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Stadler M.,Hietzing Hospital | Stadler M.,Karl Landsteiner Institute of Metabolic Diseases and Nephrology | Stadler M.,King's College London | Tomann L.,Karl Landsteiner Institute of Metabolic Diseases and Nephrology | And 11 more authors.
European Journal of Endocrinology | Year: 2014

Abstract Objective: To stop smoking is commonly associated with significant weight gain, but the mechanisms for this are poorly understood. We assessed the effects of smoking cessation on body weight, insulin sensitivity, b-cell function, and appetite. Subjects and methods: Twenty-seven long-term smokers (nZ27; nine females/18 males, 28G1 years, 22.9G0.6 kg/m2) attending an ambulatory smoking cessation program in a community hospital in Vienna, Austria were examined at baseline (Visit A; still smoking) and after a minimum of 3 months of smoking abstinence (Visit B; nZ14); relapsed smokers were not followed up. Participants underwent 3-h oral glucose tolerance tests and body composition measurements at each study visit. Fasting (QUICKI) and dynamic (oral glucose insulin sensitivity (OGIS)) insulin sensitivity and b-cell secretion (insulinogenic index 140 (IGI40)) were calculated. Food intake was quantified with a free choice buffet. Fasting plasma concentrations of neuropeptide-Y (NPY), peptide-YY (PYY), glucagon-like peptide 1 (GLP1), leptin, ghrelin, and visfatin were measured. Results: After O3 months' smoking abstinence, body weight, and fat mass were increased (C4 and C22% respectively, P!0.05) and fasting insulin sensitivity deteriorated (QUICKI: post, 0.37G0.02 vs baseline, 0.41G0.2; P!0.05), while OGIS remained unchanged throughout. IGI40 increased by 31% after O3 months' smoking abstinence (P!0.01). Carbohydrate ingestion increased after stopping smoking (P!0.05). NPY fasting levels were increased after O3 months (P!0.05), PYY, GLP1, leptin, ghrelin, and visfatin were unchanged. Conclusion: Smoking cessation is associated with transient metabolic changes including increased b-cell secretion in response to glucose and fasting insulin resistance. These alterations may be associated with or contribute to the body weight gain after smoking cessation. © 2014 European Society of Endocrinology Printed in Great Britain.


Anderwald C.-H.,CNR Institute of Biomedical Engineering | Anderwald C.-H.,Medical University of Vienna | Anderwald C.-H.,Community Pharmacy | Anderwald C.-H.,Specialized Hospital Complex Agathenhof | And 13 more authors.
Diabetes Care | Year: 2012

OBJECTIVE - Obesity leads to severe long-term complications and reduced life expectancy. Roux-en-Y gastric bypass (RYGB) surgery induces excessive and continuous weight loss in (morbid) obesity, although it causes several abnormal anatomical and physiological conditions. RESEARCH DESIGN AND METHODS - To distinctively unveil effects of RYGB surgery on b-cell function and glucose turnover in skeletal muscle, liver, and gut, nondiabetic, morbidly obese patients were studied before (pre-OP, five female/one male, BMI: 49 ± 3 kg/m2, 43 ± 2 years of age) and 7 ± 1 months after (post-OP, BMI: 37 ± 3 kg/m2) RYGB surgery, compared with matching obese (CONob, five female/one male, BMI: 34 ± 1 kg/m2, 48 ± 3 years of age) and lean controls (CON lean, five female/one male, BMI: 22 ± 0 kg/m2, 42 ± 2 years of age). Oral glucose tolerance tests (OGTTs), hyperinsulinemic-isoglycemic clamp tests, and mechanistic mathematical modeling allowed determination of whole-body insulin sensitivity (M/I), OGTT and clamp test β-cell function, and gastrointestinal glucose absorption. RESULTS - Post-OP lost (P < 0.0001) 35 ± 3 kg body weight. M/I increased after RYGB, becoming comparable to CONob, but remaining markedly lower than CONlean (P < 0.05). M/I tightly correlated (τ = 20.611, P < 0.0001) with fat mass. During OGTT, post-OP showed ≥15%reduced plasma glucose from120 to 180 min (≤4.5mmol/L), and 29-fold elevated active glucagon-like peptide-1 (GLP-1) dynamic areas under the curve, which tightly correlated (r = 0.837, P < 0.001) with 84% increased β-cell secretion. Insulinogenic index (0-30 min) in post-OP was ≥29% greater (P < 0.04). At fasting, post-OP showed approximately halved insulin secretion (P < 0.05 vs. pre-OP). Insulin-stimulated insulin secretion in post-OP was 52%higher than before surgery, but 1-2 pmol/min2 lower than in CON ob/CONlean (P < 0.05). Gastrointestinal glucose absorption was comparable in pre-OP and post-OP, but 9-26%lower from 40 to 90 min in post-OP than in CONob/CONlean (P < 0.04). CONCLUSIONS - RYGB surgery leads to decreased plasma glucose concentrations in the third OGTT hour and exaggerated β-cell function, for which increased GLP-1 release seems responsible, whereas gastrointestinal glucose absorption remains unchanged but lower than in matching controls. © 2012 by the American Diabetes Association.


