Gut-Hormone Profile in Cœliac Disease

Besterman, H S; Bloom, Stephen R.; Sarson, D. L.; Blackburn, A M; Johnston, D I; Patel, Hitendra; Stewart, James S.; Modigliani, R; Guérin, Sylvie; Mallinson, C. N.

doi:10.1016/s0140-6736(78)92994-x

Cited by 209 publications

(101 citation statements)

References 20 publications

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“…neurotensin and the enteroglucagons, are elevated (27). It is possible that the small pancreatic responses to feeding that have been recorded in celiacs (10) are mediated by enteropancreatic nervous reflexes of the type postulated by Soloman and Grossman in the dog (28).…”

Section: Discussionmentioning

confidence: 97%

Identification and measurement of molecular variants of cholecystokinin in duodenal mucosa and plasma. Diminished concentrations in patients with celiac disease.

Calam¹,

Ellis²,

Dockray³

1982

J. Clin. Invest.

151

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A B S T R A C T The amount and type of cholecystokinin (CCK) in duodenal extracts and plasma of celiac patients and normal subjects was studied by radioimmunoassay and gel filtration. In both groups there were similar patterns of molecular forms in extracts of duodenal biopsies, but concentrations in celiac disease were significantly depressed. In boiling water extracts of duodenal mucosa from both groups a factor with the properties of the COOH-terminal octapeptide of cholecystokinin predominated, but there were also significant amounts of a larger molecular weight form. In acid extracts of mucosa a factor with the properties of the 33 or 39 residue form was identified in amounts that were -25% those of CCK8; there were also similar amounts of an acid-soluble form that had an apparent molecular weight higher than CCK39. Plasma immunoreactive cholecystokinin was studied after concentration by immunoaffinity adsorption and fractionation by gel filtration. In normal subjects fasting CCK-like immunoreactivity was <0.8 pmol/liter, and after a light breakfast increased to 2.0±0.7(range 1.0 to 4.8) pmol/liter; CCK8-like activity accounted for all the increased immunoreactivity. In five of six celiac patients the concentrations of both fasting and postprandial CCK-like immunoreactivity in plasma were undetectable (<0.8 pmol/liter). We conclude that diminished production and release of CCK could account for the impaired pancreatic and gall bladder responses to intraluminal stimuli in celiac disease.

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Section: Discussionmentioning

confidence: 97%

Identification and measurement of molecular variants of cholecystokinin in duodenal mucosa and plasma. Diminished concentrations in patients with celiac disease.

Calam¹,

Ellis²,

Dockray³

1982

J. Clin. Invest.

151

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“…90 Further, such secretion is reduced in patients with intestinal malabsorption. 91 More recently, membrane receptors for GIP were identified in osteoblasts, osteocytes and osteoclasts, 92,93 and GIP was shown to increase bone-specific alkaline phosphatase activity and to promote bone turnover both in vitro and in vivo. 93 Further, GIP inhibits osteoclast differentiation, resulting in decreased resorption.…”

Section: Impact Of Bariatric Surgery On Bone Metabolismmentioning

confidence: 99%

Bariatric surgery and bone disease: from clinical perspective to molecular insights

et al. 2012

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“…Malabsorption has been shown to augment the secretion of enteroglucagon. 67 Since GLP-1 and enteroglucagon (glicentin) are co-secreted, GLP-1 responses can be predicted to be pronounced under conditions of incomplete absorption of nutrients, such as in response to malassimilation caused by consumption of contaminated substances. In a recent debate by Nauck, 68 it was suggested that under such abnormal circumstances, a signal from the lower gut (e.g.…”

Section: Integration Of Peripheral and Central Glp-1 Pathways Regulatmentioning

confidence: 99%

Glucagon-like peptide-1 (7–36) amide: a central regulator of satiety and interoceptive stress

Dijk

Thiele

1999

Neuropeptides

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INTRODUCTIONIngestion of food is a necessary and pleasant occupation that allows humans and other species to maintain caloric homeostasis and a certain level of body weight. Ironically, in doing so, one's 'milieu interieur' is put at risk because meal-induced fuel excursions can have deleterious effects on metabolic (e.g. glycosylation causing loss of enzymatic efficacy) and cardiovascular (e.g. triglyceride accumulation, increased blood pressure, etc.) processes. 1,2 To reduce these perturbations to a minimum, evolution has provided many species (including humans and rodents) with a fine-tuned system enabling ingested nutrients to be anticipated, efficiently digested, and stored. 3 One of these mechanisms includes passage of nutrients through the digestive tract, triggering the release of a number of peptides from endocrine cells located in the wall of various parts of the gastrointestinal tract. These peptides serve important functions in facilitating the process of nutrient digestion/storage. Among these, the truncated (i.e. 7-36) amidated form of glucagon-like peptide-1 (GLP-1) has attracted considerable attention over the last several years. Firstly, because of its remarkable peripheral insulinotropic effects that could be useful for clinical purposes. Secondly, because more recent data suggest an important role of this peptide in the central nervous system (CNS) control of ingestive behavior. Although the present paper mainly focusses on the latter issue, a short review of peripheral GLP mechanisms is necessary for a better understanding of the processes that relate GLP-1 to food intake. GLP-1 FROM THE GASTROINTESTINAL TRACTGLP-1 is processed from proglucagon in mucosal L cells of the distal portion of the ileum and in the A cells of the pancreas. Ingested food, particularly when rich in carbohydrates, causes the level of circulating GLP-1 (mainly of ileal origin) to increase, and in turn, GLP-1 potently stimulates the secretion of insulin from pancreatic B cells via receptor-mediated processes (for reviews, see refs 4 and 5). In contrast, it reduces the secretion of glucagon, at least under ad libitum feeding conditions. 6 While GLP-1 may have some direct stimulatory effects on glucose clearance in peripheral tissue 7,8 (presumably via activation of specific GLP-1 receptors in liver, muscle, kidney Summary Glucagon-like peptide-1 (7-36) amide (GLP-1) is processed from proglucagon in the distal ileum as well as in the CNS. In the periphery, GLP-1 acts as an incretin factor and profoundly inhibits upper gastrointestinal motility ('ileal brake'), the latter presumably involving the CNS. Within the CNS, GLP-1 has a satiating effect, since administration of GLP-1 into the third cerebral ventricle reduces short-term food intake (and meal size), while administration of GLP-1 antagonists have the opposite effect. In addition, activation of GLP-1 receptors in certain brain regions elicits strong taste aversions. Similarities between toxin-and GLP-1-induced neuronal activity in the CNS (brain stem) suggest a role f...

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Gut-Hormone Profile in Cœliac Disease

Cited by 209 publications

References 20 publications

Identification and measurement of molecular variants of cholecystokinin in duodenal mucosa and plasma. Diminished concentrations in patients with celiac disease.

Identification and measurement of molecular variants of cholecystokinin in duodenal mucosa and plasma. Diminished concentrations in patients with celiac disease.

Bariatric surgery and bone disease: from clinical perspective to molecular insights

Glucagon-like peptide-1 (7–36) amide: a central regulator of satiety and interoceptive stress

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