Search Results
Search for other papers by Lars Peter Sørensen in
Google Scholar
PubMed
Search for other papers by Tina Parkner in
Google Scholar
PubMed
Search for other papers by Esben Søndergaard in
Google Scholar
PubMed
Search for other papers by Bo Martin Bibby in
Google Scholar
PubMed
Search for other papers by Holger Jon Møller in
Google Scholar
PubMed
Search for other papers by Søren Nielsen in
Google Scholar
PubMed
Monocyte/macrophage-specific soluble CD163 (sCD163) concentration is associated with insulin resistance and increases with deteriorating glycemic control independently of BMI. This led to the proposal of the hypothesis that obesity-associated white adipose tissue inflammation varies between individuals. The objective was to examine the effect of male overweight/obesity and type 2 diabetes mellitus (T2DM) on associations between adiposity parameters and sCD163. A total of 23 overweight/obese non-diabetic men, 16 overweight/obese men with T2DM, and a control group of 20 normal-weight healthy men were included. Body composition and regional body fat distribution were determined by whole-body dual X-ray absorptiometry scan and abdominal computed tomography (CT) scan. Serum sCD163 concentrations were determined by ELISA. Associations between adiposity parameters and sCD163 were investigated using multiple linear regression analysis. In the normal-weight healthy men, there was no significant association between adiposity parameters and sCD163, whereas in the overweight/obese non-diabetic men, measures of general and regional adiposity were positively associated with sCD163. In the overweight/obese men with T2DM, only visceral adipose tissue (VAT) and the ratio of VAT to abdominal subcutaneous adipose tissue (SAT), a measure of relative body fat distribution between VAT and SAT depots, were positively associated with sCD163. In a multivariate analysis, including VAT, upper-body SAT, and lower-body fat, adjusted for BMI and age, VAT remained a significant predictor of sCD163 in the overweight/obese T2DM men, but not in the overweight/obese non-diabetic men. Our results indicate that VAT inflammation is exaggerated in men with T2DM, and that propensity to store excess body fat viscerally is particularly detrimental in men with T2DM.
Search for other papers by Jelena Stankovic in
Google Scholar
PubMed
Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark
Search for other papers by Kurt Kristensen in
Google Scholar
PubMed
Search for other papers by Niels Birkebæk in
Google Scholar
PubMed
Search for other papers by Jens Otto Lunde Jørgensen in
Google Scholar
PubMed
Steno Diabetes Center Aarhus (SDCA), Aarhus University Hospital, Aarhus, Denmark
Search for other papers by Esben Søndergaard in
Google Scholar
PubMed
Background
The diagnosis of the polyuria–polydipsia syndrome is challenging. Copeptin is a robust biomarker of arginine vasopressin (AVP) secretion. Arginine, which stimulates growth hormone (GH), has been shown also to stimulate copeptin secretion via unknown mechanisms.
Aim
The aim was to investigate copeptin levels in response to three different GH stimulation tests in patients suspected of GH deficiency.
Methods
In this cross-sectional study, we measured plasma copeptin levels at baseline and at 60, 105, and 150 min in patients undergoing a stimulation test for growth hormone deficiency with either arginine (n = 16), clonidine (n = 8) or the insulin tolerance test (ITT) (n = 10).
Results
In patients undergoing the arginine test, the mean age was 9 years, and 10 years for clonidine. The ITT was only performed in adult patients (>18 years) with a mean age of 49 years. Copeptin level increased significantly from baseline to 60 min after arginine (P <0.01) and ITT (P < 0.01). By contrast, copeptin level tended to decrease after clonidine stimulation (P = 0.14).
Conclusion
These data support that infusion of arginine increases plasma copeptin levels and reveal a comparable response after an ITT. We hypothesize that the underlying mechanism is abrogation of somatostatin-induced AVP suppression.
Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark
Danish Diabetes Academy, Odense University Hospital, Odense, Denmark
Search for other papers by Katrine M Lauritsen in
Google Scholar
PubMed
Search for other papers by Jens Hohwü Voigt in
Google Scholar
PubMed
Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark
Search for other papers by Steen Bønløkke Pedersen in
Google Scholar
PubMed
Search for other papers by Troels K Hansen in
Google Scholar
PubMed
Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark
Search for other papers by Niels Møller in
Google Scholar
PubMed
Department of Biomedicine, Aarhus University, Aarhus, Denmark
Search for other papers by Niels Jessen in
Google Scholar
PubMed
Search for other papers by Lars C Gormsen in
Google Scholar
PubMed
Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark
Danish Diabetes Academy, Odense University Hospital, Odense, Denmark
Search for other papers by Esben Søndergaard in
Google Scholar
PubMed
SGLT2 inhibition induces an insulin-independent reduction in plasma glucose causing increased lipolysis and subsequent lipid oxidation by energy-consuming tissues. However, it is unknown whether SGLT2 inhibition also affects lipid storage in adipose tissue. Therefore, we aimed to determine the effects of SGLT2 inhibition on lipid storage and lipolysis in adipose tissue. We performed a randomized, double-blinded, placebo-controlled crossover design of 4 weeks of empagliflozin 25 mg and placebo once-daily in 13 individuals with type 2 diabetes treated with metformin. Adipose tissue fatty acid uptake, lipolysis rate and clearance were measured by 11C-palmitate PET/CT. Adipose tissue glucose uptake was measured by 18F-FDG PET/CT. Protein and gene expression of pathways involved in lipid storage and lipolysis were measured in biopsies of abdominal s.c. adipose tissue. Subjects were weight stable, which allowed us to quantify the weight loss-independent effects of SGLT2 inhibition. We found that SGLT2 inhibition did not affect free fatty acids (FFA) uptake in abdominal s.c. adipose tissue but increased FFA uptake in visceral adipose tissue by 27% (P < 0.05). In addition, SGLT2 inhibition reduced GLUT4 protein (P = 0.03) and mRNA content (P = 0.01) in abdominal s.c. adipose tissue but without affecting glucose uptake. In addition, SGLT2 inhibition decreased the expression of genes involved in insulin signaling in adipose tissue. We conclude that SGLT2 inhibition reduces GLUT4 gene and protein expression in abdominal s.c. adipose tissue, which could indicate a rebalancing of substrate utilization away from glucose oxidation and lipid storage capacity through reduced glycerol formation.