Stadler M.,Hietzing Hospital | Stadler M.,Karl Landsteiner Institute of Metabolic Diseases and Nephrology | Stadler M.,Medical University of Vienna | Storka A.,Medical University of Vienna | And 11 more authors.
Clinical Endocrinology | Year: 2010

Objective: In type 1 diabetes mellitus (T1DM), the release of many hormones, not only from beta-cells, but also from adipocytes (adipokines) may be altered. After successful pancreas-kidney-transplantation (PKTx), T1DM patients can revert to a nondiabetic metabolism, but it is unclear whether alterations of adipokines are still present after PKTx. Design, patients and measurements Concentrations of adipokines [visfatin, retinol-binding protein-4 (RBP-4), adiponectin, high molecular weight (HMW) adiponectin] were measured at fasting in 10 PKTx and in 19 T1DM. Nondiabetic healthy controls (CON, n = 9) and six nondiabetic patients after kidney transplantation (KTx) were examined as control groups. In PKTx, KTx and CON, indices of insulin sensitivity (OGIS) and beta cell function (adaptation index, AI) were calculated from 75 g oral glucose tolerance test (OGTT) data. Results Fasting serum visfatin (T1DM: 56 ± 4 μg/l, PKTx: 42 ± 6 μg/l, KTx: 39 ± 3 μg/l, CON: 40 ± 3 μg/l) and RBP-4 (T1DM: 490 ± 26 μg/l, PKTx: 346 ± 39 μg/l, KTx: 401 ± 13 μg/l, CON: 359 ± 36 μg/l) was increased by 40% and 36%, respectively (each P < 0·03) in T1DM only. Levels were positively correlated with HbA1c in all subjects (visfatin: r = 0·43, P < 0·004; RBP-4: r = 0·46, P < 0·03). Fasting plasma adiponectin was 80% higher in T1DM and in PKTx (T1DM: 18 ± 2 mg/l, PKTx: 18 ± 3 mg/l, KTx: 12 ± 3 mg/l, CON: 10 ± 1 mg/l; P < 0·04) and was positively correlated with diabetes duration (r = 0·37, P < 0·02). HMW/total adiponectin ratio was increased in T1DM (P < 0·02). PKTx displayed a normoglycaemic metabolism as insulin sensitive as CON, but AI was lower than in CON and KT (P < 0·01). Conclusions T1DM after successful PKTx show normal fasting visfatin and RBP-4 levels and HMW-adiponectin/adiponectin-ratio, which are elevated in T1DM, whereas total adiponectin levels are similarly increased in T1DM and PKTx patients. © 2010 Blackwell Publishing Ltd.


Stadler M.,Hietzing Hospital | Stadler M.,Karl Landsteiner Institute of Metabolic Diseases and Nephrology | Stadler M.,Queen Mary, University of London | Krssak M.,Medical University of Vienna | And 17 more authors.
Clinical Endocrinology | Year: 2014

Background In patients with type 1 diabetes mellitus (T1DM), insulin is usually replaced systemically (subcutaneously) and not via the physiological portal route. According to previous studies, the liver's capacity to store glycogen is reduced in T1DM patients, but it remains unclear whether this is due to hyperglycaemia, or whether the route of insulin supply could contribute to this phenomenon. T1DM patients after successful pancreas-kidney transplantation with systemic venous drainage (T1DM-PKT) represent a suitable human model to further investigate this question, because they are normoglycaemic, but their liver receives insulin from the pancreas transplant via the systemic route. Materials and methods In nine T1DM-PKT, nine controls without diabetes (CON) and seven patients with T1DM (T1DM), liver glycogen content was measured at fasting and after two standardized meals employing 13C-nuclear-magnetic- resonance-spectroscopy. Circulating glucose and glucoregulatory hormones were measured repeatedly throughout the study day. Results The mean and fasting concentrations of peripheral plasma glucose, insulin, glucagon and C-peptide were comparable between T1DM-PKT and CON, whereas T1DM were hyperglycaemic and hyperinsulinaemic (P < 0·05 vs T1DM-PKT and CON). Total liver glycogen content at fasting and after breakfast did not differ in the three groups. After lunch, T1DM-PKT and T1DM had a 14% and 21% lower total liver glycogen content than CON (P < 0·02). Conclusion In spite of normalized glycaemic control, postprandial liver glycogen content was reduced in T1DM-PKT with systemic venous drainage. Thus, not even optimized systemic insulin substitution is able to resolve the defect in postprandial liver glycogen storage seen in T1DM patients. © 2013 John Wiley & Sons Ltd.


Stadler M.,Hietzing Hospital | Stadler M.,Karl Landsteiner Institute of Metabolic Diseases and Nephrology | Anderwald C.,Medical University of Vienna | Pacini G.,National Research Council Italy | And 10 more authors.
Diabetes | Year: 2010

OBJECTIVE - So far it is unclear whether chronic peripheral hyperinsulinemia per se might contribute to ectopic lipid accumulation and consequently insulin resistance. We investigated the effects of systemic instead of portal insulin release in type 1 diabetic patients after successful pancreas-kidney transplantation (PKT) with systemic venous drainage on the intracellular lipid content in liver and soleus muscle, endogenous glucose production (EGP), and insulin sensitivity. RESEARCH DESIGN AND METHODS - In nine PKT patients and nine matching nondiabetic control subjects, intrahepatocellular lipids (IHCLs) and intramyocellular lipids (IMCLs) were measured using 1H nuclear magnetic resonance spectroscopy. Fasting EGP was measured using D-[6,6-2H2]glucose tracer dilution. A 3-h 75-g oral glucose tolerance test (OGTT) allowed us to assess kinetics of glucose, free fatty acids, insulin, and C-peptide concentrations in plasma and to calculate the clamp-like index (CLIX) for insulin sensitivity and the hepatic insulin resistance (HIR) index. RESULTS - The PKT patients displayed approximately twofold increased fasting insulin (20 ± 6 vs. 9 ± 3 μU/ml; P < 0.0002) compared with that in nondiabetic control subjects and ∼10% increased fasting glucose (P < 0.02) concentrations, but during the OGTT areas under the concentration curves of C-peptide and insulin were similar. IHCL (PKT, 2.9 ± 2.5%; nondiabetic control subjects, 4.4 ± 6.6%), IMCL (PKT, 1.0 ± 0.4%; nondiabetic control subjects, 1.0 ± 0.5%), CLIX (PKT, 8 ± 2; nondiabetic control subjects, 7 ± 3), HIR (PKT, 25.6 ± 13.2; nondiabetic control subjects, 35.6 ± 20 [mg · min-1 · kg-1] x [μU/ml]), and EGP (PKT, 1.6 ± 0.2; nondiabetic control subjects, 1.7 ± 0.2 mg · min-1 · kg-1) were comparable between PKT patients and nondiabetic control subjects. IHCL was negatively correlated with CLIX in all participants (r = -0.55; P < 0.04). CONCLUSIONS - Despite fasting peripheral hyperinsulinemia because of systemic venous drainage, type 1 diabetic patients after PKT show similar IHCL, IMCL, insulin sensitivity, and fasting EGP in comparison with nondiabetic control subjects. These results suggest that systemic hyperinsulinemia per se does not cause ectopic lipid accumulation in liver and skeletal muscle. © 2010 by the American Diabetes Association.

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