Aminoacidemia and Subjective Appetite in Older Persons.Current developments in nutrition · 2021Article
- Branched-Chain Amino Acids and Brain Metabolism.Neurochemical research · 2017Review
- MicroRNA-182 Regulates Neurite Outgrowth Involving the PTEN/AKT Pathway.Frontiers in cellular neuroscience · 2017Article
- Reviewing the Effects of L-Leucine Supplementation in the Regulation of Food Intake, Energy Balance, and Glucose Homeostasis.Nutrients · 2015 · on this mapReview
- Neuronal STAT5 signaling is required for maintaining lactation but not for postpartum maternal behaviors in mice.Hormones and behavior · 2015Article
- Protein-dependent regulation of feeding and metabolism.Trends in endocrinology and metabolism: TEM · 2015Review
- SOCS3 deficiency in leptin receptor-expressing cells mitigates the development of pregnancy-induced metabolic changes.Molecular metabolism · 2015Article
- Inactivation of SOCS3 in leptin receptor-expressing cells protects mice from diet-induced insulin resistance but does not prevent obesity.Molecular metabolism · 2014Article
- Leucine acts in the brain to suppress food intake but does not function as a physiological signal of low dietary protein.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Article
- Dietary regulation of PI3K/AKT/GSK-3β pathway in Alzheimer's disease.Alzheimer's research & therapy · 2014Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leucine activates the intracellular mammalian target of the rapamycin (mTOR) pathway, and hypothalamic mTOR signaling regulates food intake. Although central infusion of leucine reduces food intake, it is still uncertain whether oral leucine supplementation is able to affect the hypothalamic circuits that control energy balance. We observed increased phosphorylation of p70s6k in the mouse hypothalamus after an acute oral gavage of leucine. We then assessed whether acute oral gavage of leucine induces the activation of neurons in several hypothalamic nuclei and in the brainstem. Leucine did not induce the expression of Fos in hypothalamic nuclei, but it increased the number of Fos-immunoreactive neurons in the area postrema. In addition, oral gavage of leucine acutely increased the 24 h food intake of mice. Nonetheless, chronic leucine supplementation in the drinking water did not change the food intake and the weight gain of ob/ob mice and of wild-type mice consuming a low- or a high-fat diet. We assessed the hypothalamic gene expression and observed that leucine supplementation increased the expression of enzymes (BCAT1, BCAT2 and BCKDK) that metabolize branched-chain amino acids. Despite these effects, leucine supplementation did not induce an anorectic pattern of gene expression in the hypothalamus. In conclusion, our data show that the brain is able to sense oral leucine intake. However, the food intake is not modified by chronic oral leucine supplementation. These results question the possible efficacy of leucine supplementation as an appetite suppressant to treat obesity.
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