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Publications (4)19.79 Total impact

  • Article: Insulin sensitivity in late gestation and early postpartum period: the role of circulating maternal adipokines.
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    ABSTRACT: Early postpartum period is characterised by a dramatic decrease in insulin resistance and significant metabolic alterations. The aims of this study were to determine the changes in circulating maternal concentrations of total adiponectin, adiponectin multimers, leptin and resistin before and after the delivery and to explore their relationship with insulin sensitivity. Twenty-seven normal pregnant women at term were included in this longitudinal study. Blood samples were taken before and 4 days after elective caesarean section. Total adiponectin, adiponectin multimers, leptin, resistin, glucose, insulin and prolactin were measured in maternal serum. Adiponectin multimers were measured before and after the delivery in eight women. (1) The mean maternal serum total adiponectin concentration was significantly higher before than after delivery while the relative distribution of circulating maternal adiponectin multimers did not change after delivery; (2) the median maternal serum concentration of leptin was significantly higher in the antepartum than in the postpartum period; (3) the median maternal serum resistin concentration was comparable before and after delivery; (4) multiple linear regression analysis revealed that antepartum insulin sensitivity was associated with maternal low body mass index, and low glucose concentrations in glucose challenge test, as well as with maternal age and increased leptin concentrations. Postpartum insulin sensitivity was associated with decreased circulating resistin concentrations. Despite increase in insulin sensitivity, early postpartum period is characterised by a decrease in maternal circulating total adiponectin and by steady concentrations of resistin and adiponectin multimers compared to the late third trimester.
    Gynecological Endocrinology 06/2011; 27(9):725-31. · 1.58 Impact Factor
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    Article: Differential expression of novel adiponectin receptor-1 transcripts in skeletal muscle of subjects with normal glucose tolerance and type 2 diabetes.
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    ABSTRACT: Adiponectin receptor-1 (AdipoR1) expression in skeletal muscle has been suggested to play an important role in insulin resistance and diabetes. We aimed at evaluating the presence of novel AdiopR1 splice variants in human muscle and their regulation under physiological and pathophysiological states. AdipoR1 5'UTR mRNA transcripts, predicted from bioinformatics data, were evaluated in fetal and adult human tissues. Expression and function of the identified transcripts were assessed in cultured human skeletal muscle cells and in muscle biopsies obtained from individuals with normal glucose tolerance (NGT) and type 2 diabetes (n = 49). Screening of potential AdipoR1 5'UTR splice variants revealed a novel highly abundant muscle transcript (R1T3) in addition to the previously described transcript (R1T1). Unlike R1T1, R1T3 expression was significantly increased during fetal development and myogenesis, paralleled with increased AdipoR1 protein expression. The 5'UTR of R1T3 was found to contain upstream open reading frames that repress translation of downstream coding sequences. Conversely, AdipoR1 3'UTR was associated with enhanced translation efficiency during myoblast-myotube differentiation. A marked reduction in muscle expression of R1T3, R1T1, and R1T3-to-R1T1 ratio was observed in individuals with type 2 diabetes compared with expression levels of NGT subjects, paralleled with decreased expression of the differentiation marker myogenin. Among NGT subjects, R1T3 expression was positively correlated with insulin sensitivity. These results indicate that AdipoR1 receptor expression in human skeletal muscle is subjected to posttranscriptional regulation, including alternative splicing and translational control. These mechanisms play an important role during myogenesis and may be important for whole-body insulin sensitivity.
    Diabetes 02/2011; 60(3):936-46. · 8.29 Impact Factor
  • Article: Total and high molecular weight adiponectin are elevated in patients with Laron syndrome despite marked obesity.
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    ABSTRACT: Patients with Laron syndrome (LS; primary GH insensitivity) caused by molecular defects of the GH receptor gene, are characterized by dwarfism, profound obesity, and hyperlipidemia. The aim of the current study was to evaluate adiponectin levels in LS, as obesity is known to be associated with low adiponectin. We studied nine untreated LS adult patients (5 males, 4 females) and six girls with LS receiving once-daily treatment by IGF1. Total and high molecular weight (HMW) adiponectin levels, adiponectin multimers distribution, and metabolic indices were analyzed in serum samples obtained during several years of follow-up. Adiponectin levels in the severely obese adult LS patients (percent body fat; females 61.0+/-2.5%, males 40.6+/-8.1%) were two- to three-fold higher than those reported for subjects of corresponding age, gender and degree of adiposity. Total adiponectin was significantly higher in females compared with males (21.4+/-3.5 vs 10.2+/-4.6 microg/ml, P<0.001). The elevated adiponectin in LS subjects was associated with an increased abundance of the HMW isoform, and positively correlated with body fat percentage (r=0.65, P=0.017) and leptin (r=0.65, P=0.012). There was no correlation between adiponectin levels (total and HMW) and the degree of insulin resistance in LS subjects or their blood lipids levels. Adiponectin was also high in young girls with LS (22.9+/-7.4 microg/ml) and did not change during long-term IGF1 replacement therapy. Adiponectin hypersecretion in LS, despite profound obesity, suggests that GH activity may negatively impact adiponectin secretion from adipocytes.
    European Journal of Endocrinology 09/2009; 161(6):837-44. · 3.42 Impact Factor
  • Article: Modulation of adiponectin and leptin during refeeding of female anorexia nervosa patients.
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    ABSTRACT: Several studies assessed adiponectin levels in anorexia nervosa (AN) patients, however, data regarding the dynamics of changes in adiponectin levels during refeeding of these patients is limited and contradicting. Our objective was to assess adiponectin levels and the distribution of its different isoforms in AN patients before and after long-term refeeding, and to relate them to alterations in body mass index, leptin, insulin sensitivity, and additional endocrine parameters. We conducted a longitudinal controlled study of 38 female adolescent malnourished AN inpatients, with 13 young, lean, healthy women serving as controls. Blood samples were obtained upon admission and thereafter at 1, 3, and 5 months (at target weight). Changes in body mass index, leptin, adiponectin, insulin sensitivity, and adiponectin multimeric forms were measured. At admission, leptin levels of AN patients were significantly lower, whereas insulin sensitivity (assessed by homeostasis model assessment-insulin resistance), adiponectin levels, and the ratio of high molecular weight (HMW) adiponectin to total adiponectin were significantly higher compared with controls. During weight recovery, leptin levels and homeostasis model assessment-insulin resistance increased significantly, whereas adiponectin and HMW adiponectin/total adiponectin ratio decreased significantly, to levels similar to controls. An initial increase in adiponectin levels was observed after 1 month of refeeding. There was no correlation between adiponectin and either T(4) or cortisol levels. Our study demonstrates hyperadiponectinemia, increased adiponectin HMW isoform, and increased insulin sensitivity in adolescent AN female patients and reversal of these findings with weight rehabilitation. We hypothesize that increased adiponectin levels may have a protective role in maintaining energy homeostasis during extreme malnourishment.
    Journal of Clinical Endocrinology &amp Metabolism 06/2007; 92(5):1843-7. · 6.50 Impact Factor