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B cell-derived nociceptin/orphanin FQ contributes to impaired glucose tolerance and insulin resistance in obesity

ABSTRACT: B cell-derived nociceptin/orphanin FQ contributes to impaired glucose tolerance and insulin resistance in obesity

PROVIDER: PRJNA1185752 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31334682_1.fastq.gz	Fastqsanger.gz
	SRR31334682_2.fastq.gz	Fastqsanger.gz
	SRR31334683_1.fastq.gz	Fastqsanger.gz
	SRR31334683_2.fastq.gz	Fastqsanger.gz
	SRR31334684_1.fastq.gz	Fastqsanger.gz

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B cell-derived nociceptin/orphanin FQ contributes to impaired glucose tolerance and insulin resistance in obesity

Project description:B cells play a significant, yet underexplored, role in modulating immune responses in obesity and type 2 diabetes. In this study, we investigate the impact of B cell-derived nociceptin/orphanin FQ (N/OFQ) on metabolic function and inflammation in the context of obesity. Using a B cell-specific Pnoc knockout mouse model (PnocΔCD19), we demonstrate that loss of N/OFQ expression in B cells improves insulin sensitivity and glucose tolerance, particularly in the context of high-fat diet (HFD)-induced obesity. PnocΔCD19 mice exhibit a marked reduction in immune cell migration markers and macrophage recruitment in liver and adipose tissue. Mechanistically, we demonstrate that N/OFQ facilitates macrophage migration, contributing to the glucose intolerance and insulin resistance associated with obesity. Overall, the immunomodulatory properties exhibited by the N/OFQ-NOP system render it a compelling therapeutic target for metabolic inflammation.

2025-05-12 | GSE281815 | GEO

B cell-derived nociceptin/orphanin FQ contributes to impaired glucose tolerance and insulin resistance in obesity [THP1]

2025-05-12 | GSE281913 | GEO

B cell-derived nociceptin/orphanin FQ contributes to impaired glucose tolerance and insulin resistance in obesity [liver]

2025-05-12 | GSE281911 | GEO

B cell-derived nociceptin/orphanin FQ contributes to impaired glucose tolerance and insulin resistance in obesity [liver]

Project description:B cell-derived nociceptin/orphanin FQ contributes to impaired glucose tolerance and insulin resistance in obesity [liver]

| PRJNA1186167 | ENA

B cell-derived nociceptin/orphanin FQ contributes to impaired glucose tolerance and insulin resistance in obesity [THP1]

Project description:B cell-derived nociceptin/orphanin FQ contributes to impaired glucose tolerance and insulin resistance in obesity [THP1]

| PRJNA1186168 | ENA

Nociceptin/orphanin FQ opioid receptor selective ligand MCOPPB as a potent senolytic drug

Project description:Nociceptin/orphanin FQ opioid receptor selective ligand MCOPPB as a potent senolytic drug

| PRJNA678239 | ENA

RiboTag enrichment of aBNST nociceptin neurons

Project description:We report the differential expression of genes in aBNST nociceptin neurons in comparison to the whole aBNST in mice

2019-11-04 | GSE135982 | GEO

Gordonia sp. FQ

Project description:Gordonia sp. FQ genome sequencing

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Natural history of insulin sensitivity and insulin secretion in the progression from normal glucose tolerance to impaired fasting glycemia and impaired glucose tolerance: the Inter99 study.

Project description:ObjectiveThe aim of this study was to describe the natural history of insulin secretion and insulin sensitivity in the development of isolated impaired fasting glycemia (i-IFG), isolated impaired glucose tolerance (i-IGT), and combined IFG/IGT.Research design and methodsBaseline and 5-year follow-up data from the Inter99 study were used. Individuals with normal glucose tolerance (NGT) at baseline and i-IFG, i-IGT, combined IFG/IGT, or NGT at the 5-year follow-up were examined with an oral glucose tolerance test (n = 3,145). Insulin sensitivity index (ISI), homeostasis model assessment of insulin sensitivity (HOMA-IS), early-phase insulin release (EPIR), and insulin secretion relative to insulin action (disposition index) were estimated.ResultsFive years before the pre-diabetes diagnoses (i-IFG, i-IGT, and IFG/IGT), ISI, HOMA-IS, EPIR, and disposition index were lower than in individuals who maintained NGT. During the 5-year follow-up, individuals developing i-IFG experienced a significant decline only in HOMA-IS, whereas individuals developing i-IGT experienced significant declines in ISI, EPIR, and disposition index. Individuals with IFG/IGT exhibited pronounced declines in ISI, HOMA-IS, EPIR, and disposition index during the 5-year follow-up.ConclusionsA stationary reduced insulin secretion followed by a decline in primarily hepatic insulin sensitivity characterizes the transition from NGT to i-IFG. In contrast, low whole-body insulin sensitivity with a secondary lack of beta-cell compensation is associated with the development of i-IGT. Thereby, i-IFG and i-IGT appear to result from different underlying mechanisms, which may have implications for the prevention and treatment of the diabetes that succeeds them.

| S-EPMC2646025 | biostudies-literature

Genetic and pharmacological evidence that endogenous nociceptin/orphanin FQ contributes to dopamine cell loss in Parkinson's disease.

Project description:To investigate whether the endogenous neuropeptide nociceptin/orphanin FQ (N/OFQ) contributes to the death of dopamine neurons in Parkinson's disease, we undertook a genetic and a pharmacological approach using NOP receptor knockout (NOP(-/-)) mice, and the selective and potent small molecule NOP receptor antagonist (-)-cis-1-methyl-7-[[4-(2,6-dichlorophenyl)piperidin-1-yl]methyl]-6,7,8,9-tetrahydro-5H-benzocyclohepten-5-ol (SB-612111). Stereological unbiased methods were used to estimate the total number of dopamine neurons in the substantia nigra of i) NOP(-/-) mice acutely treated with the parkinsonian neurotoxin 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP), ii) naïve mice subacutely treated with MPTP, alone or in combination with SB-612111, iii) rats injected with a recombinant adeno-associated viral (AAV) vector overexpressing human mutant p.A53T α-synuclein, treated with vehicle or SB-612111. NOP(-/-) mice showed a 50% greater amount of nigral dopamine neurons spared in response to acute MPTP compared to controls, which was associated with a milder motor impairment. SB-612111, given 4 days after MPTP treatment to mimic the clinical condition, prevented the loss of nigral dopamine neurons and striatal dopaminergic terminals caused by subacute MPTP. SB-612111, administered a week after the AAV injections in a clinically-driven protocol, also increased by 50% both the number of spared nigral dopamine neurons and striatal dopamine terminals, and prevented accompanying motor deficits induced by α-synuclein. We conclude that endogenous N/OFQ contributes to dopamine neuron loss in pathogenic and etiologic models of Parkinson's disease through NOP receptor-mediated mechanisms. NOP receptor antagonists might prove effective as disease-modifying agents in Parkinson's disease, through the rescue of degenerating nigral dopamine neurons and/or the protection of the healthy ones.

| S-EPMC5567676 | biostudies-literature

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