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At least 1,423 records · Page 79Linked to original sources
PubMed1992

Cloning, functional expression, and developmental regulation of a neuropeptide Y receptor from Drosophila melanogaster.

Neuropeptide Y, peptide YY, and pancreatic polypeptide are homologous 36-amino acid peptides that differ from most other peptide transmitters by having a relatively rigid conformation in aqueous solutions, defined as the pancreatic polypeptide fold, and a critical C-terminal tyrosine amide. These peptides serve as gastrointestinal hormones and neurotransmitters. A cDNA encoding a novel G protein-coupled receptor activated by neuropeptide Y was cloned from Drosophila by use of degenerate oligonucleotide primers and polymerase chain reaction amplification of cDNA prepared from transcripts expressed early in embryogenesis. The cDNA encodes a protein of 449 amino acids with the characteristics of a G protein-coupled receptor and shares significant amino acid identity with mammalian tachykinin receptors. When expressed in Xenopus oocytes, the PR4 protein is activated by mammalian neuropeptides in the order: peptide YY greater than neuropeptide Y much greater than pancreatic polypeptide. Northern analysis showed that PR4 receptor is expressed at equivalent levels in adult Drosophila head and body and that the expression of the PR4 receptor is regulated during development. The molecular characterization of this receptor should lead to a better understanding of the functional role of this important family of hormone receptors in adult organisms and during development.

Amino Acid Sequence↗
PubMed1998

[Influence of the extrinsic nervous system on exocrine pancreatic secretion in the human].

Exocrine pancreatic secretion is regulated by gastrointestinal hormone and the autonomic nervous system. The interaction of both systems is still unclear. In humans CCK mediated regulation of exocrine pancreatic secretion requires a cholinergic tonus. The CCK receptor is thought to be localized on the acinuscell and modulated by cholinergic neurons. Pancreas transplantation and percutaneous diversion of the pancreatic juice offers the opportunity to investigate pancreatic secretion under the condition of complete extrinsic denervation. In the present study the influence of denervation on exogene CCK stimulation and simultaneous cholinergic stimulation or suppression with atropine, respectively, was investigated. CCK stimulation alone showed a reduced, dose dependent increase in enzyme secretion. Simultaneous stimulation with bethachenol resulted in a 2-fold increased secretion. Atropine suppressed the low dose CCK effect completely. Whereas CCK at high doses caused a 1.5 fold increase despite atropine. After extrinsic denervation the human pancreas remains sensitive to exogene stimulation. The intrinsic system remains also intact and is sensitive to cholinergic stimulation. The extrinsic nervous system seems to be necessary for an adequate CCK response. The results are in line with the hypothesis that CCK receptors are only partly localized on the acinuscell, whereas the majority is localized in extrinsic cholinergic neurons.

Adult↗
PubMed2003

History traces of gastrointestinal motility in Poland.

The objectives of this chapter was to show how motility studies were developed and performed in Poland at the end of century to better understand pathophysiology and improve the clinicians ability to evaluate and treat patients with motility-related disorders. Some of the important historical points along the path to current understanding of the form and function of gastrointestinal motility are presented. Scarce information exists about other than Cracow and Wrocław motility centers in Poland in previous century. Lately sophisticated technology became available in Poland and more centers have begun to yield more effective strategies of treatment and enhanced understanding of the pathophysiologic mechanisms underlying GI motility disorders.

Animals↗
PubMed2005

Novel therapeutic targets for appetite regulation.

Obesity is currently the major cause of premature death in the UK, killing almost 1000 individuals per week, and worldwide, its prevalence is accelerating. Many peptides are synthesized and released from the gastrointestinal tract and, while their roles in the regulation of gastrointestinal function have been known for some time, it is now evident that they also physiologically influence eating behavior. Therefore, manipulation of gastrointestinal hormones provides the prospect of an effective and well-tolerated treatment for obesity. Whereas drugs targeting appetite-signaling neuropeptides in the brain may also affect other aspects of the central nervous system, agents based on gut hormones themselves have the advantage of targeting specific appetite circuits within the brain without producing any unacceptable side effects.

Appetite Regulation↗
PubMedDate not supplied

Physiological endocrine control of energy homeostasis and postprandial blood glucose levels.

The aim of this review is to analyze the different components and the feedback mechanisms involved in the normal control of energy homeostasis and postprandial blood glucose levels. Such control involves exogenous and endogenous factors: while the former include quantity and quality of food intake, the latter involve the balance of glucose intestinal absorption (postprandial period), glucose production and release by the liver and its consumption by peripheral tissues. Adequate secretion and peripheral metabolic effects of insulin play a key role in the control of both processes. Insulin secretion is controlled by the level of circulating substrates and by gastrointestinal hormones. The mechanism for the immediate control of blood glucose levels is modulated by energy homeostasis, with the participation of the above mentioned hormones and others produced at the classical endocrine system and adipose tissue, whose actions integrate at the central nervous system. The alteration of such delicate mechanism of control causes diseases such as diabetes; therefore, identification of the multiple components of this mechanism and comprehension of its normal function would facilitate the selection of effective strategies for diabetes prevention and treatment.

