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CLINICAL STUDY |
H Leth, Medical Research Laboratories, Clinical Institute, Aarhus University Hospital, Aarhus C, Denmark
J Kroustrup, Department of Endocrinology, Aalborg Sygehus, Aarhus University Hospital, Aalborg, Denmark
J Larsen, Department of Gastric Surgery, Aalborg Sygehus, Aarhus University Hospital, Aalborg, United Kingdom
K Andersen, Aarhus, United Kingdom
A Flyvbjerg, Medical Research Laboratories, Clinical Institute, Aarhus University Hospital, Aarhus C, Denmark
J Frystyk, Medical Research Laboratories, Clinical Institute, Aarhus University Hospital, Aarhus C, Denmark
Correspondence: Jan Frystyk, Email: jan{at}frystyk.dk
Abstract
Background: Adiponectin circulates in the three major subforms: high-molecular-weight (HMW)-, middle-molecular-weight (MMW)- and low-molecular-weight (LMW)-adiponectin, of which HMW-adiponectin appears to be the primary active form. There is consensus that serum total adiponectin is inversely related to body weight and increases following weight loss. However, the impact of weight loss on the molecular distribution of adiponectin is less settled.
Objective: To investigate the molecular distribution of adiponectin in serum from severely obese individuals before and after gastric banding (GB), and compare those with HOMA values and meal-stimulated glucose and insulin levels.
Design: Twenty-three (12 women) severely obese individuals were studied before and 6.6±0.2 months after GB, reducing their BMI from 59.3±1.8 to 52.7±1.6 kg/m2. HMW-, MMW- and LMW-adiponectin were measured after FPLC-separation using a validated immunoassay.
Results: Serum total adiponectin increased significantly after GB (from 6.06±0.35 to 6.53±0.40 mg/l; P<0.05), primarily caused by an increase in HMW-adiponectin (from 2.39±0.21 to 2.87±0.27 mg/l; P<0.001). LMW-adiponectin increased slightly (from 0.79±0.03 to 0.89±0.05 mg/l; P<0.01), while MMW-adiponectin remained unchanged (2.88±0.13 vs. 2.76±0.12 mg/l; P=NS). The relative distribution of the adiponectin subforms changed as the HMW-fraction (HMW-adiponectin/total adiponectin) increased (P<0.001) and the MMW-fraction decreased (P<0.001). However, changes in adiponectin correlated neither with the weight reduction nor with changes in metabolic parameters.
Conclusion: This study demonstrates that the HMW-subform is up-regulated after weight loss, indicating that the three major subforms of adiponectin are regulated differently. The lack of correlation between serum adiponectin and improvements in insulin sensitivity may be related to the severe degree of obesity.
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