The abdomen
Peter Kopelman, Dame Jane Dacre in Handbook of Clinical Skills, 2019
The gastrointestinal tract is responsible for the ingestion of food, the absorption of nutrients from food and the excretion of unabsorbed waste products. This process is controlled by the autonomic nervous system, together with hormones including gastrin, secretin and cholecystokinin. The musculature of the alimentary tract is composed of smooth muscle from the mid-oesophagus to the external anal sphincter. Smooth muscle has an innate tone that permits sustained and sometimes powerful contraction over long periods of time. The excretory function of the kidney regulates water and electrolyte secretion to maintain blood volume, blood pressure and plasma electrolyte composition. The 1-hydroxyl group of active vitamin D is added in the kidney, so disorders of calcium and phosphate homeostasis are a common problem in chronic kidney disease. Erythropoietin, which drives erythrocyte production in the bone marrow, is produced by fibroblasts in the renal medulla in response to hypoxia.
The Small IntestineSecretions, Digestion and Motility
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
The small intestine may be divided into three parts: duodenum, jejunum and ileum. Exocrine secretions are produced by acinar cells and the ductal cells of the pancreas. Pancreatic juice is secreted under both neural and hormonal influences. Pancreatic secretion is stimulated by cholecystokinin, secretin and acetylcholine. Various intestinal secretions are produced by the intestinal epithelium. Proteins found in the intestines are derived from endogenous sources (secretory proteins and desquamated cells) and exogenous proteins (dietary protein). Most protein digestion results from the actions of pancreatic proteolytic enzymes. The first step in fat digestion is emulsification by bile acids and lecithin. Functionally, intestinal motility is important for mixing of food and digestive secretions; ensuring maximal contact of luminal contents with the mucosa and propagation of luminal contents from the duodenum to the colon. Propulsive motility in the small intestine is partially provided by peristalsis.
Glucagon
Ben Greenstein in Rapid Revision in Endocrinology, 2017
This chapter presents a brief outline of the nature and biosynthesis of glucagon. It aims to compare and contrast glucagon and insulin in terms of synthesis control and physiological actions. The chapter discusses the given symptoms of hypersecretion of glucagon. Glucagon is released between meals when plasma fatty acids and glucose levels fall. Secretion is inhibited when energy substrates, notably plasma glucose, ketone bodies and fatty acid levels rise in plasma. The autonomic system regulates glucagon release through both sympathetic and parasympathetic stimulation. Several gastrointestinal tract hormones stimulate glucagon release, for example, cholecystokinin and vasoactive intestinal peptide. Some physiological actions of glucagon are: promotes hepatic breakdown of glycogen to glucose, promotes hepatic glucose formation from amino acids, inhibits hepatic glycogenesis, and stimulates free fatty acid conversion to ketone bodies.
Trypsin inhibitors: promising candidate satietogenic proteins as complementary treatment for obesity and metabolic disorders?
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2019
Vanessa Cristina Oliveira de Lima, Grasiela Piuvezam, Bruna Leal Lima Maciel, Ana Heloneida de Araújo Morais
The increase in non-communicable chronic diseases has aroused interest in the research of adjuvants to the classic forms of treatments. Obesity and metabolic syndrome are the main targets of confrontation because they relate directly to other chronic diseases. In this context, trypsin inhibitors, molecules with wide heterologous application, appear as possibilities in the treatment of overweight and obesity due to the action on satiety related mechanisms, mainly in the modulation of satiety hormones, such as cholecystokinin. In addition, trypsin inhibitors have the ability to also act on some biochemical parameters related to these diseases, thus, emerging as potential candidates and promising molecules in the treatment of the obesity and metabolic syndrome. Thus, the present article proposes to approach, through a systematic literature review, the advantages, disadvantages and viabilities for the use of trypsin inhibitors directed to the treatment of overweight and obesity.
Disturbed Motilin and Cholecystokinin Release in the Irritable Bowel Syndrome
Published in Scandinavian Journal of Gastroenterology, 1996
K. Sjölund, R. Ekman, S. Lindgren, J. F. Rehfeld
Background: The irritable bowel syndrome (IBS) is associated with motor abnormalities in the small intestine and colon. Neuropeptides may have an important role in initiating and regulating the intestinal motility. Motilin has been proposed to initiate the peristaltic reflex in the small intestine and cholecystokinin the gastrocolic reflex. Methods: In 18 patients with IBS and 11 healthy control subjects plasma motilin and cholecystokinin (CCK) concentrations were measured after intraluminal stimulation of water and a fat-rich meal. Results: The IBS patients had reduced motilin secretion after both water intake and the fat meal. In contrast, the fat meal elicited an exaggerated and prolonged CCK release in the IBS patients. Conclusions: Disturbed motilin and CCK release may partly be responsible for the intestinal dysmotility in the IBS patients.
Effects of high‐fat diet and cholecystokinin receptor blockade on promotion of pancreatic ductal cell tumors in the hamster
Published in Nutrition and Cancer, 1997
Margery Herrington, Thomas Gasslander, Robert Cina, Drew Fehsenfeld, Katherine Kazakoff, Parviz Pour, Thomas Adrian
The mechanism by which high‐fat diets potentiate pancreatic cancer is not known, but pancreaticotrophic hormones such as cholecystokinin (CCK) may be involved. The effect of CCK receptor blockade on carcinogenesis during the entire promotion period was investigated in Syrian Golden hamsters fed a high‐ or low‐fat diet and treated with N‐nitrosobis(2‐oxopropyl)amine (3 × 10 mg/kg at weekly intervals). One‐half of the hamsters fed a high‐fat diet received the CCK‐A receptor antagonist devazepide (25 nmol/kg/hr) for the duration of the experiment. At 39 weeks the incidence of pancreatic malignancies was significantly higher in hamsters fed the high‐fat diet than in those fed the low‐fat diet (p < 0.05). Tumor incidence was not changed by CCK receptor blockade. Potentiation of pancreatic cancer by a high‐fat diet in hamsters does not appear to be influenced by endogenous CCK during the tumor promotion period.
Related Knowledge Centers
- Enzymes
- Hormones
- Peptides
- Proteins
- Amino Acids
- Oligopeptides
- Receptors