Longitudinal associations between metabolic score for visceral fat and hyperuricemia in non-obese adults.

BACKGROUND AND AIMS: The assessment of visceral adiposity is of great significance for the prevention of hyperuricemia (HUA), especially in non-obese individuals. The metabolic score for visceral fat (METS-VF) is a newly proposed surrogate of visceral obesity. We aimed to evaluate the longitudinal associations of METS-VF with the risk of HUA in non-obese adults. METHODS AND RESULTS: A total of 16,058 non-obese adults without HUA were included for this retrospective cohort analyses. The crude incidence rate of HUA in non-obese women and men were 20.9 and 69.6 per 1000 person-years, respectively. The Cox proportional hazards model indicated that METS-VF was significantly associated with the risk of HUA in both genders. Whereas, METS-VF only had the highest HR in women, but not in men. CONCLUSIONS: METS-VF, a novel surrogate of visceral adiposity combined biochemical and anthropometric parameters, age, and gender, could be a useful tool for the hierarchical prevention and management of HUA among non-obese women.

Amelioration of oxidative stress-induced phenotype loss of parvalbumin interneurons might contribute to the beneficial effects of environmental enrichment in a rat model of post-traumatic stress disorder.

Post-traumatic stress disorder (PTSD) is a common psychiatric disease following exposure to a severe traumatic event or physiological stress, which is characterized by anxiety- and depression-like behaviors and cognitive impairment. However, the underlying mechanisms remain elusive. Parvalbumin (PV) interneurons that are susceptible to oxidative stress are a subset of inhibitory GABAergic neurons regulating the excitability of pyramidal neurons, while dysfunction of PV interneurons is casually linked to many mental disorders including PTSD. We therefore hypothesized that environmental enrichment (EE), a method of enhanced cognitive, sensory and motor stimulation, can reverse the behavioral impairments by normalizing PV interneurons in a rat model of PTSD induced by inescapable foot shocks (IFS). Behavioral changes were determined by the open field, elevated plus maze, fear conditioning, and Morris water maze tests. The levels of nicotinamide adenosine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), NOX4, PV, glutamic acid decarboxylase 67 (GAD-67), and 8-hydroxy-2-deoxyguanosine (8-OH-dG) in the hippocampus and prefrontal cortex were determined. Our results showed that in this PTSD model, rats displayed the anxiety-like behavior, enhanced fear learning behavior, and hippocampus- dependent spatial memory deficit, which were accompanied by the up-regulation of NOX2, 8-OH-dG, and down-regulation of PV and GAD-67. Notably, EE reversed all these abnormalities. These results suggest that restoration of PV interneurons by inhibiting oxidative stress in the hippocampus and prefrontal cortex might represent a mechanism through which EE reverses the behavioral impairments in a rat model of PTSD induced by IFS.