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Loss of Free Fatty Acid Receptor 2 leads to impaired islet mass and beta cell survival

ABSTRACT: Loss of Free Fatty Acid Receptor 2 leads to impaired islet mass and beta cell survival

PROVIDER: PRJNA1271074 | ENA |

REPOSITORIES: ENA

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Loss of Free Fatty Acid Receptor 2 leads to impaired islet mass and beta cell survival

Project description:The regulation of pancreatic β cell mass is a critical factor to help maintain normoglycemia during insulin resistance. Nutrient-sensing G protein-coupled receptors (GPCR) contribute to aspects of β cell function, including regulation of β cell mass. Nutrients such as free fatty acids (FFAs) contribute to precise regulation of β cell mass by signaling through cognate GPCRs, and considerable evidence suggests that circulating FFAs promote β cell expansion by direct and indirect mechanisms. Free Fatty Acid Receptor 2 (FFA2) is a β cell-expressed GPCR that is activated by short chain fatty acids, particularly acetate. Recent studies of FFA2 suggest that it may act as a regulator of β cell function. Here, we set out to explore what role FFA2 may play in regulation of β cell mass. Interestingly, Ffar2(-/-) mice exhibit diminished β cell mass at birth and throughout adulthood, and increased β cell death at adolescent time points, suggesting a role for FFA2 in establishment and maintenance of β cell mass. Additionally, activation of FFA2 with Gαq/11-biased agonists substantially increased β cell proliferation in in vitro and ex vivo proliferation assays. Collectively, these data suggest that FFA2 may be a novel therapeutic target to stimulate β cell growth and proliferation.

2025-08-08 | GSE298768 | GEO

Loss of Free Fatty Acid Receptor 2 leads to impaired islet mass and beta cell survival.

| S-EPMC4914960 | biostudies-literature

Hyperglycemia Alters the Fetal Islet Transcriptome and Leads to Progeny Islet Dysfunction

Project description:Hyperglycemia Alters the Fetal Islet Transcriptome and Leads to Progeny Islet Dysfunction

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Islet-Autonomous Inflammatory Signaling Propagates Autoimmunity and Promotes Diabetes in Nonobese Diabetic Mice

Project description:Type 1 diabetes (T1D) is an immune-mediated disease that leads to β cell dysfunction and death. However, the contribution of β cells in this process remains unclear. To understand how islet-derived pro-inflammatory signaling pathways contribute to diabetes pathogenesis, we generated inducible islet-specific Alox15 knockout mice on the NOD background. We report that islet-specific deletion of Alox15 induced a substantial increase of β-cell mass and decreased islet insulitis, and ultimately lead to a protection against spontaneous autoimmune diabetes in NOD mice. Single cell RNA-sequencing and mass spectrometry analysis revealed that islet-specific knockout of Alox15 leads to an increase of β cells expressing Pd-l1 and promotes an anti-inflammatory phenotype in myeloid cells and T cells inside the islets. Furthermore, islet- specific Alox15 deletion enhances the expansion of M2-like macrophages and regulatory T cells in the pancreatic islets and pancreatic lymph nodes. Together, these results lead to the conclusion that proinflammatory signals produced by β cells allows these cells to express immunoregulators that protects these cells of immune cell attack and promote β cell survival.

2021-02-11 | GSE166572 | GEO

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Pogz deficiency leads to abnormal behavior, transcription dysregulation and impaired cerebellar physiology

Project description:Pogz deficiency leads to abnormal behavior, transcription dysregulation and impaired cerebellar physiology

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Mettl3-mediated m6A Methylation Determines the Size of Endocrine Progenitor Pool and Postnatal Islet Mass

Project description:Mettl3-mediated m6A Methylation Determines the Size of Endocrine Progenitor Pool and Postnatal Islet Mass

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