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Antagonizing cholecystokinin A receptor in the lung attenuates obesity-induced airway hyperresponsiveness.
Nat Commun
January 2023
Program in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, 02115, USA.
Obesity increases asthma prevalence and severity. However, the underlying mechanisms are poorly understood, and consequently, therapeutic options for asthma patients with obesity remain limited. Here we report that cholecystokinin-a metabolic hormone best known for its role in signaling satiation and fat metabolism-is increased in the lungs of obese mice and that pharmacological blockade of cholecystokinin A receptor signaling reduces obesity-associated airway hyperresponsiveness.
View Article and Find Full Text PDFIntraperitoneal CCK and fourth-intraventricular Apo AIV require both peripheral and NTS CCK1R to reduce food intake in male rats.
Endocrinology
May 2014
Departments of Pathology and Laboratory Medicine (C.C.L., W.S.D., S.K.H., M.G., A.L., P.T.) and Psychiatry and Behavioral Neuroscience (S.C.W.), Metabolic Diseases Institute, University of Cincinnati, Cincinnati, Ohio 45237-0507.
Apolipoprotein AIV (Apo AIV) and cholecystokinin (CCK) are secreted in response to fat consumption, and both cause satiation via CCK 1 receptor (CCK-1R)-containing vagal afferent nerves to the nucleus of the solitary tract (NTS), where Apo AIV is also synthesized. Fasted male Long-Evans rats received ip CCK-8 or fourth-ventricular (i4vt) Apo AIV alone or in combination. Food intake and c-Fos proteins (a product of the c-Fos immediate-early gene) were assessed.
View Article and Find Full Text PDFLuminal melatonin stimulates pancreatic enzyme secretion via activation of serotonin-dependent nerves.
Pharmacol Rep
February 2014
Department of Medical Physiology, Faculty of Health Sciences, Jagiellonian University School of Medicine, Michałowskiego 12, PL 31-126 Kraków, Poland.
Background: Serotonin (5-HT) is released from enterochromaffin cells in the gastrointestinal tract. 5-HT, via the activation of 5-HT2 and 5-HT3 receptors on vagal fibers, mediates pancreatic secretion through the mechanism independent from cholecystokinin. Melatonin (5-HT derivative) or L-tryptophan (melatonin or 5-HT precursor) given systemically or intraduodenally to the rats stimulate amylase secretion, but the mechanism is not clear.
View Article and Find Full Text PDFEffect of ghrelin receptor antagonist on meal patterns in cholecystokinin type 1 receptor null mice.
Physiol Behav
May 2011
Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine, UC Davis, Davis, CA 95616, USA.
Vagal afferent neurons (VAN) express the cholecystokinin (CCK) type 1 receptor (CCK₁R) and, as predicted by the role of CCK in inducing satiation, CCK₁R⁻/⁻ mice ingest larger and longer meals. However, after a short fast, CCK₁R⁻/⁻ mice ingesting high fat (HF) diets initiate feeding earlier than wild-type mice. We hypothesized that the increased drive to eat in CCK₁R⁻/⁻ mice eating HF diet is mediated by ghrelin, a gut peptide that stimulates food intake.
View Article and Find Full Text PDFCholecystokinin and hypothalamic corticotrophin-releasing factor participate in endotoxin-induced hypophagia.
Exp Physiol
April 2011
Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Avenida Bandeirantes 3900, 14049-900 Ribeirao Preto, Sao Paulo, Brazil.
Cholecystokinin (CCK) provides a meal-related signal that activates brainstem neurons, which have reciprocal interconnections with the hypothalamic paraventricular nucleus. Neurons that express corticotrophin-releasing factor (CRF) in the hypothalamus possess anorexigenic effects and are activated during endotoxaemia. This study investigated the effects of CCK(1) receptor blockade on lipopolysaccharide (LPS)-induced hypophagia and hypothalamic CRF neuronal activation.
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