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 inScandinavian journal of clinical and laboratory investigation Vol. 66; no. 7; pp. 559 - 566
Main Authors Dullaart, R. P. F., Riemens, S. C., Boomsma, F.
Format Journal Article
LanguageEnglish
Published 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.
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.
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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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References Jensen M. D. (CIT0012) 1991; 40
Boomsma F. (CIT0003) 2005; 11
Boomsma F. (CIT0002) 2003; 1647
CIT0010
CIT0020
CIT0001
Abella A. (CIT0017) 2004; 47
Abella A. (CIT0007) 2003; 59
Van Dijk J. (CIT0014) 1995; 663
Salmi M. (CIT0009) 2002; 161
Lukaski H. C. (CIT0011) 1985; 41
Boomsma F. (CIT0008) 2005; 48
Meszaros Z. (CIT0018) 1999; 48
Visentin V. (CIT0004) 2004; 12
Matthews D. R. (CIT0013) 1985; 28
Boomsma F. (CIT0015) 2001; 44
Stolen C. M. (CIT0016) 2004; 95
Smith D. J. (CIT0005) 1998; 188
Boomsma F. (CIT0019) 1999; 42
Enrique‐Tarancon G. (CIT0006) 1998; 273
References_xml – volume: 663
  start-page: 43
  year: 1995
  ident: CIT0014
  publication-title: J Chromatogr
  doi: 10.1016/0378-4347(94)00408-W
– volume: 41
  start-page: 810
  year: 1985
  ident: CIT0011
  publication-title: Am J Clin Nutr
  doi: 10.1093/ajcn/41.4.810
– volume: 11
  start-page: RA 112
  year: 2005
  ident: CIT0003
  publication-title: Med Sci Monit
– volume: 48
  start-page: 1002
  year: 2005
  ident: CIT0008
  publication-title: Diabetologia
  doi: 10.1007/s00125-005-1716-4
– ident: CIT0001
  doi: 10.1093/emboj/20.15.3893
– volume-title: Definition, diagnosis classification of diabetes mellitus and its complications, Report of a World Health Organization consultation. Part 1: diagnosis and classification of diabetes mellitus.
  ident: CIT0010
– volume: 40
  start-page: 406
  year: 1991
  ident: CIT0012
  publication-title: Metabolism
  doi: 10.1016/0026-0495(91)90152-M
– volume: 48
  start-page: 113
  year: 1999
  ident: CIT0018
  publication-title: Metabolism
  doi: 10.1016/S0026-0495(99)90019-7
– volume: 12
  start-page: 547
  year: 2004
  ident: CIT0004
  publication-title: Obes Res
  doi: 10.1038/oby.2004.62
– ident: CIT0020
  doi: 10.1016/S0026-0495(03)00028-3
– volume: 1647
  start-page: 48
  year: 2003
  ident: CIT0002
  publication-title: Biochim Biophys Acta
  doi: 10.1016/S1570-9639(03)00047-5
– volume: 188
  start-page: 17
  year: 1998
  ident: CIT0005
  publication-title: J Exp Med
  doi: 10.1084/jem.188.1.17
– volume: 47
  start-page: 429
  year: 2004
  ident: CIT0017
  publication-title: Diabetologia
  doi: 10.1007/s00125-004-1346-2
– volume: 273
  start-page: 8025
  year: 1998
  ident: CIT0006
  publication-title: J Biol Chem
  doi: 10.1074/jbc.273.14.8025
– volume: 28
  start-page: 412
  year: 1985
  ident: CIT0013
  publication-title: Diabetologia
  doi: 10.1007/BF00280883
– volume: 44
  start-page: 388
  year: 2001
  ident: CIT0015
  publication-title: Diabetologia
  doi: 10.1007/s001250051632
– volume: 42
  start-page: 233
  year: 1999
  ident: CIT0019
  publication-title: Diabetologia
  doi: 10.1007/s001250051143
– volume: 59
  start-page: 153
  year: 2003
  ident: CIT0007
  publication-title: J Physiol Biochem
  doi: 10.1007/BF03179910
– volume: 161
  start-page: 2255
  year: 2002
  ident: CIT0009
  publication-title: Am J Pathol
  doi: 10.1016/S0002-9440(10)64501-4
– volume: 95
  start-page: 50
  year: 2004
  ident: CIT0016
  publication-title: Circ Res
  doi: 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
URI https://www.tandfonline.com/doi/abs/10.1080/00365510600863879
https://www.ncbi.nlm.nih.gov/pubmed/17101547
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