Year: 2020
Type: article
Abstract: Fatty acid oxidation inhibition is one approach to reducing blood glucose levels in type II diabetes. Skeletal muscle specific Carnitine Palmitoyltransferase 1b knockout mice (Cpt1bm-/-) cannot transport long-chain fatty acids into the mitochondria to be oxidized in order to produce energy. Cpt1bm-/- mice have debilitated fat oxidation, less fat mass and improved glucose utilization compared to control C57BL/6 mice fed a 25% fat diet.\nWe hypothesized that CPT1b inhibition could reduce fat mass and lower blood glucose levels in a genetic mouse model of obesity and diabetes. To test this, we bred Cpt1bm-/- mice to AY mice. AY mice, also referred to as lethal yellow mice, are mutated at the mouse agouti locus causing a yellow coat. AY mice are prone to obesity, diabetes, tumors and cancers. The goal of this study was to determine the effect of extended inhibition of fatty acid transport into skeletal muscle mitochondria in AY: Cpt1bm-/- mice.\nCompared to AY mice, AY: Cpt1bm-/- mice were more insulin sensitive and glucose tolerant. AY: Cpt1bm-/- mice showed improved performance on glucose and insulin tolerance tests despite minimal differences in fat mass between groups. However, liver weights of AY: Cpt1bm-/- mice were significantly less than liver weights of AY mice.
Source: Civil War Book Review
Author: Stone, Allison
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W6981399638