Animals↗
PubMedDate not supplied

[Neuropeptides in Alzheimer's disease].

INTRODUCTION: Of approximately 200 peptides that are known to exist in the body, 80 carry out functions as neurotransmitters and about 20 have been linked to Alzheimer's disease (AD). DEVELOPMENT: In this article we review the most salient studies that have been conducted on neuropeptides such as corticotropin-releasing hormone, thyrotropin-releasing hormone, somatostatin, neuropeptide Y, oxytocin, arginine vasopressin, galanin and insulin, as well as the insulin-like growth factors, the glucagon-like peptides, vasoactive intestinal peptide, cholecystokinin, substance P, opioid peptides and the neuropeptide NAP. Although attempts are made to find a causal association with AD, in many cases the findings are contradictory or not very conclusive. CONCLUSIONS: The most notable points could be the reduction in substance P in the cerebral cortex, hippocampus, basal ganglia and cephalospinal fluid; the diminished levels of somatostatin in the same structures except for the basal ganglia; the reduction in the amount of vasopressin except in the temporal lobe; and the increased levels of dynorphin and leucine enkephalin.

Alzheimer Disease↗
PubMed2006

Therapies for the treatment of type 2 diabetes mellitus based on incretin action.

Orally ingested glucose leads to a much higher insulin response than intravenous glucose leading to identical postprandial plasma glucose excursions. This phenomenon, termed ''incretin effect'' comprises up to 60% of the postprandial insulin secretion and is diminished in type 2 diabetes. The gastrointestinal hormones glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) promote the incretin effect. Type 2 diabetes is characterized by an incretin defect: while GIP does not stimulate insulin secretion, GLP-1 action is still preserved under supraphysiological concentrations. GLP-1 stimulates insulin secretion only under hyperglycaemic conditions, therefore it does not cause hypoglycaemia. Furthermore, GLP-1 inhibits glucagon secretion and delays gastric emptying. In vitro and animal data demonstrated that GLP-1 increases beta cell mass by stimulating islet cell neogenesis and by inhibiting apoptosis of islets. The improvement of beta cell function can be indirectly observed from the increased insulin secretory capacity of humans receiving GLP-1. In contrast to GIP, GLP-1 may represent an attractive therapeutic method for type 2 diabetes due to its multiple effects also including the simulation of satiety in the central nervous system by acting as transmitter or by crossing the blood brain barrier. Native GLP-1 is degraded rapidly upon intravenous or subcutaneous administration and is therefore not feasible for routine therapy. Long-acting GLP-1 analogs (e.g. Liraglutide) and exendin-4 (Exenatide, Byetta) that are resistant to degradation, called ''incretin mimetics'' are approved (Exenatide, Byetta) or in clinical trials. DPP-4-inhibitors (e.g. Vildagliptin), Sitagliptin and Saxagliptin) that inhibit the enzyme DPP-4 responsible for incretin degradation are also under study.

Animals↗
PubMed2002

[Conservative therapy of chronic pancreatitis].

Conservative therapy is applied to various extent in all subjects with chronic pancreatitis. It includes removal of the provoking agent (most frequently alcohol abuse and biliary disease), dietary regimen, treatment of pain, maldigestion, and diabetes. Removal of the provoking agent prevents progression of the disease and relieves intensity of the main symptoms, particularly of pain. Diet in remission should include approximately 1g of protein/kg body mass. Fat intake should be encouraged within limits of individual tolerance. With low caloric intake carbohydrates should be enriched up to 65 - 70% of total energy intake. Abdominal pain may be due to a complication or to the underlying disease itself. For this reason one approach cannot be effective in all subjects. Conservative methods represent the first line of pain therapy. They include alcohol withdrawal, analgesics, narcotics and negative trypsin-induced feedback control of pancreatic secretion. Pancreatin medication is the cornerstone of maldigestion therapy. This is indicated with weight loss and/or symptoms associated with steatorrhea or with 15 - 20 g stool fat/day without additional symptoms. The effect may be evaluated by increase of body mass, decrease of loose stools and by markers of the nutritional status. Adequate replacement therapy with pancreatic enzymes influences also elaboration and secretion of some gastrointestinal hormones. The appearance of secondary diabetes makes abstinence from alcohol again mandatory. Food intake should be divided into 5 - 6 daily doses and adequate enzyme replacement should be applied. Peroral antidiabetics may be considered at the early stage, but many of these patients ultimately require insulin therapy. Its dosage should be adjusted to glucose urinary losses rather than to adhere to tight normoglycemia because of the increased risk of hypoglycemia. The therapeutic options in chronic pancreatitis may stabilize the disease and prevent its progression. The patients may be at the best asymptomatic, but not cured.

Humans↗