THE EFFECT OF CHRONIC HYPERGLYCEMIA ON THE ISLET B-CELL RESPONSIVENESS IN NEWLY DIAGNOSED TYPE-2 DIABETES

被引：14

作者：

GJESSING, HJ

REINHOLD, B

PEDERSEN, O

机构：

[1] Division of Endocrinology and Metabolism, University Clinic of Internal Medicine, Århus Amtssyghus, Århus

[2] Department of Endocrinology M, Odense University Hospital, Odense

[3] Central Laboratory, Fredericia Hospital, Fredericia

来源：

DIABETIC MEDICINE | 1992年 / 9卷 / 07期

关键词：

TYPE-2; DIABETES; GLUCOSE POTENTIATION; PLASMA C-PEPTIDE; INSULIN KINETICS; ISLET B-CELL FUNCTION;

D O I：

10.1111/j.1464-5491.1992.tb01853.x

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The aim of the present study was to evaluate the effect of chronic hyperglycaemia on the pancreatic B-cell response to stimulation with a standard mixed meal or intravenous glucagon in 7 subjects with newly diagnosed Type 2 diabetes. Stimulation was performed at mean chronic fasting hyperglycaemia of 11.8 +/- 0.7 (SEM) mmol l-1 and at normoglycaemia obtained by an intravenous infusion of regular insulin followed by an insulin wash-out peroid. The incremental plasma C-peptide area under the curve after stimulation with the meal was similar at normo- and hyperglycaemia. In contrast, prestimulatory plasma C-peptide and the incremental plasma C-peptide area under the curve after stimulation with glucagon were significantly higher at chronic hyperglycaemia than at normoglycaemia (p < 0.01 and p < 0.05). In conclusion, chronic hyperglycaemia as seen in newly diagnosed Type 2 diabetes is associated with a complete lack of potentiation of postprandial islet B-cell secretion but a partly preserved potentiation of basal and post-glucagon islet B-cell secretion.

引用

页码：601 / 604

页数：4

共 21 条

[1]

Ward KW, Bolgiano DC, Mcknight B., Halter JB, Porte D., Diminished B‐cell secretory capacity in patients with noninsulin dependent diabetes mellitus, J Clin Invest, 74, pp. 1318-1328, (1984)

[2]

Gjessing HJ, Reinholdt B., Pedersen O., The plasma C‐peptide and insulin responses to stimulation with intravenous glucagon and a mixed meal in well‐controlled Type 2 (non‐insulin‐dependent) diabetes mellitus: dependency on acutely established hyperglycaemia, Diabetologia, 32, pp. 858-863, (1989)

[3]

Laury MC, Takao F., Bailbe D., Penicaud L., Portha B., Picon L., Et al., Differential effects of prolonged hyperglycaemia on in vivo and in vitro insulin secretion in rats, Endocrinology, 128, pp. 2526-2533, (1991)

[4]

Unger RH, Grundy S., Hyperglycaemia as an inducer as well as a consequence of impaired islet cell function and insulin resistance: implications for the management of diabetes, Diabetologia, 28, pp. 119-121, (1985)

[5]

Rossetti L., Giaccari A., DeFronzo RA., Glucose toxicity, Diabetes Care, 13, pp. 610-630, (1990)

[6]

Leahy JL., Natural history of beta‐cell dysfunction in NIDDM, Diabetes Care, 13, pp. 992-1010, (1990)

[7]

Robertson RP., Type II diabetes, glucose ‘non‐sense,’ and islet desensitization, Diabetes, 38, pp. 1501-1505, (1989)

[8]

Grodsky GM., A new phase of insulin secretion. How will it contribute to our understanding of beta‐cell function?, Diabetes, 38, pp. 673-678, (1989)

[9]

Rasmussen H., Zawalich KC, Ganesan S., Calle R., Zawalich WS., Physiology and pathophysiology of insulin secretion, Diabetes Care, 13, pp. 655-666, (1990)

[10]

Faber OK, Binder C., C‐peptide response to glucagon. A test for the residual beta‐cell function in diabetes mellitus, Diabetes, 26, pp. 605-610, (1977)

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