학술논문

Dysregulated growth hormone‐insulin‐like growth factor‐1 axis in adult type 1 diabetes with long duration.
Document Type
Article
Source
Clinical Endocrinology. Oct2018, Vol. 89 Issue 4, p424-430. 7p. 3 Charts, 3 Graphs.
Subject
*SOMATOTROPIN
*INSULIN
*TYPE 1 diabetes
*UPPER extremity deep vein thrombosis
*BLOOD sampling
Language
ISSN
0300-0664
Abstract
Summary: Context: In type 1 diabetes (T1D), dysregulation of the GH‐IGF‐1 axis has been reported. Whether this is related to upper extremity impairments (UEI) is unknown. Objective: Examine differences in GH‐IGF‐1 axis between T1D on subcutaneous insulin treatment and matched controls without diabetes and possible associations between GH‐IGF‐1 axis and UEI. Design: Cross‐sectional population‐based study. Patients with T1D, onset <35 years, duration ≥ 20 years, <67 years old and controls were invited to answer questionnaires and take blood samples. Subjects: A total of 605 patients with T1D and 533 controls accepted to participate. Outcomes: Fasting levels of IGF‐1, IGF‐1 Z‐score, IGFBP‐1, IGFBP‐3, C‐peptide, GH and UEI. Results: Patients with T1D had lower IGF‐1 and IGFBP‐3 and higher IGFBP‐1 and GH than controls. The difference in IGF‐1 persisted with age. Insulin dose was associated with increasing IGF‐1 Z‐score but even at a very high insulin dose (>1U/kg) IGF‐1 Z‐score was subnormal compared to controls. IGF‐1 Z‐score was unaffected by glycaemic control (HbA1c) but increased with residual insulin secretion, (C‐peptide 1‐99 pmol/L). IGFBP‐1 was associated with fasting blood glucose, negatively in controls and positively in patients with T1D probably reflecting insulin resistance and insulin deficiency, respectively. There was no association between lower IGF‐1 Z‐score and UEI in T1D. Conclusion: In adult T1D with fair glycaemic control, the GH‐IGF‐1 axis is dysregulated exhibiting GH resistance, low IGF‐1 and elevated IGFBP‐1. Subcutaneous insulin cannot normalize these changes while endogenous insulin secretion has marked effects on IGF‐1 pointing to a role of portal insulin. [ABSTRACT FROM AUTHOR]