Inflammation and decreased cardiovagal modulation are linked to stress and depression at 36th week of pregnancy in gestational diabetes mellitus.

Stress and depression have been reported in gestational diabetes mellitus (GDM). Though inflammation and oxidative stress are associated with depression, there are no reports of link of cardiometabolic risks (CMR) to stress and depression in GDM. Normal pregnant women (control group, n = 164) and women with GDM (study group, n = 176) at 36th week of gestation were recruited for the study. Blood pressure (BP), body composition, heart rate variability (HRV), glycated hemoglobin (HbA1C), markers of insulin resistance, oxidative stress, inflammation and endothelial dysfunction, were assessed. Perceived stress score (PSS), quality of life (QoL) scale, Indian diabetic risk score (IDRS) and Edinburg postnatal depression score (EPDS) were assessed. Association of potential contributors to PSS and EDPS were assessed by correlation and regression analyses. There was significant increase in PSS, EPDS, IDRS scores, HbA1C, malondialdehyde (MDA) (oxidative stress marker) and high-sensitive C-reactive protein and interleukin-6 (inflammatory markers), and significant decrease in total power (TP) of HRV (marker of cardiovagal modulation), QoL and nitric oxide (endothelial dysfunction marker) in study group compared to control group. Though many cardiometabolic risk parameters were correlated with PSS and EPDS, the significant independent association was observed for TP, HbA1C, MDA and interleukin-6. However, interleukin-6 had maximum contribution to PSS (ß = 0.550, p < 0.001) and EPDS (ß = 0.393, p < 0.001) as demonstrated by multiple regression analysis. Inflammation, oxidative stress, glycation status and decreased cardiovagal modulation are associated with stress and depression at 36th week of gestation in GDM.

Effects of gender on sympathovagal imbalance, prehypertension status, and cardiovascular risks in first-degree relatives of type 2 diabetics.

BACKGROUND: Although cardiovascular (CV) risks are reported in first-degree relatives (FDRs) of type 2 diabetics, effects of gender on sympathovagal imbalance (SVI) and CV risks in these subjects have not been investigated. METHODS: Body mass index (BMI), blood pressure variability parameters including baroreflex sensitivity (BRS), spectral indices of heart rate variability, autonomic function tests, insulin resistance, lipid profile, inflammatory markers (interleukin 6, high-sensitivity C-reactive protein, tumor necrosis factor α) and oxidative stress (OS) marker were measured and analyzed in control group (without family history of diabetes; 65 women, 60 men) and study group (FDRs of type 2 diabetics; 52 women, 49 men) subjects. RESULTS: BMI, heart rate, blood pressure, rate-pressure product, stroke volume, left-ventricular ejection time, cardiac output, total peripheral resistance, homeostatic model of insulin resistance, lipid profile, inflammatory and OS markers, and ratio of low-frequency to high-frequency power of heart rate variability (LF-HF ratio), a sensitive marker of SVI, were significantly increased, and BRS was significantly decreased in study group men compared with women. SVI was more intense in men and was due to concomitant sympathetic activation and vagal inhibition. There was no SVI in control subjects. Multiple regression analysis demonstrated independent contribution of BMI, homeostatic model of insulin resistance, atherogenic index, inflammatory and OS markers, and BRS to LF-HF ratio. Logistic regression analysis demonstrated significant prediction of prehypertension status and rate-pressure product (markers of CV risk) by LF-HF, which was more prominent in men. CONCLUSIONS: SVI is more intense in male FDRs of type 2 diabetics, and SVI is associated with increased CV risk due to insulin resistance, dyslipidemia, inflammation, and oxidative stress in these subjects.

Sympathovagal imbalance contributes to prehypertension status and cardiovascular risks attributed by insulin resistance, inflammation, dyslipidemia and oxidative stress in first degree relatives of type 2 diabetics.

BACKGROUND: Though cardiovascular (CV) risks are reported in first-degree relatives (FDR) of type 2 diabetics, the pathophysiological mechanisms contributing to these risks are not known. We investigated the association of sympathovagal imbalance (SVI) with CV risks in these subjects. SUBJECTS AND METHODS: Body mass index (BMI), basal heart rate (BHR), blood pressure (BP), rate-pressure product (RPP), spectral indices of heart rate variability (HRV), autonomic function tests, insulin resistance (HOMA-IR), lipid profile, inflammatory markers, oxidative stress (OS) marker, rennin, thyroid profile and serum electrolytes were measured and analyzed in subjects of study group (FDR of type 2 diabetics, n = 72) and control group (subjects with no family history of diabetes, n = 104). RESULTS: BMI, BP, BHR, HOMA-IR, lipid profile, inflammatory and OS markers, renin, LF-HF (ratio of low-frequency to high-frequency power of HRV, a sensitive marker of SVI) were significantly increased (p<0.0001) in study group compared to the control group. SVI in study group was due to concomitant sympathetic activation and vagal inhibition. There was significant correlation and independent contribution of markers of insulin resistance, dyslipidemia, inflammation and OS to LF-HF ratio. Multiple-regression analysis demonstrated an independent contribution of LF-HF ratio to prehypertension status (standardized beta 0.415, p<0.001) and bivariate logistic-regression showed significant prediction (OR 2.40, CI 1.128-5.326, p = 0.002) of LF-HF ratio of HRV to increased RPP, the marker of CV risk, in study group. CONCLUSION: SVI in FDR of type 2 diabetics occurs due to sympathetic activation and vagal withdrawal. The SVI contributes to prehypertension status and CV risks caused by insulin resistance, dyslipidemia, inflammation and oxidative stress in FDR of type 2 diabetics.