Search Results
You are looking at 1 - 4 of 4 items for :
- Abstract: Adrenal x
- Abstract: Addisons x
- Abstract: Adrenaline x
- Abstract: Androgens x
- Abstract: Catecholamines x
- Abstract: hyperplasia x
- Abstract: Cushings x
- Abstract: Glucocorticoids x
- Abstract: Medulla x
- Abstract: Noradrenaline x
- Metabolic Syndrome and Diabetes x
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Pernille H Hellmann in
Google Scholar
PubMed
Clinical Research, Steno Diabetes Center Copenhagen, Herlev, Denmark
Search for other papers by Jonatan I Bagger in
Google Scholar
PubMed
Search for other papers by Katrine R Carlander in
Google Scholar
PubMed
Search for other papers by Katrine B Hansen in
Google Scholar
PubMed
Search for other papers by Julie L Forman in
Google Scholar
PubMed
Search for other papers by Joachim Størling in
Google Scholar
PubMed
Search for other papers by Elizaveta Chabanova in
Google Scholar
PubMed
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Jens Holst in
Google Scholar
PubMed
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Clinical Research, Steno Diabetes Center Copenhagen, Herlev, Denmark
Search for other papers by Tina Vilsbøll in
Google Scholar
PubMed
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Clinical Research, Steno Diabetes Center Copenhagen, Herlev, Denmark
Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Search for other papers by Filip K Knop in
Google Scholar
PubMed
Objectives
Preclinically, curcumin has been shown to protect against glucocorticoid-induced insulin resistance. We evaluated the effect of curcumin administered with prednisolone in healthy overweight or obese men.
Methods
In a double-blind, parallel-group trial, 24 overweight/obese non-diabetic men were randomised to one of three intervention groups (A) prednisolone placebo+curcumin placebo, (B) prednisolone (50 mg/day)+curcumin placebo or (C) prednisolone and curcumin (400 mg/day). Curcumin or curcumin placebo treatment started 1 day prior to 10-day prednisolone or prednisolone placebo treatment. The primary endpoint was change in prednisolone-induced insulin resistance assessed by homeostatic model assessment of insulin resistance (HOMA2-IR). Other endpoints included anthropometric measurements, magnetic resonance spectroscopy-assessed hepatic fat content, blood pressure, circulating metabolic markers and continuous glucose monitoring measures.
Results
Baseline characteristics (mean ± s.d): age 44.2 ± 13.7 years, BMI 30.1 ± 3.5 kg/m2, HbAlc 33.3 ± 3.2 mmol/mol, HOMA2-IR 1.10 ± 0.45 and fasting plasma glucose 5.2 ± 0.4 mmol/L. Prednisolone significantly increased HOMA2-IR (estimated treatment difference 0.36 (95% CI 0.16; 0.57)). Co-treatment with curcumin had no effect on HOMA2-IR (estimated treatment difference 0.08 (95% CI −0.13; 0.39)). Prednisolone increased HbAlc, insulin, C-peptide, glucagon, blood pressure, mean interstitial glucose, time spent in hyperglycaemia and glucose variability, but no protective effect of curcumin on any of these measures was observed.
Conclusions
In this double-blind, placebo-controlled parallel-group study involving 24 overweight or obese men randomised to one of three treatment arms, curcumin treatment had no protective effect on prednisolone-induced insulin resistance or other glucometabolic perturbations.
Search for other papers by Yi Jia in
Google Scholar
PubMed
Search for other papers by Yanan Yang in
Google Scholar
PubMed
Search for other papers by Jing Qu in
Google Scholar
PubMed
Search for other papers by Lijun Yin in
Google Scholar
PubMed
Search for other papers by Xiaohui Wang in
Google Scholar
PubMed
Adipokine chemerin plays important roles in disorders of glucose and lipid metabolism of obesity and obesity-related diseases, and exercise-induced improvement of glucose and lipid metabolism is closely related to the decrease of chemerin, but the mechanisms by which chemerin regulates glucose and lipid metabolism remain unclarified. Hypotestosterone induces male obesity and disorders of glucose and lipid metabolism through androgen receptor (AR) and its target genes: glucose and lipid metabolism-related molecules (including FOXO1, PEPCK, PGC-1α, and SCD1). Recently, the link between them has been reported that chemerin modulated the secretion of androgen. In this study, global chemerin knockout (chemerin (−/−)) mice were established to demonstrate the roles of chemerin in regulating blood glucose and blood lipid of mice under diet (high-fat (HFD) and normal diet) and exercise interventions and then to explore its mechanisms (AR – glucose and lipid metabolism enzymes). We found that the blood lipid and adipocyte size were low accompanied by the improvements in the levels of serum testosterone, gastrocnemius AR, and gastrocnemius FOXO1, SCD1, and PGC-1α in HFD chemerin (−/−) mice, but exercise-induced improvements of these indicators in HFD WT mice were attenuated or abolished in HFD chemerin (−/−) mice. In conclusion, the decrease of chemerin improved the blood lipid profile of HFD male mice at sedentary and exercise states, mediated partly by the increases of testosterone and AR to regulate glucose and lipid metabolism enzymes. To our knowledge, it is the first report that chemerin’s regulation of glucose and lipid metabolism might be mediated by testosterone and AR in vivo.
