Increased Gut Glucagon Release as Pathogenetic Factor in Reactive Hypoglycæmia?

Rehfeld, J. F.; Heding, L. G.; Holst, Jens J.

doi:10.1016/s0140-6736(73)90193-1

Cited by 49 publications

(16 citation statements)

References 20 publications

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“…To our knowledge, no data regarding plasma GI level during postprandial hypoglycemia are available except for one report (Rehfeld et al, 1973). Though no apparent difference in plasma GI level during OGTT could be detected between the patients with hypoglycemia and their respective controls in this series, hypoglucagonemia relative to glucose levels could be said to exist in these hypoglycemic patients since hypoglycemia stimulates glucagon secretion.…”

Section: Discussionmentioning

confidence: 58%

“…Rehfeld et al (1973) found that gut GLI concentrations were significantly increased during an oral glucose load in two out of three patients with essential reactive hypoglycemia and speculated that an increased release of gut GLI might be the pathogenetic factor in reactive hypoglycemia, since gut GLI might compete with pancreatic glucagon for the glucagon receptor sites in the liver, thus leading to a state of relative deficiency of pancreatic glucagon, which would in turn lead to inappropriate glycogenolysis with ensuing hypoglycemia. Our results confirmed their findings and further showed that the same was true in diabetic reactive as well as idiopathic reactive hypoglycemia in a large number of subjects.…”

Section: Discussionmentioning

confidence: 99%

“…No adequate information on this matter is available so far. Although changes in plasma glucagon levels have been extensively investigated in diabetics in general, there are few studies on this glucose counterregulatory factor in relation to the pathophysiology causal in this kind of hypoglycemia (Hofeldt et al, 1972;Rehfeld et al, 1973;Hopwood et al, 1975). In order to clarify the pathogenesis of the reactive hypoglycemia, the present study has been undertaken to seek the abnormality common to diabetic-reactive and idiopathic reactive hypoglycemia in plasma IRI, glucagon immunoreactivity (GI) and gut glucagon-like immunoreactivity (GLI) responses to glucose loads.…”

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confidence: 99%

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Exaggerated response of plasma glucagon-like immunoreactivity (GLI) to oral glucose in patients with reactive hypoglycemia.

et al. 1981

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In order to study the pathogenesis of reactive hypoglycemia, the responses of plasma glucose, IRI, glucagon immunoreactivity (GI) and total glucagon-like immunoreactivity (GLI) to 100g oral glucose load were investigated in twenty-six patients of normal weight with reactive hypoglycemia.Of these patients, nineteen exhibited a diabetic OGTT curve. The findings in these patients were compared to normal control subjects (N=20) and to disease-matched patients controls (N=43).The psychological status was assessed by Cornell Medical Index Health Questionnaire in most of the subjects, who also received an x ray examination of the upper gastrointestinal tract. In addition, IVGTT was performed in the hypoglycemic patiens. No apparent difference in plasma IRI response to oral glucose was observed between the hypoglycemic patients and their respective controls.Plasma total GLI concentrations were significantly increased during OGTT in both hypoglycemic groups.Following an oral glucose load, plasma GI levels were suppressed in the hypoglycemic groups to an extent similar to that in the control despite an apparent fall in their plasma glucose levels to the hypoglycemic range in the former.Radiological alterations in the upper gastrointestinal tract; deformity of the duodenal cap, gastric and/or duodenal ulcer, were found more frequently in the hypoglycemic groups. However, no characteristic change in personality was noticed in the patients.During IVGTT, neither plasma glucose nor total GLI level of the hypoglycemics differed from that of each control. The pathogenic factors responsible for reactive hypoglycemia will be discussed.

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Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Exaggerated response of plasma glucagon-like immunoreactivity (GLI) to oral glucose in patients with reactive hypoglycemia.

et al. 1981

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“…This was because the 'gut glucagons' contained the entire glucagon sequence [3,4]. Indeed, as early as 1973 we found that individuals who suffered from postprandial reactive hypoglycaemia had exaggerated secretion of 'gut glucagon' [5,6]. The predominant molecule of the 'gut glucagons' turned out to be a peptide of 69 amino acids, designated glicentin, which, as predicted [3], contained the full glucagon sequence (residues 33-61), but this molecule had no effect on insulin secretion.…”

