Plasma semicarbazide-sensitive amine oxidase is moderately decreased by pronounced exogenous hyperinsulinemia but is not associated with insulin sensitivity and body fat
Objective. Semicarbazide-sensitive amine oxidase (SSAO) is widely expressed in adipose tissue, where it may contribute to stimulation of glucose transport via GLUT4 recruitment. We tested the relationships of soluble SSAO, as reflected by its plasma activity, with insulin sensitivity and indices of...
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Published in | Scandinavian journal of clinical and laboratory investigation Vol. 66; no. 7; pp. 559 - 566 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
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England
Informa UK Ltd
2006
Taylor & Francis |
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Abstract | Objective. Semicarbazide-sensitive amine oxidase (SSAO) is widely expressed in adipose tissue, where it may contribute to stimulation of glucose transport via GLUT4 recruitment. We tested the relationships of soluble SSAO, as reflected by its plasma activity, with insulin sensitivity and indices of body fat, and determined whether insulin is involved in regulating plasma SSAO activity. Material and methods. In 24 non-diabetic subjects, the relationships of plasma SSAO activity with insulin sensitivity (M-value and free fatty acid (FFA) suppression during a 3-h hyperinsulinemic (8.3 µU kg−1 s−1), euglycemic clamp), body mass index (BMI 25.5±3.1 kg m−2), waist-hip ratio and fat mass were assessed. In 16 subjects, the effect of insulin infusion, administered at a rate of 8.3 µU kg−1 s−1 during 3 h, followed by 3-h insulin infusion at a high rate of 41.7 µU kg−1 s−1 on plasma SSAO activity was determined. In the other 8 subjects, the response of plasma SSAO activity to 24-h insulin infused at 8.3 µU kg−1 s−1 was assessed. Results. There were no relationships (all p >0.10) of plasma SSAO activity (215±60 mU L−1) with the M-value or with any indices of body fat and FFA before and after insulin suppression. Plasma SSAO activity changed by −7.2 (95% CI, −14.5 to +0.2)% after 3 h (NS) and decreased by 10.1 (95% CI, 19.2 to 1)% after 6 h of insulin infusion (p <0.05). Plasma SSAO activity did not significantly change after 8 h (change 0.4 (95% CI, −15.3 to +16.2)%, NS) and after 24 h (change −8.8 (95% CI, −27.4 to +9.7)%, NS) of insulin infusion. Conclusions. It is unlikely that circulating SSAO is a clinically important marker of insulin sensitivity on glucose and fatty acid metabolism. The reduction in plasma SSAO activity in response to pronounced hyperinsulinemia suggests that insulin is involved in the regulation of the soluble form of this enzyme. |
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AbstractList | Objective. Semicarbazide-sensitive amine oxidase (SSAO) is widely expressed in adipose tissue, where it may contribute to stimulation of glucose transport via GLUT4 recruitment. We tested the relationships of soluble SSAO, as reflected by its plasma activity, with insulin sensitivity and indices of body fat, and determined whether insulin is involved in regulating plasma SSAO activity. Material and methods. In 24 non-diabetic subjects, the relationships of plasma SSAO activity with insulin sensitivity (M-value and free fatty acid (FFA) suppression during a 3-h hyperinsulinemic (8.3 µU kg−1 s−1), euglycemic clamp), body mass index (BMI 25.5±3.1 kg m−2), waist-hip ratio and fat mass were assessed. In 16 subjects, the effect of insulin infusion, administered at a rate of 8.3 µU kg−1 s−1 during 3 h, followed by 3-h insulin infusion at a high rate of 41.7 µU kg−1 s−1 on plasma SSAO activity was determined. In the other 8 subjects, the response of plasma SSAO activity to 24-h insulin infused at 8.3 µU kg−1 s−1 was assessed. Results. There were no relationships (all p >0.10) of plasma SSAO activity (215±60 mU L−1) with the M-value or with any indices of body fat and FFA before and after insulin suppression. Plasma SSAO activity changed by −7.2 (95% CI, −14.5 to +0.2)% after 3 h (NS) and decreased by 10.1 (95% CI, 19.2 to 1)% after 6 h of insulin infusion (p <0.05). Plasma SSAO activity did not significantly change after 8 h (change 0.4 (95% CI, −15.3 to +16.2)%, NS) and after 24 h (change −8.8 (95% CI, −27.4 to +9.7)%, NS) of insulin infusion. Conclusions. It is unlikely that circulating SSAO is a clinically important marker of insulin sensitivity on glucose and fatty acid metabolism. The reduction in plasma SSAO activity in response to pronounced hyperinsulinemia suggests that insulin is involved in the regulation of the soluble form of this enzyme. Semicarbazide-sensitive amine oxidase (SSAO) is widely expressed in adipose tissue, where it may contribute to stimulation of glucose