Visceral adiposity index as a tool for cardiometabolic risk in obese older women

OBJECTIVE: To correlate anthropometric measurements, lipid profile, cardiorespiratory fitness, and visceral adiposity index (VAI) in sedentary obese older women. METHODS: Twenty-seven insufficiently active and overweight older women were included in this cross-sectional study. We evaluated their anthropometric profile (body weight and stature, body mass index, waist and hip circumferences) and body composition (fat mass, body fat percentage, and musculoskeletal mass). Venous blood samples were analyzed for high and low-density lipoproteins (HDL-c and LDL-c), triglycerides (TG), and the LDL/HDL ratio. Peak oxygen uptake (VO2 peak) was measured using an adapted Bruce test using direct spirometry. We tested data normality and applied Pearson’s correlation, assuming a p &lt; 0.05. RESULS: The following correlations were observed: VAI and HDL (r = -0.53); VAI and LDL (r = 0.35); VAI and TG (r = 0.86); VAI and TG/HDL (r = 0.99) and VAI and VO2 peak (r = -0.55), with p &le; 0.01 for all analyses. CONCLUSION: The findings suggested that VAI may be used as a tool to assess cardiometabolic risk in obese older women. Future studies should evaluate the applicability of VAI as a cardiometabolic risk factor indicator in older adults.</p

Locus coeruleus mediates cold stress-induced polycystic ovary in rats

Previous reports about the rat ovary have shown that cold stress promotes ovarian morphological alterations related to a polycystic ovary (PCO) condition through activation of the ovarian sympathetic nerves. Because the noradrenergic nucleus locus coeruleus (LC) is activated by cold stress and synaptically connected to the preganglionic cell bodies of the ovarian sympathetic pathway, this study aimed to evaluate the LC`s role in cold stress-induced PCO in rats. Ovarian morphology and endocrine and sympathetic functions were evaluated after 8 wk of chronic intermittent cold stress (4 C, 3 h/d) in rats with or without LC lesion. The effect of acute and chronic cold stress upon the LC neuron activity was confirmed by Fos protein expression in tyrosine hydroxylase-immunoreactive neurons. Cold stress induced the formation of follicular cysts, type III follicles, and follicles with hyperthecosis alongside increased plasma estradiol and testosterone levels, irregular estrous cyclicity, and reduced ovulation. Considering estradiol release in vitro, cold stress potentiated the ovarian response to human chorionic gonadotropin. Ovarian norepinephrine (NE) was not altered after 8 wk of stress. However, LC lesion reduced NE activity in the ovary of cold-stressed rats, but not in controls, and prevented all the cold stress effects evaluated. Cold stress increased the number of Fos/tyrosine hydroxylase-immunoreactive neurons in the LC, but this effect was more pronounced for acute stress as compared with chronic stress. These results show that cold stress promotes PCO in rats, which apparently depends on ovarian NE activity that, under this condition, is regulated by the noradrenergic nucleus LC