[HTML][HTML] FoxO1 deacetylation decreases fatty acid oxidation in β-cells and sustains insulin secretion in diabetes
Pancreatic β-cell dysfunction contributes to onset and progression of type 2 diabetes. In this
state β-cells become metabolically inflexible, losing the ability to select between
carbohydrates and lipids as substrates for mitochondrial oxidation. These changes lead to β-
cell dedifferentiation. We have proposed that FoxO proteins are activated through
deacetylation-dependent nuclear translocation to forestall the progression of these
abnormalities. However, how deacetylated FoxO exert their actions remains unclear. To …
state β-cells become metabolically inflexible, losing the ability to select between
carbohydrates and lipids as substrates for mitochondrial oxidation. These changes lead to β-
cell dedifferentiation. We have proposed that FoxO proteins are activated through
deacetylation-dependent nuclear translocation to forestall the progression of these
abnormalities. However, how deacetylated FoxO exert their actions remains unclear. To …