Novel function of cholecystokinin (CCK): Mediator between feeding and gonadal development
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ABSTRACT:
PROVIDER: PRJNA1119449 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29264091_1.fastq.gz | Fastqsanger.gz | |||
| SRR29264091_2.fastq.gz | Fastqsanger.gz |
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Project description:Novel function of cholecystokinin (CCK): Mediator between feeding and gonadal development
| PRJNA1119996 | ENA
Project description:We used single cell RNA sequencing (scRNA-seq)to analyze the pituitary cells in Ctenopharyngodon idellus
2025-01-29 | GSE269034 | GEO
Project description:We used single cell RNA sequencing (scRNA-seq)to analyze the hypothalamu cells in Ctenopharyngodon idellus
2025-01-29 | GSE268914 | GEO
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
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
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
Project description:At high altitude, hypoxic atmosphere decreases the oxygen partial pressure (pO2) in the body, inducing several metabolic changes in tissues and cells. Furthermore, it exerts potent anorectic effects, thus causing energy deficit. Two decades ago, a marked increase in the level of resting plasma cholecystokinin (CCK) was observed at Mt. Kanchenjunga basecamp (BC) located at 5,100 m above the sea level, compared to sea-level control values. Interestingly, acute exercise also raises plasma CCK and exerts potent anorectic effects under normoxic conditions. However, the molecular mechanism underlying these effects has not yet been established. We employed acute electrical pulse stimulation (EPS), followed by a microarray analysis, to discover novel myokines in 3D engineered muscle. Acute EPS efficiently affects the contractile function, inducing a decline of the contractile force. Surprisingly, microarray analysis revealed an EPS-induced activation of the cholecystokinin receptor (CCKR)-mediated signaling. Furthermore, Cck was constitutively expressed in 3D engineered muscle, and was upregulated by hypoxic conditions. Notably, a hypoxia responsive element (HRE) was detected in the Cck promoter of mice and humans. Our results suggested that, under hypoxic conditions, Hif-1a binding to HRE transactivated Cck expression in mice and humans. Furthermore, the plasma CCK elevation after acute exercise or at high altitude might be partly attributed to myogenic cells.
2021-04-13 | GSE135373 | GEO
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.
2013-05-23 | GSE47196 | GEO
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
Project description:Spinocerebellar Ataxias (SCAs) are a group of genetic diseases characterized by progressive ataxia and neurodegeneration, often in cerebellar Purkinje neurons. A SCA1 mouse model, Pcp2-ATXN1[30Q]D776, has severe ataxia in absence of progressive Purkinje neuron degeneration and death. Previous RNA-seq analyses identified cerebellar up-regulation of the peptide hormone Cholecystokinin (Cck) in Pcp2-ATXN1[30Q]D776 mice. Importantly, absence of Cck1 receptor (Cck1R) in Pcp2-ATXN1[30Q]D776 mice confers a progressive disease with Purkinje neuron death. A Cck1R agonist, A71623 administered to Pcp2-ATXN1[30Q]D776;Cck-/- and Pcp2-AXTN1[82Q] mice dampened Purkinje neuron pathology and associated deficits in motor performance. In addition, A71623 administration improved motor performance of Pcp2-ATXN2[127Q] SCA2 mice. Moreover, the Cck1R agonist A71623 corrected mTORC1 signaling and improved expression of calbindin in cerebella of AXTN1[82Q] and ATXN2[127Q] mice. These results indicate that manipulation of the Cck-Cck1R pathway is a potential therapeutic target for treatment of diseases involving Purkinje neuron degeneration.
2022-01-11 | GSE180969 | GEO