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Pancreatitis Independently Induced by Hypertriglyceridaemia Outlines the Immune Profiles of HTGP in Clinic.

Clin Exp Pharmacol Physiol

May 2025

State Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Druggability of Biopharmaceuticals, School of Life Science and Technology, China Pharmaceutical University, Nanjing, People's Republic of China.

Hypertriglyceridaemia (HTG) is a common and well-established aetiology of acute pancreatitis (AP). Although the underlying pathophysiology of hypertriglyceridaemic pancreatitis (HTGP) is complex, some animal models of HTAP have been successfully reproduced by repeated caerulein injections based on HTAP. However, most of the current HTGP models are critically dependent on the "two-attack" of cholecystokinin analogue, which may not be consistent with the fact of HTGP aetiologies due to ignored the initial effects of HTG in the development of HTGP.

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Cortical GABAergic interneurons (INs) are comprised of distinct types that provide tailored inhibition to pyramidal cells (PCs) and other INs, thereby enabling precise control of cortical circuit activity. INs expressing the neuropeptide vasoactive-intestinal peptide (VIP) have attracted attention recently following the discovery that they predominantly function by inhibiting dendritic-targeting somatostatin (SST) expressing INs, thereby disinhibiting PCs. This VIP-SST disinhibitory circuit motif is observed throughout the neocortex from mice to humans, and serves as a key mechanism for top-down (feedback) and context-dependent information processing.

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Gastrointestinal cholecystokinin signaling pathway drugs modulate osteogenic/cementogenic differentiation of human periodontal ligament stem cells.

J Dent

March 2025

Departamento de Prótese e Periodontia, Divisão de Periodontia, Faculdade de Odontologia de Piracicaba, Universidade Estadual de Campinas - UNICAMP, Piracicaba, São Paulo, Brasil.

Objectives: Understanding the complexities of periodontal regeneration, particularly the unpredictable osteogenic/cementogenic differentiation of low-potential PDLSCs (LOP-PDLSCs), remains challenging. Identifying new therapeutic targets is crucial for enhancing regeneration. This study investigates the modulation of the Cholecystokinin (CCK) pathway, a key signaling cascade with roles in the gastrointestinal system, as a potential osteogenic/cementogenic pathway in PDLSCs.

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Addressing the risk of malnutrition at an early stage is crucial to preventing its development, which can have a detrimental impact on physical and mental health status. This study investigates the potential role of biochemical biomarkers such as sirtuin 1 (SIRT-1), melatonin, cholecystokinin-8 (CCK-8), and total antioxidant capacity (TAC) in identifying the risk of malnutrition. This cross-sectional study assessed malnutrition risk in 153 community-dwelling older adults using the Mini Nutritional Assessment (MNA).

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Naringenin Decreases Retroperitoneal Adiposity and Improves Metabolic Parameters in a Rat Model of Western Diet-Induced Obesity.

Metabolites

February 2025

Facultad de Medicina de Mexicali, Universidad Autónoma de Baja California, Dr. Humberto Torres Sanginés, Centro Cívico, Mexicali 21000, BCN, Mexico.

Obesity is a multifactorial disease with detrimental effects on health and quality of life; unregulated satiety plays a crucial role in food intake and obesity development. Naringenin (NAR) has shown beneficial effects on lipid and carbohydrate metabolism, although its impact on adiposity and satiety remains unclear. This study reports a Western diet (WD)-induced obesity model in rats, wherein 100 mg/kg of NAR was administered as an anti-obesity agent for 8 weeks; oxidative stress, lipid profile, and satiety biomarkers were then studied, as well as in silico interaction between NAR and cholecystokinin (CCK) and ghrelin receptors.

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