Correlates of Insulin-Stimulated Glucose Disposal in Recent-Onset Type 1 and Type 2 Diabetes.
Journal
The Journal of clinical endocrinology and metabolism
ISSN: 1945-7197
Titre abrégé: J Clin Endocrinol Metab
Pays: United States
ID NLM: 0375362
Informations de publication
Date de publication:
01 06 2019
01 06 2019
Historique:
received:
21
09
2018
accepted:
23
01
2019
pubmed:
29
1
2019
medline:
28
4
2020
entrez:
29
1
2019
Statut:
ppublish
Résumé
Not only type 2 diabetes (T2D), but also type 1 diabetes (T1D), can be associated with insulin resistance, as assessed using insulin-stimulated whole-body glucose disposal (M-value). We hypothesized that different factors would affect the M-value at the onset of T1D and T2D. We examined 132 patients with T1D or T2D matched for sex, age, and body mass index with a known diabetes duration of <12 months. Multivariable linear regression analyses were applied to test the associations between glycemic control, blood lipid levels, adiponectin, and proinflammatory immune mediators and the M-value, obtained from the hyperinsulinemic-euglycemic clamp. Despite comparable age, body mass index, and near-normoglycemic control, the mean M-value was lower in those with T2D than in those with T1D. Patients with T1D had a lower waist/hip ratio and serum triglycerides but higher serum adiponectin than patients with T2D. However, the circulating proinflammatory markers were not different. Even with adjustments for glucose-lowering treatments, the fasting blood glucose correlated negatively with the M-value in both groups. However, gamma-glutamyl transferase-independently of any treatments-correlated negatively only in T2D. In contrast, serum adiponectin correlated positively with the M-values. Fasting glycemia correlated with insulin-stimulated glucose disposal in both diabetes types. However, altered liver and adipose tissue function were associated with insulin-stimulated glucose disposal only in T2D, underpinning the specific differences between these diabetes types.
Identifiants
pubmed: 30689904
pii: 5303356
doi: 10.1210/jc.2018-02057
doi:
Substances chimiques
Blood Glucose
0
Insulin
0
Lipids
0
Glucose
IY9XDZ35W2
Banques de données
ClinicalTrials.gov
['NCT01055093']
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2295-2304Informations de copyright
Copyright © 2019 Endocrine Society.