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Changes in subcutaneous white adipose tissue cellular composition and molecular programs underlie glucose intolerance in persons with HIV

ABSTRACT: Changes in subcutaneous white adipose tissue cellular composition and molecular programs underlie glucose intolerance in persons with HIV

PROVIDER: PRJNA816914 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18338200_1.fastq.gz	Fastqsanger.gz
	SRR18338200_2.fastq.gz	Fastqsanger.gz
	SRR18338201_1.fastq.gz	Fastqsanger.gz
	SRR18338201_2.fastq.gz	Fastqsanger.gz
	SRR18338202_1.fastq.gz	Fastqsanger.gz

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Changes in subcutaneous white adipose tissue cellular composition and molecular programs underlie glucose intolerance in persons with HIV

Project description:Subcutaneous adipose tissue (SAT) is a critical regulator of systemic metabolic homeostasis. Persons with HIV (PWH) have an increased risk of metabolic diseases and have significant alterations in SAT immune cells compared with the general population. We generated a comprehensive SAT atlas from 59 PWH with a spectrum of metabolic diseases to characterize cellular compositional and transcriptional changes associated with glucose intolerance and demographic characteristics. In PWH, glucose intolerance was associated with increased lipid-associated macrophages, CD4+ and CD8+ T effector memory cells, and decreased perivascular macrophages. We observed a coordinated intercellular regulatory program enriched for genes related to inflammation and lipid-processing with glucose intolerance that was also present in diabetic HIV-negative persons. Finally, CD4+ tissue resident cells were most strongly associated with altered whole tissue expression of genes related to lipid and glucose metabolism. These data provide a comprehensive assessment of SAT immune cells that may contribute to glucose intolerance.

2023-08-30 | GSE198809 | GEO

Changes in subcutaneous white adipose tissue cellular composition and molecular programs underlie glucose intolerance in persons with HIV.

Project description:IntroductionSubcutaneous adipose tissue (SAT) is a critical regulator of systemic metabolic homeostasis. Persons with HIV (PWH) have an increased risk of metabolic diseases and significant alterations in the SAT immune environment compared with the general population.MethodsWe generated a comprehensive single-cell multi-omic SAT atlas to characterize cellular compositional and transcriptional changes in 59 PWH across a spectrum of metabolic health.ResultsGlucose intolerance was associated with increased lipid-associated macrophages, CD4+ and CD8+ T effector memory cells, and decreased perivascular macrophages. We observed a coordinated intercellular regulatory program which enriched for genes related to inflammation and lipid-processing across multiple cell types as glucose intolerance increased. Increased CD4+ effector memory tissue-resident cells most strongly associated with altered expression of adipocyte genes critical for lipid metabolism and cellular regulation. Intercellular communication analysis demonstrated enhanced pro-inflammatory and pro-fibrotic signaling between immune cells and stromal cells in PWH with glucose intolerance compared with non-diabetic PWH. Lastly, while cell type-specific gene expression among PWH with diabetes was globally similar to HIV-negative individuals with diabetes, we observed substantially divergent intercellular communication pathways.DiscussionThese findings suggest a central role of tissue-resident immune cells in regulating SAT inflammation among PWH with metabolic disease, and underscore unique mechanisms that may converge to promote metabolic disease.

| S-EPMC10499182 | biostudies-literature

Single-cell analysis of adipose tissue T cells in diabetic persons with HIV reveals high proportions of clonally expanded CMV-like CD4+ T cells with cytotoxic RNA transcriptomes

Project description:Persons with HIV have a disproportionate burden of metabolic disease, including type 2 diabetes. We hypothesized that the accumulation of chronically activated T cells in the adipose tissue of HIV+ persons is a central mechanism promoting local macrophage activation, impaired adipocyte function, and the development of HIV-associated glucose intolerance. Prior studies of immune activation and HIV-associated metabolic disease have only measured circulating T cell subsets. In contrast, in our study we recruited a longitudinal cohort of HIV+ patients on antiretroviral therapy ranging from insulin sensitive to overtly diabetic, in addition to HIV-negative diabetic controls, to identify potential mechanistic linkages between adipose-resident T cell cytokine signaling, adipose tissue inflammation, and glucose intolerance in HIV+ persons. This study may also provide further insight into the role of T cells in the development of glucose intolerance in HIV-negative patients.

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DNA methylation data for older persons with vs. without mild cognitive impairment

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Factors regulating subcutaneous adipose tissue storage, fibrosis, and inflammation may underlie low systemic rates of fatty acid mobilization in insulin sensitive obese adults

Project description:Although the rate of fatty acid release from adipose tissue into the systemic circulation is very high in most obese adults, some obese adults maintain relatively low rates of fatty acid release, which helps protect them against the development of systemic insulin resistance. The primary aim of this study was to identify factors in adipose tissue that may underlie low vs. high rates of fatty acid mobilization in a relatively homogeneous cohort of obese adults. We obtained subcutaneous abdominal adipose tissue samples from 30 obese adults (BMI: 38±1 kg/m2, age: 30±2 yr) after an overnight fast. We performed microarray analysis on the adiose tissue samples.

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Endothelial TFEB improves glucose intolerance via upregulation of IRS1 and IRS2

Project description:To determine whether endothelial TFEB is critical for glucose metabolism in vivo, we utilized EC-selective TFEB knockout mice and EC selective TFEB transgenic mice fed a high fat diet (HFD). EC-TFEB knockout mice exhibited significantly impaired glucose tolerance compared with control mice. Consistently, EC-TFEB transgenic mice showed improved glucose intolerance. In primary human ECs, small interfering RNA-mediated TFEB knockdown blunts the Akt signaling. adenovirus-mediated overexpression of TFEB consistently activates Akt signaling and significantly increases glucose uptake in ECs. Mechanically, TFEB upregulates insulin receptor substrate 1 and 2 (IRS1 and IRS2). TFEB increases IRS2 transcription measured by reporter gene and chromatin immunoprecipitation assays. Furthermore, we found that TFEB increases IRS1 protein via downregulation of microRNAs (miR-335, miR-495 and miR548o). In vivo, Akt signaling in the skeletal muscle and adipose tissue was significantly impaired in EC-TFEB knockout mice and consistently improved in EC-TFEB transgenic mice on HFD

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Progressive loss of PGC-1alpha expression in aging muscle potentiates glucose intolerance and systemic inflammation

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