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Expansion of Islet-Resident Macrophages Leads to Inflammation Affecting Beta Cell Proliferation and Function in Obesity

ABSTRACT: Expansion of Islet-Resident Macrophages Leads to Inflammation Affecting Beta Cell Proliferation and Function in Obesity

PROVIDER: PRJNA438927 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6855580.fastq.gz	Fastqsanger.gz
	SRR6855581.fastq.gz	Fastqsanger.gz
	SRR6855582.fastq.gz	Fastqsanger.gz
	SRR6855583.fastq.gz	Fastqsanger.gz
	SRR6855584.fastq.gz	Fastqsanger.gz

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Expansion of Islet-Resident Macrophages Leads to Inflammation Affecting Beta Cell Proliferation and Function in Obesity

Project description:Inflammation is a key component of the pathogenesis of obesity-associated type 2 diabetes (T2D). However, the nature of T2D-associated islet inflammation and its impacts on T2D-associated beta cell abnormalities remain poorly defined. Using both diet-induced and genetically modified T2D animal models, we explore immune components of islet inflammation and define their roles in regulating beta cell function and proliferation. Our studies show that T2D-associated islet inflammation is uniquely dominated by macrophages, without the involvement of adaptive immune cells. We identify two islet macrophage populations, characterized by their distinct phenotypes, anatomical distributions and functional properties. Obesity induces a local expansion of intra-islet macrophages, independent of the replenishment from circulating monocytes. In contrast, the abundance of peri-islet macrophages is negligibly affected by obesity. Functionally, intra-islet macrophages impair beta cell function in a cell-cell contact dependent manner. In contrast, both intra- and peri-islet macrophage populations are able to promote beta cell proliferation. Together, these data provide a definitive view of the genesis of T2D-associated islet inflammation and define specific roles of islet macrophages in regulating beta cell function and proliferation.

2019-01-02 | GSE112002 | GEO

Expansion of Islet-Resident Macrophages Leads to Inflammation Affecting β Cell Proliferation and Function in Obesity.

Project description:The nature of obesity-associated islet inflammation and its impact on β cell abnormalities remains poorly defined. Here, we explore immune cell components of islet inflammation and define their roles in regulating β cell function and proliferation. Islet inflammation in obese mice is dominated by macrophages. We identify two islet-resident macrophage populations, characterized by their anatomical distributions, distinct phenotypes, and functional properties. Obesity induces the local expansion of resident intra-islet macrophages, independent of recruitment from circulating monocytes. Functionally, intra-islet macrophages impair β cell function in a cell-cell contact-dependent manner. Increased engulfment of β cell insulin secretory granules by intra-islet macrophages in obese mice may contribute to restricting insulin secretion. In contrast, both intra- and peri-islet macrophage populations from obese mice promote β cell proliferation in a PDGFR signaling-dependent manner. Together, these data define distinct roles and mechanisms for islet macrophages in the regulation of islet β cells.

| S-EPMC6701710 | biostudies-literature

Antioxidant program of islet-resident macrophages preserves β cell physiology

Project description:Macrophages residing inside mouse pancreatic islets have an activated phenotype at steady-state. To explore the molecular pathways involved in their polarization, we compared the transcriptomic signatures of islet-resident macrophages with autologous epididymal adipose tissue (EpiWAT)-resident macrophages. Our data confirmed the pro-inflammatory profile of islet marophages and revealed also strong anti-oxidant capacities compared to EpiWATcells.

2025-11-17 | GSE246999 | GEO

Antioxidant program of islet-resident macrophages preserves β cell physiology

Project description:Macrophages residing within mouse pancreatic islets display an activated phenotype at steady state, yet the molecular signatures underlying their polarization remain unclear. To investigate islet macrophage heterogeneity under physiological conditions, we isolated islet-resident immune cells from chow diet-fed adult male mice and performed single-cell RNA sequencing.

2025-11-14 | GSE245717 | GEO

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

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Antioxidant program of islet-resident macrophages preserves β cell physiology [dataset 3]

Project description:Macrophages residing inside mouse pancreatic islets have an activated phenotype at steady-state. We revealed that they also harbor an antioxidant profile driven by the cystine/glutamate antiporter SLC7A11. We thus explored the role of SLC7A11 in islet-resident macrophages under steady-state.

2025-11-17 | GSE307627 | GEO

Antioxidant program of islet-resident macrophages preserves β cell physiology

Project description:Antioxidant program of islet-resident macrophages preserves β cell physiology

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Antioxidant program of islet-resident macrophages preserves β cell physiology

Project description:Antioxidant program of islet-resident macrophages preserves β cell physiology

| PRJNA1029611 | ENA

Antioxidant program of islet-resident macrophages preserves β cell physiology

Project description:Antioxidant program of islet-resident macrophages preserves β cell physiology

| PRJNA1035525 | ENA

STING signaling in infiltrating macrophages mediates islet function in obesity

Project description:The innate immune regulator stimulator of interferon genes (STING) mediates self-DNA sensing and leads to the induction of type I interferons and inflammatory cytokines, which promotes the progression of various inflammatory and autoimmune diseases. Innate immune system plays a critical role in regulating obesity-induced islet dysfunction, whereas the potential effect of STING signaling remains unclear. Here, we demonstrate that STING is mainly expressed and activated in islet macrophages upon high-fat diet (HFD) feeding. Knocking-out STING alleviates HFD-induced islet inflammation by inhibiting the expression of pro-inflammatory cytokines and infiltration of macrophages. Mechanically, palmitic acid incubation promotes mitochondrial DNA leakage into the cytosol and subsequently activates cyclic AMP-GMP synthase (cGAS)-STING pathway in macrophages. Additionally, STING activation in macrophages impairs glucose-stimulated insulin secretion by mediating the engulfment of β cell insulin secretory granules. Genetically or pharmacologically inhibiting STING activation boosts insulin secretion and hyperglycemia. Together, these findings reveal a regulatory mechanism in controlling the islet inflammation and insulin secretion in diet-induced obesity and suggest that selective blocking of the STING activation maybe a promising strategy for treating type 2 diabetes.

2025-07-11 | GSE207876 | GEO

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