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N-terminal prosomatostatin as a risk marker for cardiovascular disease and diabetes in a general population

Hedbäck, Tore LU ; Almgren, Peter LU ; Nilsson, Peter M. LU and Melander, Olle LU orcid (2016) In Journal of Clinical Endocrinology and Metabolism 101(9). p.3437-3444
Abstract

Context: Somatostatin inhibits a range of hormones, including GH, insulin, and glucagon, but little is known about its role in the development of cardiometabolic disease. Objective: The objective of the study was to investigate whether fasting plasma concentration of N-terminal prosomatostatin (NT-proSST) is associated with the development of diabetes, coronary artery disease (CAD), and mortality. Design, Setting, and Participants: NT-proSST was measured in plasma from 5389 fasting participants of the population-based study Malmö Preventive Project, with a mean baseline age of 69.4± 6.2 years. Cox proportional hazards models adjusted for traditional cardiovascular risk factors were used to investigate the relationships between baseline... (More)

Context: Somatostatin inhibits a range of hormones, including GH, insulin, and glucagon, but little is known about its role in the development of cardiometabolic disease. Objective: The objective of the study was to investigate whether fasting plasma concentration of N-terminal prosomatostatin (NT-proSST) is associated with the development of diabetes, coronary artery disease (CAD), and mortality. Design, Setting, and Participants: NT-proSST was measured in plasma from 5389 fasting participants of the population-based study Malmö Preventive Project, with a mean baseline age of 69.4± 6.2 years. Cox proportional hazards models adjusted for traditional cardiovascular risk factors were used to investigate the relationships between baseline NT-proSST and end points, with a mean follow-up of 5.6 ± 1.4 years. Main Outcome Measures: CAD, diabetes, and mortality were measured. Results: Overall, NT-proSST (hazard ratio [HR] per SD increment of log transformed NT-proSST) was unrelated to the risk of incident diabetes (220 events; HR 1.05; 95% confidence interval [CI] 0.91- 1.20; P = .531) but was related to the risk of incident CAD (370 events; HR 1.17; 95% CI 1.06-1.30; P = .003), all-cause mortality (756 events; HR 1.24; 95% CI 1.15-1.33; P < .001), and cardiovascular mortality (283 events; HR 1.33; 95% CI 1.19-1.43; P<.001). The relationships were not linear, with most of the excess risk observed in subjects with high values of NT-proSST. Subjects in the top vs bottom decile had a severely increased risk of incident CAD (HR 2.41; 95% CI 1.45-4.01; P < .001), all-cause mortality (HR 1.84;95%CI 1.33-2.53; P<.001),andcardiovascular mortality (HR 2.44;95% CI 1.39-4.27; P < .001). Conclusion: NT-proSST was significantly and independently associated with the development of CAD, all-cause mortality, and cardiovascular mortality.

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author
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Journal of Clinical Endocrinology and Metabolism
volume
101
issue
9
pages
8 pages
publisher
Oxford University Press
external identifiers
  • pmid:27399347
  • wos:000390849100029
  • scopus:84988922701
ISSN
0021-972X
DOI
10.1210/jc.2016-1736
language
English
LU publication?
yes
id
fa120b73-b191-4d43-80a3-8e0998e35f9a
date added to LUP
2016-10-28 16:16:57
date last changed
2024-03-22 10:21:31
@article{fa120b73-b191-4d43-80a3-8e0998e35f9a,
  abstract     = {{<p>Context: Somatostatin inhibits a range of hormones, including GH, insulin, and glucagon, but little is known about its role in the development of cardiometabolic disease. Objective: The objective of the study was to investigate whether fasting plasma concentration of N-terminal prosomatostatin (NT-proSST) is associated with the development of diabetes, coronary artery disease (CAD), and mortality. Design, Setting, and Participants: NT-proSST was measured in plasma from 5389 fasting participants of the population-based study Malmö Preventive Project, with a mean baseline age of 69.4± 6.2 years. Cox proportional hazards models adjusted for traditional cardiovascular risk factors were used to investigate the relationships between baseline NT-proSST and end points, with a mean follow-up of 5.6 ± 1.4 years. Main Outcome Measures: CAD, diabetes, and mortality were measured. Results: Overall, NT-proSST (hazard ratio [HR] per SD increment of log transformed NT-proSST) was unrelated to the risk of incident diabetes (220 events; HR 1.05; 95% confidence interval [CI] 0.91- 1.20; P = .531) but was related to the risk of incident CAD (370 events; HR 1.17; 95% CI 1.06-1.30; P = .003), all-cause mortality (756 events; HR 1.24; 95% CI 1.15-1.33; P &lt; .001), and cardiovascular mortality (283 events; HR 1.33; 95% CI 1.19-1.43; P&lt;.001). The relationships were not linear, with most of the excess risk observed in subjects with high values of NT-proSST. Subjects in the top vs bottom decile had a severely increased risk of incident CAD (HR 2.41; 95% CI 1.45-4.01; P &lt; .001), all-cause mortality (HR 1.84;95%CI 1.33-2.53; P&lt;.001),andcardiovascular mortality (HR 2.44;95% CI 1.39-4.27; P &lt; .001). Conclusion: NT-proSST was significantly and independently associated with the development of CAD, all-cause mortality, and cardiovascular mortality.</p>}},
  author       = {{Hedbäck, Tore and Almgren, Peter and Nilsson, Peter M. and Melander, Olle}},
  issn         = {{0021-972X}},
  language     = {{eng}},
  month        = {{09}},
  number       = {{9}},
  pages        = {{3437--3444}},
  publisher    = {{Oxford University Press}},
  series       = {{Journal of Clinical Endocrinology and Metabolism}},
  title        = {{N-terminal prosomatostatin as a risk marker for cardiovascular disease and diabetes in a general population}},
  url          = {{http://dx.doi.org/10.1210/jc.2016-1736}},
  doi          = {{10.1210/jc.2016-1736}},
  volume       = {{101}},
  year         = {{2016}},
}