Gender Difference in the Role of Posterodorsal Amygdala on the Regulation of Food Intake, Adiposity and Immunological Responses in Albino Wistar Rats.

Lesion of posterodorsal amygdala (PDA) has been known to produce hyperphagia and obesity in animal models. However, the influence of gender on food intake (FI), body weight (BW) and immunological parameters following PDA lesion is not yet known. The present work was carried out to study the effect of gender on the regulation of FI, BW and immunological parameters following lesions of PDA in albino Wistar rats. Twenty-four albino Wistar rats were divided equally into 2 groups - PDA group and control group - with 6 male and 6 female rats in each. In the experimental group, bilateral electrolytic lesion of the respective nuclei was performed by stereotaxy and post-lesion parameters were recorded. In the control group, sham lesion was made. Male-female difference in each parameter was determined. Following PDA lesion, FI increased significantly in both male (p < 0.001) and female rats (p < 0.01) but the percentage increase in FI was significantly more in female rats (p < 0.001). BW also increased in both the sexes but the increase in BW was significant only in male rats (p < 0.05). Both male and female rats showed increase in the concentration of cluster of differentiation 4 (CD4), but the significant increase in CD4 concentration (p < 0.01) was seen only in male rats. CD8 concentration increased significantly in male rats (p < 0.05). The liver weight-BW ratio was significantly greater in female rats (p < 0.001) following PDA lesions. Lesion of PDA results in accentuation of FI and BW gain and activation of immunity. There is a gender difference in the inhibitory control of PDA on FI, BW and immunity.

Association of hypertension status and cardiovascular risks with sympathovagal imbalance in first degree relatives of type 2 diabetics.

AIMS/INTRODUCTION: As reports show cardiovascular (CV) risks in first-degree relatives (FDR) of type 2 diabetics, and autonomic imbalance predisposing to CV risks, in the present study we have assessed the contribution of sympathovagal imbalance (SVI) to CV risks in these subjects. MATERIALS AND METHODS: Body mass index (BMI), waist-to-hip ratio (WHR), basal heart rate (BHR), blood pressure (BP), rate pressure product (RPP), and spectral indices of heart rate variability (HRV) were reordered and analyzed in FDR of type 2 diabetics (study group, n = 293) and in subjects with no family history of diabetes (control group, n = 405). RESULTS: The ratio of low-frequency (LF) to high-frequency (HF) power of HRV (LF-HF), a sensitive marker of SVI, was significantly increased (P < 0.001) in the study group compared with the control group. The SVI in the study group was due to concomitant sympathetic activation (increased LF) and vagal inhibition (decreased HF). In the study group, the LF-HF ratio was significantly correlated with BMI, WHR, BHR, BP and RPP. Multiple regression analysis showed an independent contribution of LF-HF to hypertension status (P = 0.000), and bivariate logistic regression showed significant prediction (odds ratio 2.16, confidence interval 1.130-5.115) of LF-HF to increased RPP, the marker of CV risk, in the study group. CONCLUSIONS: Sympathovagal imbalance in the form of increased sympathetic and decreased parasympathetic activity is present in FDR of type 2 diabetics. Increased resting heart rate, elevated hypertension status, decreased HRV and increased RPP in these subjects make them vulnerable to CV risks. SVI in these subjects contributes to CV risks independent of the degree of adiposity.

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.

Association of sympathovagal imbalance with cardiovascular risks in young prehypertensives.

