Insulin resistance and metabolism: organ crosstalk

The goal of this program is to implement an inventory of the different animal models, tissues and cell cultures used.

Model of crosstalk between diverse organs and pancreatic beta cells under both physiological and insulin-resistant states. The different factors represented may have the potential to enhance glucose-stimulated insulin secretion or beta-cell proliferation (as IGF-1—insulin-like growth factor-1; GLP-1—glucagon-like peptide-1; kisspeptin1 and SCFAs—short-chain fatty acids) or negatively contribute to reduce functional beta-cell mass during type 2 diabetes progression (as leptin, CXCL10 and EVs—extracellular vesicles—from inflamed adipocytes or insulin-resistant muscle cells).