Mice lacking neutral amino acid transporter B(0)AT1 (Slc6a19) have elevated levels of FGF21 and GLP-1 and improved glycaemic control.

ABSTRACT:

Objective

Type 2 diabetes arises from insulin resistance of peripheral tissues followed by dysfunction of β-cells in the pancreas due to metabolic stress. Both depletion and supplementation of neutral amino acids have been discussed as strategies to improve insulin sensitivity. Here we characterise mice lacking the intestinal and renal neutral amino acid transporter B(0)AT1 (Slc6a19) as a model to study the consequences of selective depletion of neutral amino acids.

Methods

Metabolic tests, analysis of metabolite levels and signalling pathways were used to characterise mice lacking the intestinal and renal neutral amino acid transporter B(0)AT1 (Slc6a19).

Results

Reduced uptake of neutral amino acids in the intestine and loss of neutral amino acids in the urine causes

SUBMITTER: Jiang Y 

PROVIDER: S-EPMC4421019 | biostudies-literature | 2015 May

REPOSITORIES: biostudies-literature