Search for other papers by Sarantis Livadas in
Google Scholar
PubMed
Search for other papers by Christina Bothou in
Google Scholar
PubMed
Search for other papers by Justyna Kuliczkowska-Płaksej in
Google Scholar
PubMed
Search for other papers by Ralitsa Robeva in
Google Scholar
PubMed
Search for other papers by Andromahi Vryonidou in
Google Scholar
PubMed
Search for other papers by Jelica Bjekic Macut in
Google Scholar
PubMed
Search for other papers by Ioannis Androulakis in
Google Scholar
PubMed
Search for other papers by Milica Opalic in
Google Scholar
PubMed
Search for other papers by Zadalla Mouslech in
Google Scholar
PubMed
Search for other papers by Andrej Milewicz in
Google Scholar
PubMed
Search for other papers by Alessandra Gambineri in
Google Scholar
PubMed
Search for other papers by Dimitrios Panidis in
Google Scholar
PubMed
Search for other papers by Djuro Macut in
Google Scholar
PubMed
Background
Polycystic ovary syndrome (PCOS) is considered a risk factor for the development of type 2 diabetes mellitus (T2DM). However, which is the most appropriate way to evaluate dysglycemia in women with PCOS and who are at increased risk are as yet unclear.
Aim of the study
To determine the prevalence of T2DM, impaired glucose tolerance (IGT), and impaired fasting glucose (IFG) in PCOS women and potential factors to identify those at risk.
Subjects and methods
The oral glucose tolerance test (OGTT), biochemical/hormonal profile, and ovarian ultrasound data from 1614 Caucasian women with PCOS and 362 controls were analyzed in this cross-sectional multicenter study. The data were categorized according to age and BMI.
Results
Dysglycemia (T2DM, IGT, and IFG according to World Health Organization criteria) was more frequent in the PCOS group compared to controls: 2.2% vs 0.8%, P = 0.04; 9.5% vs 7.4%, P = 0.038; 14.2% vs 9.1%, P = 0.002, respectively. OGTT was essential for T2DM diagnosis, since in 88% of them basal glucose values were inconclusive for diagnosis. The presence of either T2DM or IFG was irrespective of age (P = 0.54) and BMI (P = 0.32), although the latter was associated with IGT (P = 0.021). There was no impact of age and BMI status on the prevalence of T2DM or IFG. Regression analysis revealed a role for age, BMI, fat deposition, androgens, and insulin resistance for dysglycemia. However, none of the factors prevailed as a useful marker employed in clinical practice.
Conclusions
One-third of our cohort of PCOS women with either T2DM or IGT displayed normal fasting glucose values but without confirming any specific predictor for dysglycemic condition. Hence, the evaluation of glycemic status using OGTT in all women with PCOS is strongly supported.
Search for other papers by Giovanni Fanni in
Google Scholar
PubMed
Search for other papers by Petros Katsogiannos in
Google Scholar
PubMed
Search for other papers by Bipasha Nandi Jui in
Google Scholar
PubMed
Search for other papers by Magnus Sundbom in
Google Scholar
PubMed
Search for other papers by Susanne Hetty in
Google Scholar
PubMed
Search for other papers by Maria J Pereira in
Google Scholar
PubMed
Search for other papers by Jan W Eriksson in
Google Scholar
PubMed
Purpose
In patients with type 2 diabetes mellitus (T2DM), Roux-en-Y gastric bypass (RYGB) leads to beneficial metabolic adaptations, including enhanced incretin secretion, beta-cell function, and systemic insulin sensitivity. We explored the impact of RYGB on pituitary, pancreatic, gut hormones, and cortisol responses to parenteral and enteral nutrient stimulation in patients with obesity and T2DM with repeated sampling up to 2 years after intervention.
Methods
We performed exploratory post hoc analyses in a previously reported randomized trial. Levels of adrenocorticotropic hormone (ACTH), cortisol, growth hormone (GH), glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic peptide (GIP), peptide YY (PYY), ACTH, insulin, and glucagon were measured in 13 patients with T2DM and obesity at four different visits: before and 4, 24, and 104 weeks after RYGB; and in three sequential conditions on the same day: fasting, intravenous arginine challenge, and OGTT.
Results
RYGB surprisingly induced a rise in ACTH, cortisol, and GH levels upon an oral glucose load, together with enhanced GLP-1 and PYY responses. Fasting and post-arginine GH levels were higher after RYGB, whereas insulin, glucagon, GLP-1, GIP, and cortisol were lower. These endocrine adaptations were seen as early as 4 weeks after surgery and were maintained for up to 2 years.
Conclusion
These findings indicate adaptations of glucose sensing mechanisms and responses in multiple endocrine organs after RYGB, involving the gut, pancreatic islets, the pituitary gland, the adrenals, and the brain.
