Studies on the Physiology of Secretin

Barre, Jean La; Still, Eugene U.

doi:10.1152/ajplegacy.1930.91.2.649

Cited by 56 publications

(15 citation statements)

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“…Soon after that, a number of groups presented somehow contradictory results of assessments of the effect of duodenal mucosa extracts . The acronym “incretin”, referring INtestine seCRETion INsulin, was coined by La Barre in 1932 . Rapid development of the concept of incretin became possible after quantitative insulin measurement with radioimmunoassay (RIA) was available in 1960s …”

Section: Concept Of Incretin and The Development Of Glp‐1‐based Diabementioning

confidence: 99%

The incretin hormone GLP‐1 and mechanisms underlying its secretion

Tian

Jin

2016

Journal of Diabetes

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Highlights GLP-1 is among the two known incretin hormones which are released from the gut in response to food ingestion. Neuronal factors, other hormones, and direct nutritional contact, can trigger GLP-1 secretion. Here we present a brief summary of our current knowledge on mechanisms underlying GLP-1 secretion in response to nutrient components, hormonal factors and dietary polyphenols. Our perspective view of the role of gut microbiota on GLP-1 production and the biology of the gut GLP-1-producing cells was also presented. Abstract Glucagon-like peptide-1 (GLP-1) is a cell type-specific post-translational product of proglucagon. It is encoded by the proglucagon gene and released primarily from intestinal endocrine L-cells in response to hormonal, neuronal, and nutritional stimuli. In addition to serving as an incretin in mediating the effect of meal consumption on insulin secretion, GLP-1 exerts other functions in pancreatic islets, including regulation of β-cell proliferation and protection of β-cells against metabolic stresses. Furthermore, GLP-1 exerts numerous other functions in extrapancreatic organs, whereas brain GLP-1 signaling controls satiety. Herein we review the discovery of two incretins and the development of GLP-1-based drugs. We also describe the development of cellular models for studying mechanisms underlying GLP-1 secretion over the past 30 years. However, the main content of this review is a summary of studies on the exploration of mechanisms underlying GLP-1 secretion. We not only summarize studies conducted over the past three decades on elucidating the role of nutritional components and hormonal factors in regulating GLP-1 secretion, but also present a few very recent studies showing the possible role of dietary polyphenols. Finally, the emerging role of gut microbiota in metabolic homeostasis with the potential implication on GLP-1 secretion is discussed. Lili

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Section: Concept Of Incretin and The Development Of Glp‐1‐based Diabementioning

confidence: 99%

The incretin hormone GLP‐1 and mechanisms underlying its secretion

Tian

Jin

2016

Journal of Diabetes

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“…incretin) that was without effect on the exocrine pancreas, but lowered blood glucose concentrations, presumably by stimulating insulin secretion from the endocrine pancreas (La Barre & Still 1930). Thus, in 1930, La Barre and Still had separated a crude secretin preparation into two fractions: one that stimulated exocrine pancreatic secretion (i.e.…”

Section: The Incretin Conceptmentioning

confidence: 99%

Incretin physiology beyond glucagon‐like peptide 1 and glucose‐dependent insulinotropic polypeptide: cholecystokinin and gastrin peptides

Rehfeld

2011

Acta Physiologica

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Gastrin and cholecystokinin (CCK) are homologous hormone systems known to regulate gastric acid secretion, gallbladder emptying, and cell growth in the pancreas and stomach. They are, however, also involved in the development and secretory functions of pancreatic islet cells. For instance, foetal and neonatal islets express significant amounts of gastrin, and human as well as porcine islet cells express the gastrin/CCK-B receptor abundantly. Therefore, exogenous gastrin and CCK peptides stimulate insulin and glucagon secretion in man. Accordingly, endogenous hypergastrinaemia is accompanied by islet cell hyperplasia and increased insulin secretion. Conventionally, the effect of gastrointestinal hormones on insulin secretion (the incretin effect) has been defined and quantified in relation to oral versus intravenous glucose loadings. Under these unphysiological conditions, the release of gastrin and CCK and, hence, their effect on insulin secretion are modest in comparison with the effects of glucose-dependent insulinotropic polypeptide and glucagon-like peptide 1 (GLP-1). Consequently, the interest of CCK and gastrin in incretin research has for decades been limited. A few years ago, however, it was suggested that gastrin together with epidermal growth factor or later GLP-1 might stimulate beta cell growth and secretion. Recent studies have shown that the combination of gastrin and GLP-1 actually restores normoglycaemia in diabetic mice. Therefore, a short review of the incretin system in a broader functional context that includes gastrin and CCK peptides may be timely.

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“…The hormonal components of the enteroinsular axis have been investigated since the initial definition of the 'incretin' concept by La Barre & Still in 1930, i.e. 'the endocrine factors from the gut with insulinotropic activity which are released by nutrients, especially carbohydrates' [11]. Successive incretin candidates have included gastrin, secretin and cholecystokinin; and at present, the two leading candidates are glucose-dependent insulinotropic polypeptide (GIP) and GLP-1 (reviewed in 12).…”

Section: Hormonal Responsementioning

confidence: 99%

Glucose metabolism and the postprandial state

Lefèbvre

Scheen

1999

Eur J Clin Investigation

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Disturbances of postprandial glucose metabolism are now thought to contribute to cardiovascular disease. Postprandial glucose excursions can be affected by a number of factors, such as the types of carbohydrates ingested and the way they are metabolized. In Type 2 diabetes, factors that contribute to excessive postprandial glucose excursions include disruption of insulin secretion, insufficient inhibition of hepatic glucose production and defective glucose storage in muscle. A number of measures may attenuate excessive postprandial blood glucose excursions. These include a diet high in 'low glycaemic index' foods and treatment with drugs that improve or restore the hormonal response (e.g. the sulphonylureas and the newer beta-cell mediated insulinotropic drugs such as repaglinide), that improve insulin sensitivity or that delay gastric emptying.

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Studies on the Physiology of Secretin

Cited by 56 publications

References 0 publications

The incretin hormone GLP‐1 and mechanisms underlying its secretion

The incretin hormone GLP‐1 and mechanisms underlying its secretion

Incretin physiology beyond glucagon‐like peptide 1 and glucose‐dependent insulinotropic polypeptide: cholecystokinin and gastrin peptides

Glucose metabolism and the postprandial state

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