N-terminal prosomatostatin as a risk marker for cardiovascular disease and diabetes in a general population
(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
- Hedbäck, Tore LU ; Almgren, Peter LU ; Nilsson, Peter M. LU and Melander, Olle LU
- organization
- publishing date
- 2016-09-01
- 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
-
- scopus:84988922701
- pmid:27399347
- wos:000390849100029
- 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
- 2024-04-05 08:59:23
@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 < .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.</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}}, }