Leptin-Oxytocin Axis May Play an Important Role in Patients with Type 2 Diabetes (T2D) and Post-Traumatic Stress Disorder (PTSD): Data from the Cross-Sectional Study of African American Male Veterans.

Presentation Number: MON 592
Date of Presentation: April 3rd, 2017

Deepika Khanna*1, Arfana Akbar2, Yuval Eisenberg3, Ten EnSen4, Subhash C Kukreja3 and Elena Barengolts3
1University of Illinois college, 2University of Illinois at Chicago, 3University of Illinois at Chicago, Chicago, IL, 4Jess Brown Medical Center

Abstract

Background: Neurohypophyseal hormone oxytocin (OXT) is suggested as treatment for type 2 diabetes (T2D) and post-traumatic stress disorder (PTSD) (1). Endogenous OXT production is regulated by adipokine leptin. OXT is located downstream leptin signaling and might have a potential for improving both leptin and insulin resistance of T2D. In animal models OXT treatment was able to partly overcome leptin deficiency and/or resistance. Similar results were observed in a pilot human study. Role of OXT or leptin-OXT axis was not tested in patients with T2D and comorbid PTSD (T2D/PTSD[+]).

Objective: to investigate the hypothesis that OXT and/or leptin-OXT axis are associated with T2D and comorbid T2D/PTSD[+].

Methods: In a cross-sectional study 99 African American male (AAM) veterans with and without T2D were assessed by oral glucose tolerance test (OGTT). A PTSD diagnosis was categorized from the medical record. Urinary OXT was measured after extraction, adjusted for urinary creatinine, and log transformed prior to analysis. The selected T2D-related biomarkers comprising leptin, IGF-1, testosterone, cortisol, 25(OH)D, and C-reactive protein (CRP) were measured by standardized assays. The univariate and multivariate regression assessed predictors of T2D and T2D/PTSD comorbidity.

Results: There was high rate of chronic (95%), including psychiatric (66%) conditions. Patients with PTSD had lower BMI and accordingly lower prevalent T2D as compared to subjects with normal glucose tolerance (NGT). Comparison of T2D vs NGT showed (mean ± SD) higher serum leptin (27.7 ± 14.2 vs 10.4 ± 8.0 ng/ml, p<0.01) and lower OXT (0.69 ± 0.25 vs 0.85 ± 0.26 pg/mg Cr, p=0.045). Comparison of subjects without vs with PTSD, PTSD(-) (n=74) vs PTSD(+) (n=25) showed no difference for leptin or OXT. Similarly, no difference was observed between NGT/PTSD(-) (n=30) vs comorbid T2D/PTSD(+) (n=5) groups. Correlation analysis showed that HbA1c correlated negatively with OXT (r=-0.20) and positively with leptin (r=0.55) (p<0.05 for both). In the bivariate regression analysis a trend was observed for negative association between OXT and T2D, odds ratio (OR, 95% confidence interval [CI]) 0.52 (0.27 - 1.01, p=0.053). However, OR was rendered insignificant in fully adjusted analysis. In the multiple logistic regression leptin was the only (and positive) predictor of T2D after adjustment for age and BMI, OR=1.10, CI=1.02-1.19 (p=0.02). Similarly, only BMI was a significant positive predictor of comorbid T2D/PTSD, OR=2.48, CI 1.31-4.71 (p=0.006).

Conclusion: BMI was confirmed as the most important predictor for T2D and T2D/PTSD comorbidity. In addition, the observed associations suggested that OXT and leptin-OXT axis might play a role in glycemic control and as markers for T2D. Further research should corroborate the data in other populations and investigate usefulness of OXT for remediation of T2D and T2D/PTSD comorbidity.

 

Nothing to Disclose: DK, AA, YE, TE, SCK, EB