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Novel function of cholecystokinin (CCK): Mediator between feeding and gonadal development

ABSTRACT: Novel function of cholecystokinin (CCK): Mediator between feeding and gonadal development

PROVIDER: PRJNA1119449 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29264091_1.fastq.gz	Fastqsanger.gz
	SRR29264091_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Novel function of cholecystokinin (CCK): Mediator between feeding and gonadal development

Project description:Novel function of cholecystokinin (CCK): Mediator between feeding and gonadal development

| PRJNA1119996 | ENA

Synaptic and Intrinsic Plasticity Mediated by CCK-type Signaling Coordinates Behavioral Changes During Motivational State Shifts

Project description:Transitions from hunger to satiety involve multiple behavioral changes, including modulation and inhibition of feeding behavior. Cholecystokinin (CCK), a key satiety peptide in mammals, plays a critical role in these processes, though whether and how CCK might induce satiety via synaptic and intrinsic plasticity remain unclear. Here, we demonstrate that CCK acts as a classical brain-gut peptide in a protostome, mollusk Aplysia. CCK neurons, located in the gut, project centrally to release CCK at the site of the feeding pattern generator. In vivo, CCK reduced food intake, while in vitro, it shifted motor patterns towards egestion and inhibited feeding programs. Mechanistically, CCK primarily modulated the excitability of the egestive-promoting B20 interneuron and suppressed synaptic inputs to protraction motoneurons, thereby altering program type and inhibiting feeding program generation. These findings highlight the importance of both synaptic and intrinsic plasticity in specific circuit elements for implementing motivational shifts induced by satiety peptides.

2025-05-17 | GSE296741 | GEO

Novel function of cholecystokinin (CCK): Mediator between feeding and gonadal development

Project description:We used single cell RNA sequencing (scRNA-seq)to analyze the pituitary cells in Ctenopharyngodon idellus

2025-01-29 | GSE269034 | GEO

Novel function of cholecystokinin (CCK): Mediator between feeding and gonadal development

Project description:We used single cell RNA sequencing (scRNA-seq)to analyze the hypothalamu cells in Ctenopharyngodon idellus

2025-01-29 | GSE268914 | GEO

Cholecystokinin (CCK) Is a Mediator Between Nutritional Intake and Gonadal Development in Teleosts.

Project description:Nutritional intake is closely linked to gonadal development, although the mechanisms by which food intake affects gonadal development are not fully understood. Cholecystokinin (CCK) is a satiety neuropeptide derived from the hypothalamus, and the present study observed that hypothalamic CCK expression is significantly influenced by food intake, which is mediated through blood glucose levels. Interestingly, CCK and its receptors were observed to exhibit a high expression in the hypothalamus-pituitary-gonad (HPG) axis of grass carp (Ctenopharyngodon idellus), suggesting that CCK is potentially involved in regulating fish reproduction through the HPG axis. Further investigations revealed that CCK could significantly stimulate the expression of gonadotropin-releasing hormone-3 (GnRH3) in the hypothalamus. In addition, single-cell RNA sequencing showed that cckrb was highly enriched in pituitary follicle-stimulating hormone (FSH) cells. Further study confirmed that CCK can significantly induce FSH synthesis and secretion in primary cultured pituitary cells. Additionally, with primary cultured ovary cells as a model, the in vitro experiment demonstrated that CCK directly induces the expression of lhr, fshr, and cyp19a1a mRNA. This indicates that hypothalamic CCK may act as a nutrient sensor involved in regulating gonadal development in teleosts.

| S-EPMC11763773 | biostudies-literature

Effect of CCK-8s injection (20 ug/kg BW i.p.) on mRNA translational activity in hypothalamic oxytocin neurons of mice fed standard chow or high-fat/high-sugar diet (RiboTag;TRAP)

