Background In subcutaneous adipose tissue (SAT), higher stearoyl-CoA desaturase-1 (SCD1) expression has been related to improved insulin sensitivity in thiazolidinedione-treated type 2 diabetes mellitus patients. In animal models, deficiency of the free fatty acid receptor (FFAR) 2 associated with higher and FFAR4-deficiency with lower insulin sensitivity. We hypothesized that increased FFAR2 expression and reductions in FFAR4 and SCD1 expression in SAT of type 2 diabetes mellitus patients associate positively with insulin resistance and impaired beta cell function. Methods Twenty-five type 2 diabetes mellitus patients and 25 glucose-tolerant humans (CON) matched for sex, age, and BMI underwent mixed-meal tests to assess insulin sensitivity (OGIS) and beta cell function (?AUC(C-peptide)0-180 min/ ?AUC(glucose)0-180 min) in a cross-sectional study. Gene and protein expression of SCD1 and FFAR2/4 were quantified in SAT biopsies. Results Insulin sensitivity was 14% and beta cell function 71% (both p < 0.001) lower in type 2 diabetes mellitus patients. In type 2 diabetes mellitus, SCD1 mRNA was fivefold (p < 0.001) and protein expression twofold (p < 0.01) lower. While FFAR2/4 mRNA and protein expression did not differ between groups, FFAR2 protein levels correlated negatively with beta cell function only in CON (r = -0.74, p < 0.01). However, neither SCD1 nor FFAR2/4 protein expression correlated with insulin sensitivity in both groups. Conclusions Type 2 diabetes patients have lower SCD1, which does not associate with insulin resistance. Only in nondiabetic humans, FFAR2 associated with impaired beta cell function.

Reduced expression of stearoyl-CoA desaturase-1, but not free fatty acid receptor 2 or 4 in subcutaneous adipose tissue of patients with newly diagnosed type 2 diabetes mellitus

Tura A;
2018

Abstract

Background In subcutaneous adipose tissue (SAT), higher stearoyl-CoA desaturase-1 (SCD1) expression has been related to improved insulin sensitivity in thiazolidinedione-treated type 2 diabetes mellitus patients. In animal models, deficiency of the free fatty acid receptor (FFAR) 2 associated with higher and FFAR4-deficiency with lower insulin sensitivity. We hypothesized that increased FFAR2 expression and reductions in FFAR4 and SCD1 expression in SAT of type 2 diabetes mellitus patients associate positively with insulin resistance and impaired beta cell function. Methods Twenty-five type 2 diabetes mellitus patients and 25 glucose-tolerant humans (CON) matched for sex, age, and BMI underwent mixed-meal tests to assess insulin sensitivity (OGIS) and beta cell function (?AUC(C-peptide)0-180 min/ ?AUC(glucose)0-180 min) in a cross-sectional study. Gene and protein expression of SCD1 and FFAR2/4 were quantified in SAT biopsies. Results Insulin sensitivity was 14% and beta cell function 71% (both p < 0.001) lower in type 2 diabetes mellitus patients. In type 2 diabetes mellitus, SCD1 mRNA was fivefold (p < 0.001) and protein expression twofold (p < 0.01) lower. While FFAR2/4 mRNA and protein expression did not differ between groups, FFAR2 protein levels correlated negatively with beta cell function only in CON (r = -0.74, p < 0.01). However, neither SCD1 nor FFAR2/4 protein expression correlated with insulin sensitivity in both groups. Conclusions Type 2 diabetes patients have lower SCD1, which does not associate with insulin resistance. Only in nondiabetic humans, FFAR2 associated with impaired beta cell function.
2018
Istituto di Neuroscienze - IN -
Inglese
8
1
9
https://www.ncbi.nlm.nih.gov/pubmed/30190473
Sì, ma tipo non specificato
Receptors
G-Protein-Coupled
Fatty Acids
Nonesterified
glucose-stimulated insulin
This work was supported by the Ministry of Culture and Science of the State of North Rhine-Westphalia (MIWF NRW) and the German Federal Ministry of Health (BMG). This study was supported in part by a grant of the Federal Ministry for Research (BMBF) to the German Center for Diabetes Research (DZD e.V.).
14
info:eu-repo/semantics/article
262
Bodis, K; Kahl, S; Simon, Mc; Zhou, Z; Sell, H; Knebel, B; Tura, A; Strassburger, K; Burkart, V; Mussig, K; Markgraf, D; Alhasani, H; Szendroedi, J; R...espandi
01 Contributo su Rivista::01.01 Articolo in rivista
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.14243/359811
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