Glucagon- and Glicentin-Producing Cells

Orci, Lelio; Bordi, Cesare; Unger, Roger H; Perrelet, Alain

doi:10.1007/978-3-642-68866-9_4

Cited by 13 publications

(5 citation statements)

References 46 publications

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“…Similar cells have not been found in humans, however (120). The majority of the intestinal proglucagon-derived peptides are secreted from the L-cells, which differ clearly from the A-cells by their granule morphology (224). A-cell granules show a distinct halo of less electron-dense material surrounding a core of dense material, whereas the granules of the L-cells are homogeneous without halo formation.…”

Section: Proglucagon Distributionmentioning

confidence: 60%

“…As expected, antisera directed against the midregion of glucagon ("side viewing") stain the pancreatic A-cells as well as the intestinal L-cells, whereas antibodies against the free COOH terminus of glucagon (which is not exposed in the L-cells) only stain the A-cells. Antisera against the NH 2 -terminal, non-glucagon part of glicentin stain both the A-cells and the L-cells because they react with GRPP in the pancreas and with glicentin in the gut (224). As expected from their common origin, both GLP-1 and GLP-2 show complete coexistence with glucagon (side-viewing antisera) upon immunohistochemical examination (189,227,229).…”

Section: Proglucagon Distributionmentioning

confidence: 99%

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The Physiology of Glucagon-like Peptide 1

Holst¹

2007

Physiological Reviews

2,670

2,385

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Glucagon-like peptide 1 (GLP-1) is a 30-amino acid peptide hormone produced in the intestinal epithelial endocrine L-cells by differential processing of proglucagon, the gene which is expressed in these cells. The current knowledge regarding regulation of proglucagon gene expression in the gut and in the brain and mechanisms responsible for the posttranslational processing are reviewed. GLP-1 is released in response to meal intake, and the stimuli and molecular mechanisms involved are discussed. GLP-1 is extremely rapidly metabolized and inactivated by the enzyme dipeptidyl peptidase IV even before the hormone has left the gut, raising the possibility that the actions of GLP-1 are transmitted via sensory neurons in the intestine and the liver expressing the GLP-1 receptor. Because of this, it is important to distinguish between measurements of the intact hormone (responsible for endocrine actions) or the sum of the intact hormone and its metabolites, reflecting the total L-cell secretion and therefore also the possible neural actions. The main actions of GLP-1 are to stimulate insulin secretion (i.e., to act as an incretin hormone) and to inhibit glucagon secretion, thereby contributing to limit postprandial glucose excursions. It also inhibits gastrointestinal motility and secretion and thus acts as an enterogastrone and part of the “ileal brake” mechanism. GLP-1 also appears to be a physiological regulator of appetite and food intake. Because of these actions, GLP-1 or GLP-1 receptor agonists are currently being evaluated for the therapy of type 2 diabetes. Decreased secretion of GLP-1 may contribute to the development of obesity, and exaggerated secretion may be responsible for postprandial reactive hypoglycemia.

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Section: Proglucagon Distributionmentioning

confidence: 60%

Section: Proglucagon Distributionmentioning

confidence: 99%

The Physiology of Glucagon-like Peptide 1

Holst¹

2007

Physiological Reviews

2,670

2,385

View full text Add to dashboard Cite

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“…Whilst intestinal morphology was not dramatically altered by bypass surgery, it seemed reasonable to further investigate gut hormone populations in the AL and BPL of ND- and HFD-RYGB rats. GLP-1 has long been advocated as the chief hormonal protagonist for RYGB induced metabolic benefits [ 19 ], originating largely from L-cells located in the ileum [ 20 ]. As such, GLP-1 delays gastric emptying, promotes satiety together with weight loss and improves glucose tolerance through stimulation of glucose-dependent insulin secretion [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

