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Adipocyte-secreted lipids mediate adipose tissue and pancreas organ crosstalk

Grant number: 23/10725-4
Support Opportunities:Scholarships abroad - Research Internship - Post-doctor
Start date: January 31, 2024
End date: January 30, 2025
Field of knowledge:Biological Sciences - Biochemistry - Metabolism and Bioenergetics
Principal Investigator:Luiz Osório Silveira Leiria
Grantee:Fernanda Almeida de Oliveira
Supervisor: Stefan Offermanns
Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Institution abroad: Max Planck Society, Bad Nauheim, Germany  
Associated to the scholarship:21/03785-5 - Adipocyte-secreted lipids mediate adipose tissue and pancreas organ crosstalk, BP.PD

Abstract

Obesity is a pandemic with increasing prevalence and is a major independent risk factor for type 2 diabetes development and many other diseases. Insulin resistance can be observed in the early stages of obesity induced type 2 diabetes. Increased level of circulating insulin is usually noticed before hyperglycemia. Indeed, it can be observed two weeks after a high fat diet challenge. Hyperinsulinemia itself can contribute to many obesity-derived comorbidities and increase adiposity. On the other hand, lipolysis of the adipose tissue is strongly regulated by insulin and seen to be one of the first pathways affected by insulin resistance. There is evidence supporting the idea that lipolysis of adipose tissue can increase insulin secretion by releasing free fatty-acids or oxylipins capable of stimulating beta-cells but the hypothesis that dysregulated adipocyte lipolysis could be the hyperinsulinemia trigger remains untested and the molecular mediator and/or its receptor are unknown. Our aim is to identify the mediator and the corresponding receptor, which probably is a G-protein-mediated receptor (GPCR), to which the insulinotropic lipid can bind on the ²-cells, thereby uncovering new inter-organ pathways regulating the hyperinsulinemia in the context of obesity/T2DM. (AU)

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