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

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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 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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  • Cardiac and Cardiovascular Systems
Original languageEnglish
Pages (from-to)3437-3444
Number of pages8
JournalJournal of Clinical Endocrinology and Metabolism
Volume101
Issue number9
Publication statusPublished - 2016 Sep 1
Publication categoryResearch
Peer-reviewedYes