L-Leucine is an essential branched-chain amino acid (BCAA), which activates the mTOR signaling pathway[1].
L-Leucine (10 mM) treatment impairs endocrine progenitor cell development[1].In E13.5 rat pancreatic explants, in absence of added L-Leucine, Ngn3 mRNA levels increased after 1 day of culture, peaked on day 3, and then decreased. When L-Leucine is added, a dramatic decrease is observed in Ngn3 mRNA levels. This decrease in Ngn3 mRNA levels was paralleled by a decrease in the number of Ngn3-expressing cells (4728±408 vs. 959±28; PNgn3, its target Insm1, and insulin[1]. Leucine stimulates protein synthesis in skeletal muscle of neonatal pigs by enhancing mTORC1 activation. L-Leucine increases intracellular HIF-1α levels and activates the HIF-1α signaling pathway, and these two effects are mediated by the mTOR signaling pathway. This process results in Ngn3 repression and, consequently, decreases β-cell differentiation[1].
References:
[1]. Rachdi L, et al. L-leucine alters pancreatic β-cell differentiation and function via the mTor signaling pathway. Diabetes. 2012 Feb;61(2):409-17.
















