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Residual insulin secretion is not coupled to a maintained glucagon response to hypoglycaemia in long-term type 1 diabetes.
J Intern Med. 2002 Oct; 252(4):342-51.JI

Abstract

OBJECTIVES

To evaluate the influence of residual beta-cell function on glucagon secretion and glucose counter-regulation following hypoglycaemia in type 1 diabetes.

DESIGN AND SUBJECTS

The hormonal counter-regulatory responses to standardized insulin-induced hypoglycaemia were investigated, 18 patients with type 1 diabetes of long duration and 12 healthy subjects were investigated. Nine of the diabetic patients (diabetes duration 17 +/- 1 years) had residual insulin secretion, as reflected by persistent urinary C-peptide excretion. The other nine diabetic patients (diabetes duration 21 +/- 1 years) were C-peptide negative.

RESULTS

Similar hypoglycaemic nadirs were found in all groups (2.1-2.3 mmol L-1), whereas the recovery of plasma glucose levels was delayed similarly in the diabetic groups. In the control subjects, plasma glucagon increased ( approximately 50%). No significant glucagon response was registered in either of the two diabetic groups. The maximum plasma adrenaline and pancreatic polypeptides (PP) responses to hypoglycaemia were comparable in the two diabetic patient groups; the peak values being lower (P < 0.05) than in the controls. Plasma noradrenaline, growth hormone and cortisol responses to hypoglycaemia were similar in all three groups.

CONCLUSION

Residual beta-cell function in patients with long-term type 1 diabetes is not accompanied by preservation of the glucagon response to hypoglycaemia. As the two markers of autonomic function (adrenaline and PP) were similarly reduced in the two diabetic groups, the findings instead favour the concept that the defective glucagon secretory response to hypoglycaemia is because of autonomic nervous dysfunction.

Authors+Show Affiliations

Department of Medicine M:63, Huddinge University Hospital, Karolinska Institutet, S-141 86 Stockholm, Sweden. stefan.sjoberg@cme.hs.sll.seNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

12366607

Citation

Sjöberg, S, et al. "Residual Insulin Secretion Is Not Coupled to a Maintained Glucagon Response to Hypoglycaemia in Long-term Type 1 Diabetes." Journal of Internal Medicine, vol. 252, no. 4, 2002, pp. 342-51.
Sjöberg S, Ahrén B, Bolinder J. Residual insulin secretion is not coupled to a maintained glucagon response to hypoglycaemia in long-term type 1 diabetes. J Intern Med. 2002;252(4):342-51.
Sjöberg, S., Ahrén, B., & Bolinder, J. (2002). Residual insulin secretion is not coupled to a maintained glucagon response to hypoglycaemia in long-term type 1 diabetes. Journal of Internal Medicine, 252(4), 342-51.
Sjöberg S, Ahrén B, Bolinder J. Residual Insulin Secretion Is Not Coupled to a Maintained Glucagon Response to Hypoglycaemia in Long-term Type 1 Diabetes. J Intern Med. 2002;252(4):342-51. PubMed PMID: 12366607.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Residual insulin secretion is not coupled to a maintained glucagon response to hypoglycaemia in long-term type 1 diabetes. AU - Sjöberg,S, AU - Ahrén,B, AU - Bolinder,J, PY - 2002/10/9/pubmed PY - 2002/11/26/medline PY - 2002/10/9/entrez SP - 342 EP - 51 JF - Journal of internal medicine JO - J Intern Med VL - 252 IS - 4 N2 - OBJECTIVES: To evaluate the influence of residual beta-cell function on glucagon secretion and glucose counter-regulation following hypoglycaemia in type 1 diabetes. DESIGN AND SUBJECTS: The hormonal counter-regulatory responses to standardized insulin-induced hypoglycaemia were investigated, 18 patients with type 1 diabetes of long duration and 12 healthy subjects were investigated. Nine of the diabetic patients (diabetes duration 17 +/- 1 years) had residual insulin secretion, as reflected by persistent urinary C-peptide excretion. The other nine diabetic patients (diabetes duration 21 +/- 1 years) were C-peptide negative. RESULTS: Similar hypoglycaemic nadirs were found in all groups (2.1-2.3 mmol L-1), whereas the recovery of plasma glucose levels was delayed similarly in the diabetic groups. In the control subjects, plasma glucagon increased ( approximately 50%). No significant glucagon response was registered in either of the two diabetic groups. The maximum plasma adrenaline and pancreatic polypeptides (PP) responses to hypoglycaemia were comparable in the two diabetic patient groups; the peak values being lower (P < 0.05) than in the controls. Plasma noradrenaline, growth hormone and cortisol responses to hypoglycaemia were similar in all three groups. CONCLUSION: Residual beta-cell function in patients with long-term type 1 diabetes is not accompanied by preservation of the glucagon response to hypoglycaemia. As the two markers of autonomic function (adrenaline and PP) were similarly reduced in the two diabetic groups, the findings instead favour the concept that the defective glucagon secretory response to hypoglycaemia is because of autonomic nervous dysfunction. SN - 0954-6820 UR - https://www.unboundmedicine.com/medline/citation/12366607/Residual_insulin_secretion_is_not_coupled_to_a_maintained_glucagon_response_to_hypoglycaemia_in_long_term_type_1_diabetes_ DB - PRIME DP - Unbound Medicine ER -