Silencing the FABP3 gene in insulin-secreting cells reduces fatty acid uptake and protects against lipotoxicity.

ABSTRACT:

Background

Long-term exposure of pancreatic islets to fatty acids (FAs), common in obesity, metabolic syndrome, and type 2 diabetes, leads to a compensatory hyperactivity followed by inflammation, apoptosis, dysfunctional beta cells, and results in insulin dependence of the patient. Restriction of fatty uptake by islet beta cells may protect them from lipotoxicity.

Purpose

Pancreatic islet beta cells express the fatty acid binding protein 3 (FABP3) to bind FAs and to orchestrate lipid signals. Based on this, we investigated whether downregulation of FABP3, by Fabp3 silencing, might slow lipid metabolism and protect against lipotoxicity in insulin-secreting cells.

Results

Neither Fabp3 silencing, nor overexpression affected the glucose-stimulated insulin secretion in a

SUBMITTER: Hyder A 

PROVIDER: S-EPMC11628584 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature