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Adipokines in type 1 diabetes after successful pancreas transplantation: normal visfatin and retinol-binding-protein-4, but increased total adiponectin fasting concentrations

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Summary 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.
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Document Type: Research Article

Affiliations: 1: Medical University Vienna, Department of Clinical Pharmacology, Vienna, Austria 2: Karl Landsteiner Institute of Metabolic Diseases and Nephrology, Vienna, Austria 3: Medical University Vienna, Division of Endocrinology and Metabolism, Department of Internal Medicine 3, Vienna, Austria 4: Metabolic Unit, Institute of Biomedical Engineering, ISIB-CNR, Padua, Italy

Publication date: June 1, 2010

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