Project description:Oxytocin-expressing paraventricular hypothalamic neurons (PVN^OT neurons) integrate afferent signals from the gut including cholecystokinin (CCK) to adjust whole-body energy homeostasis. However, the molecular underpinnings by which PVN^OT neurons orchestrate gut-to-brain feeding control remain unclear. Here, we show that mice undergoing selective ablation of PVNOT neurons fail to reduce food intake in response to CCK and develop hyperphagic obesity on chow diet. Notably, exposing wildtype mice to a high-fat/high-sugar (HFHS) diet recapitulates this insensitivity towards CCK, which is linked to diet-induced transcriptional and electrophysiological aberrations specifically in PVNOT neurons. Restoring OT pathways in DIO mice via chemogenetics or polypharmacology sufficiently re-establishes CCK?s anorexigenic effects. Lastly, by single-cell profiling, we identify a specialized PVN^OT neuronal subpopulation with increased ?-opioid signaling under HFHS diet, which restrains their CCK-evoked activation. In sum, we here document a novel (patho)mechanism by which PVN^OT signaling uncouples a gut-brain satiation pathway under obesogenic conditions.

2023-09-07 | GSE242245 | GEO

Behavioural and neurochemical mechanisms underpinning the synergistic feeding-suppressive effect of GLP-1/CCK combinatorial therapy

Project description:Behavioural and neurochemical mechanisms underpinning the synergistic feeding-suppressive effect of GLP-1/CCK combinatorial therapy

| PRJNA560362 | ENA

Immunoglobulin-like domain receptor 1 mediates fat-stimulated cholecystokinin secretion.

Project description:Cholecystokinin (CCK) is a satiety hormone produced by discrete enteroendocrine cells scattered among absorptive cells of the small intestine. CCK is released into blood following a meal; however, the mechanisms inducing hormone secretion are largely unknown. Ingested fat is the major stimulant of CCK secretion. We recently identified a novel member of the lipoprotein remnant receptor family known as immunoglobulin-like domain containing receptor 1 (ILDR1) in intestinal CCK cells and postulated that this receptor conveyed the signal for fat-stimulated CCK secretion. In the intestine, ILDR1 is expressed exclusively in CCK cells. Orogastric administration of fatty acids elevated blood levels of CCK in wild type but not ILDR1-deficient mice, although the CCK secretory response to trypsin inhibitor was retained. The uptake of fluorescently labeled lipoproteins in ILDR1-transfected CHO cells and release of CCK from isolated intestinal cells required a unique combination of fatty acid plus HDL. CCK secretion secondary to ILDR1 activation is associated with increased [Ca2+]i consistent with regulated hormone release. These findings demonstrate that ILDR1 regulates CCK release through a mechanism dependent on fatty acids and lipoproteins and that absorbed fatty acids regulate gastrointestinal hormone secretion. GFP positive cells from CCK-EGFP transgenic mice were isolated by FACS and the expression profile was compared with an equal number of non-fluorescent intestinal cells.

2013-05-23 | E-GEOD-47196 | biostudies-arrayexpress

Transcription profiling of mouse fundic mucosa in the presence/absence of gastrin and in gastrin-CCK double knockout mice

Project description:Fundic mucosa gene expression in wildtype vs gastrin knockout, gastrin replaced gastrin KO and gastrin-CCK double knockout mice; Fundic mucosal scraping RNA were isolated from WT, Gastrin Knockout, Gastrin replaced KO and Gastrin-CCK double knockout mice. Targets from three biological replicates of each were generated and the expression profiles were determined using Affymetrix murine 430A arrays. Comparisons between the sample groups allow the identification of genes with gastrin responsiveness and Gastrin-CCK double effect . Experiment Overall Design: 3 WT, 3 Gastrin KO, 3 Gastrin replaced KO and 3 Gastrin-CCK double Knockout fundic RNA replicates were analyzed

2008-06-13 | E-GEOD-4810 | biostudies-arrayexpress

RNAseq anaysis of hippocamal cck cells of SMARCA3 cKO mice

Project description:Purpose: To identify gene expression changes in CCK neurons of hippocsmpus of SMARCA3 cKO mice Method: Translating Ribosome Affinity Purification (TRAP) to isolate RNA from CCK+ cells and, cDNA synthesis and next generation RNAseq using Illumina Nextseq sequencer. Results: Biostatistical analysis identified 1378 genes that were altered by SMARCA3 cKO.

2023-02-11 | GSE141481 | GEO

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