Glucagon Secretion in Patients with Hypoparathyroidism: Effect of Serum Calcium on Glucagon Release

Torella, Roberto; Giugliano, Dario; Scognamiglio, Giuseppe; Passariello, N.; Tirelli, A

doi:10.1210/jcem-54-2-229

Cited by 6 publications

(2 citation statements)

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“…As shown in results fasting glucagon and also insulin stimulated glucagon levels were almost identical in each group. Discordance of our results with those of Torella et al (1982) is possibly due to their different experimental conditions in that they studied the effect of arginine stimulus on the endocrine response of the pancreas. As is known, when the glucose concentrations are abruptly dropped from 80 to 25 mg/ 100 ml the alpha-cell responded with a two phase pattern of glucagon output (Gordon, Knowlton and Martin 1974).…”

Section: Discussioncontrasting

confidence: 82%

“…On the other hand some investigators have documented that lack of calcium in the medium resulted in enhanced glucagon secretion (Leclercq-Meyer, Marchand and Malaisse 1973;Leclercq-Meyer, Rebolledo, Marchand and Malaisse 1975). More recently it was observed that glucagon secretion in response to arginine infusion in hypocalcaemic hypoparathyroid patients decreased markedly, but following correction of hypocalcaemia acutely, it returned to normal (Torella, Giugliano, Scognamiglio, Passariello and Tirelli 1982).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Pancreatic Glucagon Secretion in Hypoparathyroidism, Lack of Effect of Serum Calcium on Glucagon Release

Gedik¹,

Koray²,

Istanbullu³

1983

Horm Metab Res

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The key role of calcium in the release of insulin is well recognized (Grodsky and Benett 1966;Milner and Hales 1967). However, little is known about the effects of this cation on glucagon secretion from pancreatic alpha-cell and there are conflicting results concerning this subject. In the present study we evaluated glucagon responses to insulin induced hypoglycemia in patients with hypoparathyroidism before and after correction of hypocalcemia. Materials and MethodsThe subjects for this study comprised two groups. Group 1 consisted of 7 patients of both sexes who had hypocalcaemia due to either idiopathic (five cases) or secondary hypoparathyroidism (two cases). They were nondiabetic, nonobese and had no family history of metabolic and endocrine diseases. After an overnight fast, an i.v. insulin tolerance test was performed with 0.1 U of regularly insulin per kg of body weight. Blood samples for analysis of glucose, serum calcium and plasma immunoreactive pancreatic glucagon were collected from an antecubital vein before and after insulin injection, at 15 min. intervals for 120 min. After the first experiment was completed vitamin D 3 treatment was started. When the serum calcium levels reached normal, the same experiment was repeated on every subject. Group 2 (control group) consisted of 7 normal, healthy volunteers of both sexes. They were prepared for the experiment in the same way as for group 1. The nature and purpose of the study was explained and formal consent obtained.Blood glucose was measured by Somogyi method. Serum calcium determinations were done by an Atomic Absorption Spectrophotometer (Perkin-Elmer Model 103). For plasma pancreatic glucagon determinations, plasma samples were prepared by adding 1000 IU of Trasylol + 2 mg of EDTA Na per ml of blood. The plasma was kept frozen until beginning of the dosage.Plasma glucagon was assayed with commercially available glucagon assay kits (Glucagon PEG Kit, Biodata, S.p. A Viale Tunisia 50 Milano, Italy). The basal values of pancreatic glucagon, in fasting subjects at rest, ranging between 50-250 pg/ml. ResultsThe mean serum calcium concentration in hypocalcaemic hypoparathyroid patients was 5.9 ± 1.5 mg/100 ml. Treatment with vitamin D 3 raised the serum calcium concentration to 8.9 ± 0.5 mg/100 ml. (P< 0.05). In control group (group 2) the mean serum calcium level was 9.4 ±0.5 mg/ml. The mean basal calcium level of untreated patients was significantly lower than those of normal controls (P<0.05) but there were no significantly differences between control group and after treatment (P> 0.05).Mean blood glucose levels during i.v. insulin administration are shown in Figure 1. The nadir of blood glucose level was at 30 min in each group no statistical significance was found in mean glucose levels during i.v. insulin administration in hypo-and normocalcaemic conditions as well as in control group. Mean basal fasting plasma pancreatic glucagon levels were 99.6 ± 19.6 pg/ml (group 1, before treatment), 91.7 ± 15.9 pg/ml (group 1, after treatment) and 102.5 ± 20...

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Section: Discussioncontrasting

confidence: 82%

Section: Discussionmentioning

confidence: 99%