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      Association of ADRB1 and UCP3 Gene Polymorphisms with Insulin Sensitivity but Not Obesity

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          Background: The uncoupling proteins (UCPs) and β-adrenoceptors (ADRBs) are important for energy balance and may be involved in the pathogenesis of insulin resistance. Obesity is strongly hunted by insulin resistance and susceptibility genes for the two conditions could be separate or common. Variations within the UCPs and ADRBs genes may give important clues to their involvement in disease. Methods: A total of four single nucleotide polymorphisms (SNPs) in the genes UCP1, UCP2, UCP3, and ADRB1 were examined for association with obesity and insulin sensitivity (HOMA<sub>IR</sub>) in obese (n = 292) and healthy non-obese (n = 481) females. Results: None of the SNPs was associated with obesity status or body mass index. However, ADRB1 (rs1801253) was nominally associated with serum insulin (nominal p = 0.034) and HOMA<sub>IR</sub> (nominal p = 0.022). UCP3 (rs1800006) was in post-hoc analysis nominally associated with serum insulin and HOMA<sub>IR</sub> (nominal p = 0.013 and 0.048, respectively). UCP1 and UCP2 showed no association with insulin sensitivity. Conclusion: Polymorphisms in ADRB1 and UCP3 may contribute to insulin resistance rather than obesity among Swedish women.

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          Most cited references 20

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          Mice lacking mitochondrial uncoupling protein are cold-sensitive but not obese.

          The mitochondrial uncoupling protein (UCP) in the mitochondrial inner membrane of mammalian brown adipose tissue generates heat by uncoupling oxidative phosphorylation. This process protects against cold and regulates energy balance. Manipulation of thermogenesis could be an effective strategy against obesity. Here we determine the role of UCP in the regulation of body mass by targeted inactivation of the gene encoding it. We find that UCP-deficient mice consume less oxygen after treatment with a beta3-adrenergic-receptor agonist and that they are sensitive to cold, indicating that their thermoregulation is defective. However, this deficiency caused neither hyperphagia nor obesity in mice fed on either a standard or a high-fat diet. We propose that the loss of UCP may be compensated by UCP2, a newly discovered homologue of UCP; this gene is ubiquitously expressed and is induced in the brown fat of UCP-deficient mice.
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            Disruption of the uncoupling protein-2 gene in mice reveals a role in immunity and reactive oxygen species production.

            The gene Ucp2 is a member of a family of genes found in animals and plants, encoding a protein homologous to the brown fat uncoupling protein Ucp1 (refs 1-3). As Ucp2 is widely expressed in mammalian tissues, uncouples respiration and resides within a region of genetic linkage to obesity, a role in energy dissipation has been proposed. We demonstrate here, however, that mice lacking Ucp2 following targeted gene disruption are not obese and have a normal response to cold exposure or high-fat diet. Expression of Ucp2 is robust in spleen, lung and isolated macrophages, suggesting a role for Ucp2 in immunity or inflammatory responsiveness. We investigated the response to infection with Toxoplasma gondii in Ucp2-/- mice, and found that they are completely resistant to infection, in contrast with the lethality observed in wild-type littermates. Parasitic cysts and inflammation sites in brain were significantly reduced in Ucp2-/- mice (63% decrease, P<0.04). Macrophages from Ucp2-/- mice generated more reactive oxygen species than wild-type mice (80% increase, P<0.001) in response to T. gondii, and had a fivefold greater toxoplasmacidal activity in vitro compared with wild-type mice (P<0.001 ), which was absent in the presence of a quencher of reactive oxygen species (ROS). Our results indicate a role for Ucp2 in the limitation of ROS and macrophage-mediated immunity.
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              Homeostasis model assessment closely mirrors the glucose clamp technique in the assessment of insulin sensitivity: studies in subjects with various degrees of glucose tolerance and insulin sensitivity


                Author and article information

                Horm Res Paediatr
                Hormone Research in Paediatrics
                S. Karger AG
                December 2007
                04 December 2007
                : 69
                : 1
                : 31-36
                aDepartment of Molecular Medicine, National Public Health Institute/Department of Medical Genetics, University of Helsinki, Biomedicum, Helsinki, Finland; bDepartment of Medicine, Huddinge, Karolinska Institutet, Karolinska University Hospital and cDepartment of Bioscience and Nutrition, Karolinska Institutet, Stockholm, Sweden, and dDepartment of Genetics, University of Leicester, Leicester, UK
                111793 Horm Res 2008;69:31–36
                © 2007 S. Karger AG, Basel

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                Page count
                Tables: 4, References: 28, Pages: 6
                Original Paper


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