transport via GLUT4 recruitment. We tested the relationships of soluble SSAO, as reflected by its plasma activity, with insulin sensitivity and indices of body fat, and determined whether insulin is involved in regulating plasma SSAO activity. In 24 non-diabetic subjects, the relationships of plasma SSAO activity with insulin sensitivity (M-value and free fatty acid (FFA) suppression during a 3-h hyperinsulinemic (8.3 microU kg-1 s-1), euglycemic clamp), body mass index (BMI 25.5 +/- 3.1 kg m-2), waist-hip ratio and fat mass were assessed. In 16 subjects, the effect of insulin infusion, administered at a rate of 8.3 microU kg-1 s-1 during 3 h, followed by 3-h insulin infusion at a high rate of 41.7 microU kg-1 s-1 on plasma SSAO activity was determined. In the other 8 subjects, the response of plasma SSAO activity to 24-h insulin infused at 8.3 microU kg-1 s-1 was assessed. There were no relationships (all p > 0.10) of plasma SSAO activity (215 +/- 60 mU L-1) with the M-value or with any indices of body fat and FFA before and after insulin suppression. Plasma SSAO activity changed by -7.2 (95% CI, -14.5 to +0.2)% after 3 h (NS) and decreased by 10.1 (95% CI, 19.2 to 1)% after 6 h of insulin infusion (p < 0.05). Plasma SSAO activity did not significantly change after 8 h (change 0.4 (95% CI, -15.3 to +16.2)%, NS) and after 24 h (change -8.8 (95% CI, -27.4 to +9.7)%, NS) of insulin infusion. It is unlikely that circulating SSAO is a clinically important marker of insulin sensitivity on glucose and fatty acid metabolism. The reduction in plasma SSAO activity in response to pronounced hyperinsulinemia suggests that insulin is involved in the regulation of the soluble form of this enzyme. Semicarbazide-sensitive amine oxidase (SSAO) is widely expressed in adipose tissue, where it may contribute to stimulation of glucose transport via GLUT4 recruitment. We tested the relationships of soluble SSAO, as reflected by its plasma activity, with insulin sensitivity and indices of body fat, and determined whether insulin is involved in regulating plasma SSAO activity.OBJECTIVESemicarbazide-sensitive amine oxidase (SSAO) is widely expressed in adipose tissue, where it may contribute to stimulation of glucose transport via GLUT4 recruitment. We tested the relationships of soluble SSAO, as reflected by its plasma activity, with insulin sensitivity and indices of body fat, and determined whether insulin is involved in regulating plasma SSAO activity.In 24 non-diabetic subjects, the relationships of plasma SSAO activity with insulin sensitivity (M-value and free fatty acid (FFA) suppression during a 3-h hyperinsulinemic (8.3 microU kg-1 s-1), euglycemic clamp), body mass index (BMI 25.5 +/- 3.1 kg m-2), waist-hip ratio and fat mass were assessed. In 16 subjects, the effect of insulin infusion, administered at a rate of 8.3 microU kg-1 s-1 during 3 h, followed by 3-h insulin infusion at a high rate of 41.7 microU kg-1 s-1 on plasma SSAO activity was determined. In the other 8 subjects, the response of plasma SSAO activity to 24-h insulin infused at 8.3 microU kg-1 s-1 was assessed.MATERIAL AND METHODSIn 24 non-diabetic subjects, the relationships of plasma SSAO activity with insulin sensitivity (M-value and free fatty acid (FFA) suppression during a 3-h hyperinsulinemic (8.3 microU kg-1 s-1), euglycemic clamp), body mass index (BMI 25.5 +/- 3.1 kg m-2), waist-hip ratio and fat mass were assessed. In 16 subjects, the effect of insulin infusion, administered at a rate of 8.3 microU kg-1 s-1 during 3 h, followed by 3-h insulin infusion at a high rate of 41.7 microU kg-1 s-1 on plasma SSAO activity was determined. In the other 8 subjects, the response of plasma SSAO activity to 24-h insulin infused at 8.3 microU kg-1 s-1 was assessed.There were no relationships (all p > 0.10) of plasma SSAO activity (215 +/- 60 mU L-1) with the M-value or with any indices of body fat and FFA before and after insulin suppression. Plasma SSAO activity changed by -7.2 (95% CI, -14.5 to +0.2)% after 3 h (NS) and decreased by 10.1 (95% CI, 19.2 to 1)% after 6 h of insulin infusion (p < 0.05). Plasma SSAO activity did not significantly change after 8 h (change 0.4 (95% CI, -15.3 to +16.2)%, NS) and after 24 h (change -8.8 (95% CI, -27.4 to +9.7)%, NS) of insulin infusion.RESULTSThere were no relationships (all p > 0.10) of plasma SSAO activity (215 +/- 60 mU L-1) with the M-value or with any indices of body fat and FFA before and after insulin suppression. Plasma SSAO activity changed by -7.2 (95% CI, -14.5 to +0.2)% after 3 h (NS) and decreased by 10.1 (95% CI, 19.2 to 1)% after 6 h of insulin infusion (p < 0.05). Plasma SSAO activity did not significantly change after 8 h (change 0.4 (95% CI, -15.3 to +16.2)%, NS) and after 24 h (change -8.8 (95% CI, -27.4 