Doubling the amount of the branched chained amino acid (BCAA) leucine in a high-fat diet reversed many of negative metabolic effects associated with metabolic syndrome and caused an improvement in glucose tolerance and insulin signaling in a recent mouse study (PLoS ONE. May 23;6(6): e21187. DOI:10.1371/journal.pone.0021187). This study demonstrates how a single, simple dietary factor—leucine—can modify insulin resistance by acting on multiple tissues and at multiple levels of metabolism.
American researchers placed mice on either a normal or high-fat diet; both groups had twice the normal amount of dietary leucine added to their drinking water. After eight weeks on a high-fat diet, mice developed obesity, fatty liver, inflammatory changes in adipose tissue and insulin resistance, as well as alterations in metabolomic profile of amino acid metabolites, glucose and cholesterol metabolites, and fatty acids in liver, muscle, fat and serum.
However, doubling dietary leucine reversed many of the metabolite abnormalities and caused a marked improvement in glucose tolerance and insulin signaling even though the mice still gained weight. Increased dietary leucine was also associated with a decrease in liver disease and a decrease in inflammation in adipose tissue.
These data indicate that modest changes in a single environmental/nutrient factor can modify multiple metabolic and signaling pathways and modify high-fat diet induced metabolic syndrome by acting at a systemic level on multiple tissues. These data also suggest that increasing dietary leucine may provide an adjunct in the management of obesity-related insulin resistance.
Last year, leucine was found to not help muscle recovery, but this current study may give the miconutrient new life in metabolic syndrome products as opposed to sports nutrition products.