Section: Discovery Of Glucagon-like Peptide-1mentioning

confidence: 98%

Glucagon-like peptide-1: from extract to agent. The Claude Bernard Lecture, 2005

2006

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The incretin hormones are intestinal polypeptides that enhance postprandial insulin secretion. Gastric inhibitory polypeptide (GIP) was initially thought to regulate gastric acid secretion, whereas glucagon-like peptide-1 (GLP-1) was discovered as a result of a systematic search for intestinal insulinotropic products of proglucagon gene expression. The incretin effect is markedly impaired or absent in patients with type 2 diabetes because of decreased secretion of GLP-1 and a loss of the insulinotropic effects of GIP. Metabolic control can be restored or greatly improved by administration of exogenous GLP-1, but this peptide is almost immediately degraded by dipeptidyl peptidase IV (DPP-IV), and therefore has little clinical value. DPP-IV-resistant analogues (incretin mimetics) have been identified or developed, and inhibitors of DPP-IV have also proved effective in protecting endogenous GLP-1 (and GIP) from degradation. Both principles have been tested in clinical studies. The incretin mimetics, administered by sc injection, have demonstrated lasting improvement in HbA 1 c in patients insufficiently treated with conventional oral therapy, and their use has been associated with steady weight loss for up to 2 years. The DPP-IV inhibitors, given once or twice daily by mouth, also appear to provide lasting improvement in HbA 1 c, but are weight-neutral. The first incretin mimetic has reached the market in the US, and applications for approval of the first inhibitors are expected to be filed early in 2006.

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“…In gastrectomized patients, the secretion of intestinal glucagon-like immunoreactivity (GLI) observed throughout the course of an oral glucose tolerance test (OGTT) is more intense (three-fivefold) than in normal subjects [1,2,3,4,5,6]. Arising from these findings, speculation has been made about the possible implication of high levels of circulating GLI in the pathogenesis of some aspects of the postgastrectomy syndrome, such as dumping [5] and reactive hypoglycaemia [6]. However, the aforementioned condition, induced by the ingestion of a large amount of glucose solution, is obviously not a physiological situation.…”

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Effect of food ingestion on intestinal glucagon-like immunoreactivity (GLI) secretion in normal and gastrectomized subjects

et al. 1977

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Summary. This work was undertaken to compare the intestinal GLI responses to oral glucose (1.75 g/kg, 25% sol.), to a carbohydrate-rich meal (carbohydrate content about 1.75 g/kg) and to a protein meal (250-400 g grilled lean beef) in normal (n = 6) and gastrectomized (n = 6) subjects. As expected, after glucose administration the elevation of plasma GLI was more pronounced in the gastrectomy group (-500% above baseline) than in the controls (= 75% above baseline). However, the gastrectomized patients responded to the carbohydrate meal with a very slight elevation of circulating GLI (= 45% above baseline), similar to that found in the controls (= 70% above baseline). After the protein meal, a small increase of GLI was also observed in both groups. -In conclusion, in gastrectomized subjects the ingestion of natural foodstuffs is followed by a normal elevation of plasma GLI, thereby suggesting the exclusion of this factor from involvement in the constellation of postgastrectomy syndrome. In these patients, the exaggerated rise in GLI after oral glucose is not representative of increments after physiological stimuli.Key words: Gastrectomized and normal subjects, glucose and food ingestion, glucagon, intestinal glucagon-like immunoreactivity (GLI), insulin. In gastrectomized patients, the secretion of intestinal glucagon-like immunoreactivity (GLI) observed throughout the course of an oral glucose tolerance test (OGTT) is more intense (three-fivefold) than in normal subjects [1,2,3,4,5,6]. Arising from these findings, speculation has been made about the possible implication of high levels of circulating GLI in the pathogenesis of some aspects of the postgastrectomy syndrome, such as dumping [5] and reactive hypoglycaemia [6]. However, the aforementioned condition, induced by the ingestion of a large amount of glucose solution, is obviously not a physiological situation.To obtain information about the effect of ingestion of natural foodstuffs on GLI secretion, in the present work we have examined the plasma GLI levels after consumption of carbohydrate and protein-rich meals in normal and gastrectomized subjects. Materials and MethodsThe control group consisted of six healthy volunteers (four males and two females) whose ages ranged from 24 to 46 years. None of them appeared to be obese (+ 10% ideal body weight according to the Metropolitan Life Insurance Company tables). The test group consisted of six male subjects who had undergone subtotal gastric resection (Billroth II) because of the presence of a benign ulcer not controllable by medical treatment. Their ages ranged from 32 to 48 years. None of them were underweight by more than 10% of the ideal body weight and none suffered from other apparent illness.All individuals were subjected to three tests. First, to an oral glucose tolerance test; glucose (1.75 g per kg of body weight) was taken as a 25%

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Increased Gut Glucagon Release as Pathogenetic Factor in Reactive Hypoglycæmia?

Cited by 49 publications

References 20 publications

Exaggerated response of plasma glucagon-like immunoreactivity (GLI) to oral glucose in patients with reactive hypoglycemia.

Exaggerated response of plasma glucagon-like immunoreactivity (GLI) to oral glucose in patients with reactive hypoglycemia.

Glucagon-like peptide-1: from extract to agent. The Claude Bernard Lecture, 2005

Effect of food ingestion on intestinal glucagon-like immunoreactivity (GLI) secretion in normal and gastrectomized subjects

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