Although cardiovascular (CV) risks have been reported in prehypertension, their link to sympathovagal imbalance (SVI) has not been investigated. In the present study, we have assessed the factors contributing to SVI and the prediction of CV risk by SVI in prehypertensives. Body mass index, CV parameters such as heart rate, systolic blood pressure (BP), diastolic BP, mean arterial pressure, rate-pressure product (RPP), stroke volume, left ventricular ejection time, cardiac output, total peripheral resistance, baroreflex sensitivity recorded by continuous blood pressure variability monitoring using Finapres, autonomic function tests recorded by spectral analysis of heart rate variability (HRV), and heart rate and BP responses to standing, deep breathing, and isometric handgrip, and biochemical parameters such as homeostatic model assessment of insulin resistance, lipid risk factors, inflammatory markers, thyroid profile, and renin and oxidative stress parameters were analyzed in young normotensives (n = 118) and prehypertensives (n = 58). Contribution of CV risks to low-frequency/high-frequency (LF/HF) ratio of HRV, the marker of SVI, was determined by multiple regression analysis, and prediction of SVI to RPP, a known CV risk, was assessed by logisitic regression adjusted for body mass index. BP variability, HRV, and autonomic function test parameters were significantly altered in prehypertensives and these parameters were correlated with LF/HF. Insulin resistance, dyslipidemia, inflammation, and oxidative stress contributed to SVI in prehypertensives. LF/HF and baroreflex sensitivity had significant prediction of RPP in prehypertensives. In conclusion, SVI in young prehypertensives is due to both increased sympathetic and decreased vagal tone. CV risks are linked to SVI and SVI predicts cardiac risk in prehypertensives.

Sympathovagal imbalance in young prehypertensives: importance of male-female difference.

INTRODUCTION: Although the prevalence of prehypertension is high, the pathophysiological mechanisms and the effects of gender in its causation have not yet been fully understood. METHODS: Body mass index, waist-to-hip ratio, basal heart rate, blood pressure, rate pressure product and spectral indices of heart rate variability were reordered and analyzed in young normotensive (n = 344) and prehypertensive (n = 69) subjects. Each group was categorized into male and female subgroups. RESULTS: Ratio of low-frequency to high-frequency powers (LF-HF ratio) of heart rate variability spectrum, the sensitive marker of sympathovagal imbalance (SVI), was significantly more increased (P < 0.001) in male prehypertensives compared with female prehypertensives. Although SVI in prehypertensives was found to be due to both sympathetic activation in the form of increased low-frequency power normalized (increased LFnu) and vagal inhibition in the form of decreased high-frequency power normalized (decreased HFnu), contribution of vagal withdrawal was more in males. LF-HF ratio was significantly correlated with body mass index, waist-to-hip ratio, basal heart rate, blood pressure and rate pressure product by Pearson correlation analysis. Furthermore, multiple regression analysis demonstrated an independent relationship between LF-HF ratio and gender (P = 0.000) and prehypertension status (P = 0.000) in both normotensives and prehypertensives. CONCLUSIONS: Vagal inhibition plays an important role in addition to sympathetic activation in alteration of SVI in the genesis of prehypertension, especially in males. Gender and prehypertension status play important role in the causation of SVI. It was suggested that vagal tone of prehypertensives should be maintained at a higher level to prevent their further rise in blood pressure.

Effect of gender on sympathovagal imbalance in prehypertensives.

Although recently the incidence of prehypertension has increased considerably, the pathophysiological mechanisms and the effects of gender in its causation have not yet been fully elucidated. Therefore, in this study body mass index (BMI), waist-hip ratio (WHR), basal heart rate (BHR), blood pressure (BP), rate pressure product (RPP), and spectral indices of heart rate variability (HRV) were reordered and analyzed in normotensive and prehypertensive males and females. It was observed that low frequency-high frequency (LF-HF) ratio, the sensitive indicator of sympathovagal imbalance (SVI), is significantly more (P < .001) in male prehypertensives compared with female prehypertensives. Although SVI in prehypertensives was found to be due to both sympathetic activation and vagal inhibition, contribution of vagal withdrawal was prominent in males. The LF-HF ratio was significantly correlated with BMI, WHR, BHR, BP, and RPP, which was more prominent in male prehypertensives and the degree of correlation was more for WHR and diastolic pressure. It was concluded that vagal inhibition plays an important role in critical alteration of SVI in the genesis of prehypertension, especially in males, and WHR could be a better indicator of SVI in prehypertensives. It was suggested that prehypertensives should improve their vagal tone to restore the sympathovagal homeostasis.