Abstract
BackgroundThe hormone somatostatin inhibits growth hormone release from the pituitary gland and is theoretically linked to diabetes and diabetes related complications. This study aimed to investigate the relationship between levels of the stable somatostatin precursor, N-terminal prosomatostatin (NT-proSST), with mortality in type 2 diabetes (T2DM) patients.MethodsIn 1,326 T2DM outpatients, participating in this ZODIAC prospective cohort study, Cox proportional hazards models were used to investigate the independent relationship between plasma NT-proSST concentrations with all-cause and cardiovascular mortality.ResultsMedian concentration of NT-proSST was 592 [IQR 450–783] pmol/L. During follow-up for 6 [3–10] years, 413 (31%) patients died, of which 176 deaths (43%) were attributable to cardiovascular causes. The age and sex adjusted hazard ratios (HRs) for all-cause and cardiovascular mortality were 1.48 (95%CI 1.14 - 1.93) and 2.21 (95%CI 1.49 - 3.28). However, after further adjustment for cardiovascular risk factors there was no independent association of log NT-proSST with mortality, which was almost entirely attributable to adjustment for serum creatinine. There were no significant differences in Harrell’s C statistics to predict mortality for the models with and without NT-proSST: both 0.79 (95%CI 0.77 – 0.82) and 0.81 (95%CI 0.77 – 0.84).ConclusionsNT-proSST is unsuitable as a biomarker for cardiovascular and all-cause mortality in stable outpatients with T2DM.
Highlights
The hormone somatostatin inhibits growth hormone release from the pituitary gland and is theoretically linked to diabetes and diabetes related complications
In type 2 diabetes mellitus (T2DM), somatostatin lowers glucose concentrations by inhibiting glucagon secretion [9,10] and abnormalities in the growth hormone (GH)-insulin-like growth factor-1 (IGF-1) axis have been associated with increased cardiovascular risk in T2DM [11,12,13]
In univariate Cox regression analyses the log NT-proSST was significantly associated with all-cause (HR 2.80, 95% Confidence interval (CI) 2.17 - 3.60) and cardiovascular mortality (HR 3.86, 95% CI 2.64 - 5.62)
Summary
The hormone somatostatin inhibits growth hormone release from the pituitary gland and is theoretically linked to diabetes and diabetes related complications. This study aimed to investigate the relationship between levels of the stable somatostatin precursor, N-terminal prosomatostatin (NT-proSST), with mortality in type 2 diabetes (T2DM) patients. Somatostatin is secreted by gastric and pancreatic D-cells in response to meal ingestion through stimulation of the autonomic nervous system [2,3,4]. It suppresses the release of insulin-like growth factor-1 (IGF-1), vasoactive intestinal polypeptide, gastrin, secretin, and pancreatic polypeptides and exerts a range of physiological effects, such as modifying intestinal. The long-term predictive capabilities of stable plasma NT-proSST concentrations in stable outpatients with T2DM have not been studied
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
