Inhibitory effect of enterostatin on the beta cell response to digestive insulinotropic peptides

Rodriguez-Gallardo, J.; Silvestre, Ramona A.; Marco, José

doi:10.1038/sj.ijo.0800927

Cited by 8 publications

(7 citation statements)

References 28 publications

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“…Since both peptides exert their insulinotropic activity by activating the adenylate cyclase/cyclic AMP system, the interference of this pathway by enterostatin may be considered. Enterostatin (100 nM) did not modify the insulin response to CCK-8 and carbachol, substances which activate phosphoinositol turnover within the beta cell [227].…”

Section: Enterostatin Receptor Ligandsmentioning

confidence: 93%

“…No effects of enterostatin on food intake were observed in healthy volunteers [226]. Enterostatin has also been found to inhibit insulin release in perifused rat pancreas [227] and in isolated rat islets [228]. In isolated rat islets enterostatin reduced glucose (16.7 mM) stimulated insulin secretion at concentrations below 1 nM, while it did not significantly reduce insulin release in the presence of neither 3.3 mM nor 5.6 mM glucose.…”

Section: Enterostatin Receptor Ligandsmentioning

confidence: 95%

See 1 more Smart Citation

Inhibition of Insulin Secretion as a New Drug Target in the Treatment of Metabolic Disorders

Hansen¹,

Arkhammar²,

Bödvarsdóttir³

et al. 2004

CMC

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The pattern of insulin release is crucial for regulation of glucose and lipid haemostasis. Deficient insulin release causes hyperglycemia and diabetes, whereas excessive insulin release can give rise to serious metabolic disorders, such as nesidioblastosis (Persistent Hyperinsulinemic Hypoglycemia of Infancy, PHHI) and might also be closely associated with development of type 2 diabetes and obesity. Type 2 diabetes is characterized by fasting hyperinsulinemia, insulin resistance and impaired insulin release, i.e. reduced first phase insulin release and decreased insulin pulse mass. The beta cell function of patients with type 2 diabetes slowly declines and will ultimately result in beta cell failure and increasing degrees of hyperglycemia. Type 2 diabetes, in combination with obesity and cardiovascular disorders, forms the metabolic syndrome. It has been possible to improve beta cell function and viability in preclinical models of type 1 and type 2 diabetes by reducing insulin secretion to induce beta cell rest. Clinical studies have furthermore indicated that inhibitors of insulin release will be of benefit in treatment or prevention of diabetes and obesity. Pancreatic beta cells secrete insulin in response to increased metabolism and by stimulation of different receptors. The energy status of the beta cell controls insulin release via regulation of open probability of the ATP sensitive potassium (K(ATP)) channels to affect membrane potential and the intracellular calcium concentration [Ca(2+)](i). Other membrane bound receptors and ion channels and intracellular targets that modulate [Ca(2+)](i)will affect insulin release. Thus, insulin release is regulated by e.g. somatostatin receptors, GLP-1 receptors, muscarinic receptors, cholecystokinin receptors and adrenergic receptors. Although the relationship between hyperinsulinemia and certain metabolic diseases has been known for decades, only a few inhibitors of insulin release have been characterized in vitro and in vivo. These include the K(ATP) channel openers diazoxide and NN414 and the somatostatin receptor agonist octreotide.

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Section: Enterostatin Receptor Ligandsmentioning

confidence: 93%

Section: Enterostatin Receptor Ligandsmentioning

confidence: 95%

Inhibition of Insulin Secretion as a New Drug Target in the Treatment of Metabolic Disorders

Hansen¹,

Arkhammar²,

Bödvarsdóttir³

et al. 2004

CMC

View full text Add to dashboard Cite

show abstract

“…In addition to the pancreas, enterostatin-immunoreactive cells are also present in the antrum and proximal small intestine. Enterostatin selectively reduces fat intake, decreases insulin secretion [63], and also increases energy expenditure by activating brown adipose tissue during high-fat feeding [64]. In addition, recent data obtained from rodent experiments suggest that enterostatin changes lipid and carbohydrate metabolic pathways [65].…”

Section: Enterostatinmentioning

confidence: 97%

Physiology of gut hormones: an overview

Wittert

Chapman

2006

Current Opinion in Endocrinology and Diabetes

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Purpose of reviewThus far more than 30 peptides have been identified as being expressed within the digestive tract, making the gut the largest endocrine organ in the body. Understanding of the physiology of many of these peptides has progressed rapidly. This paper provides an overview of advances in our understanding of the physiology of ghrelin, motilin, cholecystokinin, glucagon-like peptide-1 and oxyntomodulin, glucose-dependent insulinotropic peptide, gastrin-releasing peptide, enterostatin, galanin, and gut leptin. Recent findingsThe review highlights how, in anticipation of and in response to food intake of a particular amount and composition, changes in gastrointestinal hormone synthesis and release occur in order to regulate and coordinate gastrointestinal function, appetite control, and intermediary metabolism. Abnormalities of gut hormones in disorders such as diabetes mellitus, disorders of body weight, and eating disorders are highlighted. The paucity of data relating to the human physiology of enterostatin, galanin, and gut leptin stands in contrast to the other hormones discussed and highlights areas for further investigation. Summary An increase in the understanding of the physiology of gut hormones and their role in integrating food intake and intermediary metabolism have led to novel therapies for the management of diabetes mellitus and also has the potential for new approaches for the management of disorders of food intake and body weight.

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“…Effects on endocrine secretion of rat beta cells (121) Galanin Innervation, (98) presence of a galanin-like peptide in rat islets (122) Studies on RIN5AH beta cell lines indicate galanin binding sites (122) Effects on endocrine secretion of the RIN5mF beta cell line (incretin hormone) (123) Gastric inhibitory polypeptide Expressed in beta cells (124) GIP acts as an incretin hormone, (124) effects on endocrine secretion of rat islets (125) Gastrin Acts as a growth factor in foetal mice, (126) present in rat insulinoma cell lines (127) CCK-B receptor on rat islets (103) Islet regeneration in diabetes mellitus (128) …”

Section: Receptor Localisation Bioactivitymentioning

confidence: 99%

Bioactive peptides, networks and systems biology

Boonen

Creemers

Schoofs³

2009

BioEssays

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Bioactive peptides are a group of diverse intercellular signalling molecules. Almost half a century of research on this topic has resulted in an enormous amount of data. In this essay, a general perspective to interpret all these data will be given. In classical endocrinology, neuropeptides were thought of as simple signalling molecules that each elicit one response. However, the fact that the total bioactive peptide signal is far from simple puts this view under pressure. Cells and tissues express many different bioactive peptides and they are also able to respond to many different bioactive peptides, indicating that multiple receptors and signal transduction pathways are present in a single cell. Therefore, the authors suggest that the bioactive peptide signalling system should be regarded in the context of network and systems biology. Bioactive peptides can best be viewed as an extension of the protein interaction network that allows regulating and fine-tuning the metabolism of the different cells and tissues in the body. The cell thus responds to the 'peptidome' instead of to a single peptide. The intracellular part of this signalling network consists of the various signalling transduction cascades. Recently, new systems biology approaches have emerged for the modelling of cell signalling. The network and systems biology approach is also able to shed new light on the evolution of intercellular signalling.

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Inhibitory effect of enterostatin on the beta cell response to digestive insulinotropic peptides

Cited by 8 publications

References 28 publications

Inhibition of Insulin Secretion as a New Drug Target in the Treatment of Metabolic Disorders

Inhibition of Insulin Secretion as a New Drug Target in the Treatment of Metabolic Disorders

Physiology of gut hormones: an overview

Bioactive peptides, networks and systems biology

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