RYGB surgery has modest effects on intestinal morphology and gut hormone populations in the bypassed biliopancreatic limb but causes reciprocal changes in GLP-2 and PYY in the alimentary limb

et al. 2023

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Roux-en-Y gastric-bypass (RYGB) induced alterations in intestinal morphology and gut-cell hormone expression profile in the bypassed biliopancreatic-limb (BPL) versus the alimentary-limbs (AL) are poorly characterised. This pilot study has therefore explored effects following RYGB in high-fat-diet (HFD) and normal-diet (ND) rats. Female Wistar rats (4-week-old) were fed HFD or ND for 23-weeks prior to RYGB or sham surgeries. Immunohistochemical analysis of excised tissue was conducted three-weeks post-surgery. After RYGB, intestinal morphology of the BPL in both HFD and ND groups was unchanged with exception of a small decrease in villi width in the ND-RYGB and crypt depth in the HFD-RYGB group. However, in the AL, villi width was decreased in ND-RYGB rats but increased in the HFD-RYGB group. In addition, crypt depth decreased after RYGB in the AL of HFD rats. GIP positive cells in either limb of both groups of rats were unchanged by RYGB. Similarly, there was little change in GLP-1 positive cells, apart from a small decrease of numbers in the villi of the BPL in HFD rats. RYGB increased GLP-2 cell numbers in the AL of ND-RYGB rats, including in both crypts and villi. This was associated with decreased numbers of cells expressing PYY in the AL of ND-RYGB rats. The BPL appears to maintain normal morphology and unchanged enteroendocrine cell populations despite being bypassed in RYGB-surgery. In contrast, in the AL, villi area is generally enhanced post-RYGB in ND rats with increased numbers of GLP-2 positive cells and decreased expression of PYY.

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“…Komórki wydzielania wewnętrznego przypominające komórki α trzustki występują w błonie śluzowej jelita cienkiego i jelita grubego (66). Większość jelitowych peptydów pochodzących od proglukagonu jest wydzielana przez komórki L, które różnią się od komórek α morfologią ziarnistości (65). Peptydy wytwarzane przez komórki α i L zostały zidentyfikowane na poziomie komórkowym metodą immunocytochemiczną.…”

Section: Dystrybucja Proglukagonuunclassified

Distribution and function of glucagon-like peptide 1 (GLP-1) in the digestive tract of mammals and the clinical use of its analogues

Górska¹,

Arciszewski²

2023

Medycyna Weterynaryjna

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Recently, interest in glucagon-like peptide-1 (GLP-1) and other peptides derived from preproglucagon has increased significantly. GLP-1 is a 30-amino acid peptide hormone produced in L-type enteroendocrine cells as a response to food intake. GLP-1 is rapidly metabolized and inactivated by the dipeptidyl peptidase IV enzyme before the hormone leaves the intestine, which increases the likelihood that GLP-1 action is transmitted through sensory neurons in the intestine and liver through the GLP-1 receptor. The main actions of GLP-1 are to stimulate insulin secretion (i.e. act as incretin hormone) and inhibit glucagon secretion, thus contributing to the reduction of postprandial glucose spikes. GLP-1 also inhibits motility and gastrointestinal secretion, and therefore acts as part of the „small bowel brake” mechanism. GLP-1 also appears to be a physiological regulator of appetite and food intake. Because of these effects, GLP-1 or GLP-1 receptor agonists are now increasingly used to treat type 2 diabetes. Reduced GLP-1 secretion may contribute to the development of obesity, and excessive secretion may be responsible for postprandial reactive hypoglycemia. The use of GLP-1 agonists opens up new possibilities for the treatment of type 2 diabetes and other metabolic diseases. In the last two decades, many interesting studies covering both the physiological and pathophysiological role of GLP-1 have been published, and our understanding of GLP-1 has broadened significantly. In this review article, we have tried to describe our current understanding of how GLP-1 works as both a peripheral hormone and as a central neurotransmitter in health and disease. We focused on its biological effects on the body and the potential clinical application in relation to current research.

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Glucagon- and Glicentin-Producing Cells

Cited by 13 publications

References 46 publications

The Physiology of Glucagon-like Peptide 1

The Physiology of Glucagon-like Peptide 1

RYGB surgery has modest effects on intestinal morphology and gut hormone populations in the bypassed biliopancreatic limb but causes reciprocal changes in GLP-2 and PYY in the alimentary limb

Distribution and function of glucagon-like peptide 1 (GLP-1) in the digestive tract of mammals and the clinical use of its analogues

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