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Serum adiponectin in a population sample of 64-year-old women in relation to glucose tolerance, family history of diabetes, autoimmunity, insulin sensitivity, C-peptide, and inflammation

Behre, Carl Johan, 1968 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberglaboratoriet,Institute of Medicine, Department of Molecular and Clinical Medicine,Wallenberg Laboratory
Brohall, Gerhard, 1952 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberglaboratoriet,Institute of Medicine, Department of Molecular and Clinical Medicine,Wallenberg Laboratory
Hulthe, Johannes, 1970 (författare)
Gothenburg University,Göteborgs universitet,Wallenberglaboratoriet,Wallenberg Laboratory
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Fagerberg, Björn, 1943 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Wallenberglaboratoriet,Institute of Medicine, Department of Molecular and Clinical Medicine,Wallenberg Laboratory
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 (creator_code:org_t)
Elsevier BV, 2006
2006
Engelska.
Ingår i: Metabolism: Clinical and Experimental. - : Elsevier BV. - 0026-0495 .- 1532-8600. ; 55:2, s. 188-94
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • The aim of the study was to describe serum adiponectin levels in a population-based sample of women with different degrees of glucose tolerance and to examine if the variability in serum adiponectin was explained by family history of diabetes, obesity, insulin resistance, glycemia, and inflammation. Repeated oral glucose tolerance tests were used in a screening procedure of a cohort of 64-year-old women to identify those with diabetes mellitus n = 210) and impaired glucose tolerance (n = 201). A random sample of women with normal glucose tolerance (NGT, n = 186) was also included. The examination included history of first-degree relatives with diabetes, anthropometry, measurement of circulating adiponectin, glutamic acid decarboxylase antibodies, blood glucose, HbA1c, insulin, proinsulin, C-peptide, high-sensitivity C-reactive protein, and homeostasis model assessment. Serum adiponectin concentration was lowest among diabetic women, highest in the random-sample NGT group, and intermediate in the impaired glucose tolerance group. This difference was partly explained by homeostasis model assessment, C-peptide, family history, and high-sensitivity C-reactive protein (R2 = 0.33, P < .001), but obesity and glycemia did not contribute to this variability in serum adiponectin. A family history of diabetes was associated with low serum adiponectin concentration independently of obesity, glycemia, or insulin sensitivity (P = .002). Glutamic acid decarboxylase-positive diabetic women (n = 17) had similar serum adiponectin as the NGT group in spite of hyperglycemia. In conclusion, serum adiponectin was lowered in women with type 2 diabetes mellitus, and this difference could only be partly explained by insulin resistance, insulin secretion, family history of diabetes, and inflammation. Family history of diabetes was independently associated with hypoadiponectinemia. Autoimmune diabetic women did not have low adiponectin levels.

Nyckelord

Adiponectin/blood/immunology/metabolism
Autoantibodies/blood
Blood Glucose/*metabolism
C-Reactive Protein/metabolism
Cohort Studies
Diabetes Mellitus
Type 1/*blood/immunology/metabolism
Female
Glucose Intolerance/*metabolism
Glucose Tolerance Test
Hemoglobin A
Glycosylated/metabolism
Humans
Middle Aged
Obesity/blood

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