IRI-Secretion in MOD with and without SU (5 Year Control)

Lohmann, Dieter; Hj, Verlohren

doi:10.1055/s-2007-999236

Cited by 5 publications

(3 citation statements)

References 4 publications

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“…1, no consistent impairment of beta-cell function was seen in relation to the duration of diabetes. Thus far the results are in agreement with results from preliminary prospective studies with a follow-up period of five years (15,16). Since there are no longitudinal studies with longer followup and in¬ cluding a large number of patients, a clear sequence of events can only be hypothesized from cross-sectional data like this.…”

Section: Introductionsupporting

confidence: 87%

Treatment failures: A common problem in the management of patients with type II diabetes

Groop

Pelkonen

1983

Acta Endocrinologica

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Secondary failure is a common problem in the treatment of patients with type II diabetes. The underlying mechanisms are reviewed, and special interest is focused on the assessment of insulin secretion and insulin sensitivity. Impaired beta-cell function seems to be the major cause of secondary drug failure in patients with normal weight, whereas insulin resistance is of greater importance in obese patients. The importance of Cpeptide determinations to detect patients needing insulin is emphasized. The concept of progressive deterioration of beta-cell function with time in type II diabetes is challenged. Different treatment modalities for the management of patients with secondary drug failure are discussed and special interest is focused on the combination of insulin and sulfonylureas in the management of secondary failure patients with slightly impaired insulin secretion.

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Section: Introductionsupporting

confidence: 87%

Treatment failures: A common problem in the management of patients with type II diabetes

Groop

Pelkonen

1983

Acta Endocrinologica

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“…The results were compared with those obtained in 27 healthy volunteers. To investigate the insulin secretion pattern and carbohydrate tolerance in relation to the duration of the disease, 38 non-insulin-dependent diabetics (24 patients on a purely dietetic treatment, 14 patients with an additional treatment of glibenclamide were repeatedly investigated immediately after manifestation of diabetes, 4 weeks later, and after 5 years (Lohmann and Verlohren, 1980). In vitro study.…”

Section: Methodsmentioning

confidence: 99%

“…All patients were characterized by missing or reduced insulin secretion during an oral glucose load (lOOg). Insulin content, 3H-leucine incorporation into (pro)insulin, and insulin release from the isolated islets were examined (Jahr et al, 1980;Jahr et al, 1983;Lohmann et al, 1980). These data were compared with those under in vivo conditions.…”

Section: Methodsmentioning

confidence: 99%

Insulin Secretion in Type II Diabetics: In Vivo and in Vitro Investigation¹)

Hj¹,

Jahr²

2009

Exp Clin Endocrinol Diabetes

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Many cases of type II diabetes present an anomaly of insulin secretion which is characterized by a missing, reduced, or delayed glucose-stimulated insulin output from the beta cell. We aimed at finding out whether this characteristic disorder is a consequence of reduced beta cell mass or of a more functional disturbance. In the latter case it was to be clarified whether the disturbed beta cell "glucoreceptor" function represents a qualitative or rather a quantitative difference. By the evaluation of insulin secretion and of carbohydrate tolerance during oral and/or intravenous intake of glucose, and after intravenous application of tolbutamide or glucagon the defective insulin secretion in type II diabetics was found to represent a more functional disturbance which could not be explained by reduction of beta cell mass. Thus it was concluded that the anomaly of insulin secretion mentioned above might be a consequence of a qualitative defect of the glucoreceptor. To prove this, isolated human islets (insulin secretion under incubation with glucose, measurements of 3H-leucine incorporation and of the insulin content) were also studied. In contrast to the in vivo results, insulin release of the isolated islets of type II diabetics was normal. From this it must be concluded that the glucoreceptor of the beta cell, which in vivo reacts in a qualitatively different manner from that of subjects with intact metabolism, is not irreversibly disturbed.(ABSTRACT TRUNCATED AT 250 WORDS)

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