to +9.7)%, NS) of insulin infusion.It is unlikely that circulating SSAO is a clinically important marker of insulin sensitivity on glucose and fatty acid metabolism. The reduction in plasma SSAO activity in response to pronounced hyperinsulinemia suggests that insulin is involved in the regulation of the soluble form of this enzyme.CONCLUSIONSIt is unlikely that circulating SSAO is a clinically important marker of insulin sensitivity on glucose and fatty acid metabolism. The reduction in plasma SSAO activity in response to pronounced hyperinsulinemia suggests that insulin is involved in the regulation of the soluble form of this enzyme. Objective. Semicarbazide-sensitive amine oxidase (SSAO) is widely expressed in adipose tissue, where it may contribute to stimulation of glucose transport via GLUT4 recruitment. We tested the relationships of soluble SSAO, as reflected by its plasma activity, with insulin sensitivity and indices of body fat, and determined whether insulin is involved in regulating plasma SSAO activity. Material and methods. In 24 non-diabetic subjects, the relationships of plasma SSAO activity with insulin sensitivity (M-value and free fatty acid (FFA) suppression during a 3-h hyperinsulinemic (8.3 µU kg −1 s −1 ), euglycemic clamp), body mass index (BMI 25.5±3.1 kg m −2 ), waist-hip ratio and fat mass were assessed. In 16 subjects, the effect of insulin infusion, administered at a rate of 8.3 µU kg −1 s −1 during 3 h, followed by 3-h insulin infusion at a high rate of 41.7 µU kg −1 s −1 on plasma SSAO activity was determined. In the other 8 subjects, the response of plasma SSAO activity to 24-h insulin infused at 8.3 µU kg −1 s −1 was assessed. Results. There were no relationships (all p >0.10) of plasma SSAO activity (215±60 mU L −1 ) with the M-value or with any indices of body fat and FFA before and after insulin suppression. Plasma SSAO activity changed by −7.2 (95% CI, −14.5 to +0.2)% after 3 h (NS) and decreased by 10.1 (95% CI, 19.2 to 1)% after 6 h of insulin infusion (p <0.05). Plasma SSAO activity did not significantly change after 8 h (change 0.4 (95% CI, −15.3 to +16.2)%, NS) and after 24 h (change −8.8 (95% CI, −27.4 to +9.7)%, NS) of insulin infusion. Conclusions. It is unlikely that circulating SSAO is a clinically important marker of insulin sensitivity on glucose and fatty acid metabolism. The reduction in plasma SSAO activity in response to pronounced hyperinsulinemia suggests that insulin is involved in the regulation of the soluble form of this enzyme. |
Author | Dullaart, R. P. F. Riemens, S. C. Boomsma, F. |
Author_xml | – sequence: 1 givenname: R. P. F. surname: Dullaart fullname: Dullaart, R. P. F. email: r.p.f.dullaart@int.umcg.nl organization: Department of Endocrinology, Groningen University Medical Center, University of Groningen, Groningen, The Netherlands – sequence: 2 givenname: S. C. surname: Riemens fullname: Riemens, S. C. email: r.p.f.dullaart@int.umcg.nl organization: Department of Endocrinology, Groningen University Medical Center, University of Groningen, Groningen, The Netherlands – sequence: 3 givenname: F. surname: Boomsma fullname: Boomsma, F. email: r.p.f.dullaart@int.umcg.nl organization: Department of Endocrinology, Groningen University Medical Center, University of Groningen, Groningen, The Netherlands |
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Cites_doi | 10.1016/0378-4347(94)00408-W 10.1093/ajcn/41.4.810 10.1007/s00125-005-1716-4 10.1093/emboj/20.15.3893 10.1016/0026-0495(91)90152-M 10.1016/S0026-0495(99)90019-7 10.1038/oby.2004.62 10.1016/S0026-0495(03)00028-3 10.1016/S1570-9639(03)00047-5 10.1084/jem.188.1.17 10.1007/s00125-004-1346-2 10.1074/jbc.273.14.8025 10.1007/BF00280883 10.1007/s001250051632 10.1007/s001250051143 10.1007/BF03179910 10.1016/S0002-9440(10)64501-4 10.1161/01.RES.0000134630.68877.2F |
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Snippet | Objective. Semicarbazide-sensitive amine oxidase (SSAO) is widely expressed in adipose tissue, where it may contribute to stimulation of glucose transport via... Semicarbazide-sensitive amine oxidase (SSAO) is widely expressed in adipose tissue, where it may contribute to stimulation of glucose transport via GLUT4... |
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SubjectTerms | Adipose Tissue - enzymology Amine Oxidase (Copper-Containing) - blood Biomarkers - blood Body fat Humans Hyperinsulinism - chemically induced Hyperinsulinism - enzymology insulin Insulin - blood insulin sensitivity M-value Male semicarbazide-sensitive amine oxidase |
Title | Plasma semicarbazide-sensitive amine oxidase is moderately decreased by pronounced exogenous hyperinsulinemia but is not associated with insulin sensitivity and body fat |
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