Regulation of Pancreatic Glucagon Secretion During a Continuous Glucose Infusion in Early and Overt Diabetics

Schulz, B; Ziegler, M.; Witt, Sabine; Rjasanowski, I; Heinke, P.; Bibergeil, H

doi:10.1530/acta.0.0890329

Cited by 8 publications

(8 citation statements)

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“…Growth hormone concentration was determined by radioimmunoassay [24]. Pancreatic glucagon was measured with specific antiserum R4 which did not cross-react with porcine gut glucagon-like immunoreactivity in the physiological range [25]. Non-esterified fatty acids (NEFA) were estimated according to Duncombe [26] and glycerol concentrations according to Eggstein and Kreutz [27],…”

Section: Methodsmentioning

confidence: 99%

Tolbutamide does not alter insulin requirement in Type 1 (insulin-dependent) diabetes

et al. 1984

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We examined whether tolbutamide has any acute or short-term effects on insulin action in Type 1 (insulin-dependent) diabetes. A euglycaemic glucose clamp was performed in seven Type 1 diabetic patients without clinical insulin resistance by infusing glucose at a constant rate of 0.01 mmol X kg-1 X min-1 for 3h together with a simultaneous insulin infusion using an 'artificial pancreas'. The insulin infusion rate required to maintain blood glucose at 6.7 mmol/l at a set low glucose infusion rate provides an index of insulin action in vivo. The euglycaemic clamp was performed on 3 separate days in the same patient: (1) in the basal state; (2) during simultaneous intravenous tolbutamide infusion of 0.5 g/h, and (3) after treatment with 2.5 g tolbutamide/day for 6 days in addition to insulin. The insulin infusion rate needed to maintain the set blood glucose level did not differ significantly between the three experimental conditions (1.2 +/- 0.2 versus 1.3 +/- 0.3 versus 1.2 +/- 0.3 U/h). Plasma glucagon, growth hormone, non-esterified fatty acid and glycerol levels did not differ between control or sulphonylurea treatment studies. The results suggest that tolbutamide does not exert any acute or short-term effects on insulin action in vivo in Type 1 diabetes. Our results do not provide support for the idea that this agent is a clinically useful adjunct to insulin in such patients.

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Section: Methodsmentioning

confidence: 99%

Tolbutamide does not alter insulin requirement in Type 1 (insulin-dependent) diabetes

et al. 1984

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“…The criteria for the evaluation of glucose tolerance have been described in detail elsewhere (Michaelis et al 1975;Schulz et al 1978;Ratzmann et al 1979Ratzmann et al , 1980. Glucose tolerance was estimated by deter¬ mining the area of plasma glucose below the glucose curve at 60-120 min (normal value < 850 mmol • l"1 • min'1) and the plasma glucose concentration at 150 min (normal value < 6.66 mmol/l).…”

Section: Methodsmentioning

confidence: 99%

The effect of ageing on insulin sensitivity and insulin secretion in non-obese healthy subjects

Ratzmann

Witt

Heinke

et al. 1982

Acta Endocrinologica

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The relationship of age to insulin sensitivity was studied in 74 non-obese healthy subjects with normal fasting plasma glucose concentration, ranging in age from 17 to 65 years. Glucose tolerance and early as well as late insulin responses were characterized by means of a 2 h glucose infusion test (12 mg/kg/min) primed by an initial injection of 0.33 g/kg body weight glucose. Glucose tolerance did not markedly differ between young (< 30 years; n = 31) and middle-aged subjects (31\p=n-\45 years; n = 29) but deteriorated significantly in the elder group (> 45 years; n = 14). Early and late insulin responses to glucose were not appreciably altered during ageing in this selected healthy population. For the determination of insulin sensitivity a 1 h priming dose-constant infusion technique (two 30 min periods of 8 and 16 mU/kg, insulin 'MC-Actrapid', initiated by a start injection of 1 and 2 mU/kg, respectively) was used. The percent decrease of plasma glucose, FFA and glycerol levels serves as a measure of the whole body sensitivity to exogenous insulin. Under condition of identical steady-state insulin levels the decrease in plasma glucose was significantly reduced in elderly (24 \m=+-\ 5%) vs young (34 \m=+-\ 2%) subjects (P < 0.05). However, a marked sensitivity to the antilipolytic effect of insulin was demonstrated in elderly subjects considered to be resistant to its glucose-lowering action. There was no evidence that disappeared time and metabolic clearance rate of insulin were altered with advancing age. In conclusion, the impaired insulin sensitivity to glucose metabolism seems to be the primary factor responsible for the deterioration of glucose tolerance with advancing age.

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“…It is well established that all forms of diabetes mellitus are accompanied by relative or absolute hyperglucagonemia (Unger and Orci, 1977;Unger, 1974). During treatnient with GCIIS of a short period plasma immunoreaetive glucagon levels were in the normal range of the assay as employed in our laboratory (Schulz et al, 1978;Ratzmann et al, 1978;Ratzmann et al, 1981). Albisser et al (1977) failed to demonstrate apparent alterations of the patterns of glucagon levels in insulin-dependent diabetic patients irrespective of improvement of an oral glucose tolerance test by treatment with an artificial endocrine pancreas.…”

Section: Discussionmentioning

confidence: 79%

Short-Term of the Artificial Beta-Cell (Biostator^® on Pancreatic Glucagon Response in Insulin-Dependent Diabetic (IDDM)

Kp¹,

Schneider²,

Besch³

et al. 2009

Exp Clin Endocrinol Diabetes

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The short-term effect of the glucose-controlled insulin infusion system (GCIIS) Biostator on metabolic and hormonal responses to a 2 h glucose infusion (0.33 g/kg body weight glucose i.v. followed by an infusion of 12 mg/kg/min) was studied in 8 insulin-dependent diabetic patients (IDDM). Normalization of glucose tolerance by means of GCIIS was associated with significant improvement of lipid metabolism in IDDM. Endogenous insulin secretion (C-peptide) was not altered significantly under the experimental conditions. The results demonstrate that immunoreactive glucagon response to intravenous glucose infusion was restored by treatment with GCIIS in IDDM irrespective of no prolonged duration of normoglycemia. The results provide further support that abnormal glucagon response in some IDDM is secondary to insulin deficiency.

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Regulation of Pancreatic Glucagon Secretion During a Continuous Glucose Infusion in Early and Overt Diabetics

Cited by 8 publications

References 0 publications

Tolbutamide does not alter insulin requirement in Type 1 (insulin-dependent) diabetes

Tolbutamide does not alter insulin requirement in Type 1 (insulin-dependent) diabetes

The effect of ageing on insulin sensitivity and insulin secretion in non-obese healthy subjects

Short-Term of the Artificial Beta-Cell (Biostator^® on Pancreatic Glucagon Response in Insulin-Dependent Diabetic (IDDM)

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Regulation of Pancreatic Glucagon Secretion During a Continuous Glucose Infusion in Early and Overt Diabetics

Cited by 8 publications

References 0 publications

Tolbutamide does not alter insulin requirement in Type 1 (insulin-dependent) diabetes

Tolbutamide does not alter insulin requirement in Type 1 (insulin-dependent) diabetes

The effect of ageing on insulin sensitivity and insulin secretion in non-obese healthy subjects

Short-Term of the Artificial Beta-Cell (Biostator® on Pancreatic Glucagon Response in Insulin-Dependent Diabetic (IDDM)

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Short-Term of the Artificial Beta-Cell (Biostator^® on Pancreatic Glucagon Response in Insulin-Dependent Diabetic (IDDM)