Gender difference in the association of hyperuricemia with hypertension in a middle-aged Chinese population.

In this study, we report the relationship between hyperuricemia and hypertension in a middle-aged Chinese population, emphasizing the difference of gender. The cross-sectional study was conducted among 1776 adults aged 45-60 years, who participated in the Hefei Nutrition and Health Study (2012). Hyperuricemia was defined as serum uric acid (SUA)> 420 µmol/l for men, and > 360 µmol/l for women. Hypertension was defined as systolic blood pressure (SBP) ≥ 140 mmHg or diastolic blood pressure (DBP) ≥ 90 mmHg. Anthropometric measurements and biochemical data were collected using standardized procedures. Multivariate logistic regression analysis was performed to determine the relationship between hyperuricemia and hypertension with adjustment of potential confounding factors. Body mass index (BMI), waist circumference (WC), SBP, DBP, fasting glucose, SUA and the prevalence of hyperuricemia and hypertension were significantly higher in male than in female (p < 0.001). Females had significantly higher levels of triglycerides (TG) and high-density lipoprotein (HDL)-cholesterol (5.23 ± 0.87 vs 5.12 ± 1.01, p < 0.05, 1.50 ± 0.37 vs 1.28 ± 0.41, respectively.) than males. Simple correlation analysis showed that SUA was positively associated with WC and TG. In addition, after adjusting for potential confounders, hyperuricemia was associated with increased risk of hypertension in both males and females, with odds ratios (95% CI) of 1.680 (1.110-2.543) and 1.065 (1.012-1.118), respectively. Conclusions: The association of hyperuricemia with hypertension was stronger in males than in females, and middle-aged men with hyperuricemia had greater association with hypertension. Our findings remain to be confirmed in future prospective studies.

High-pressure microfluidisation-induced changes in the antigenicity and conformation of allergen Ara h 2 purified from Chinese peanut.

BACKGROUND: Peanut allergy is one of the most serious food allergies, and Ara h 2 is one of the most important peanut allergens as it is recognised by serum immunoglobulin E from more than 90% of peanut-allergic individuals. Dynamic high-pressure microfluidisation has been widely used in food processing as a new technology. The aim of this study was to investigate the effect of high-pressure microfluidisation on the antigenicity and structure of Ara h 2. Extracted peanut allergen Ara h 2 was treated under a continuous pressure array of 60, 90, 120, 150 and 180 MPa. Immunoreactivity was measured by indirect enzyme-linked immunosorbent assay with rabbit polyclonal antibodies. Secondary structure was analysed by circular dichroism. Surface hydrophobicity and sulfhydryl groups were assessed via fluorescence and UV absorption spectra respectively. RESULTS: High-pressure microfluidisation treatment decreased the antigenicity of peanut allergen Ara h 2, changed its secondary structure and increased its UV absorption intensity and surface hydrophobicity. CONCLUSION: The change in conformation contributed to the decrease in antigenicity of Ara h 2, and the spatial conformation of peanut allergen Ara h 2 plays a critical role in its antigenicity.

[Effect of heat treatment on the antigenicity and conformation of peanut allergen Ara h 2].

Peanut allergen Ara h 2 was extracted from peanuts and was identified by SDS-PAGE and MALDI-TOF-MS. Effect of heat treatment on the antigenicity and structure of Ara h 2 was measured by indirect ELISA, CD, fluorescence and UV absorption spectra. The results showed that the antigenicity of Ara h 2 had a slight increase after being heated at 55 or 70 degrees C, while above 85 degrees C the antigenicity decreased significantly, and the antigeicity of Ara h 2 decreased with increasing temperature. The CD showed that the secondary structure of Ara h 2 was changed after heat treatment. The ANS fluorescence probe emission spectra analysis demonstrated that the heat treatment induced an increase in surface hydrophobicity of Ara h 2. The UV absorption spectra showed that the absorption maximum wavelength was increased when Ara h 2 was heated except the sample heating at 50 degrees C for 30 min. So the changes in conformation of Ara h 2 lead to the antigenicity degression.

Vitamin D-vitamin D receptor system down-regulates expression of uncoupling proteins in brown adipocyte through interaction with Hairless protein.

Our previous study showed that feeding mice with vitamin D deficiency diet markedly alleviated high-fat-diet-induced overweight, hyperinsulinemia, and hepatic lipid accumulation. Moreover, vitamin D deficiency up-regulated the expression of uncoupling protein 3 (Ucp3) in white adipose tissue (WAT) and brown adipose tissue (BAT). The present study aimed to further investigate the effects of vitamin D and vitamin D receptor (Vdr) on Ucp1-3 (Ucps) expression in brown adipocyte and the mechanism involved in it. Rat primary brown adipocytes were separated and purified. The effects of the 1,25(OH)2D3 (1,25-dihydroxyvitamin D3; the hormonal form of vitamin D) and Vdr system on Ucps expression in brown adipocytes were investigated in basal condition and activated condition by isoproterenol (ISO) and triiodothyronine (T3). Ucps expression levels were significantly down-regulated by 1,25(OH)2D3 in the activated brown adipocyte. Vdr silencing reversed the down-regulation of Ucps by 1,25(OH)2D3, whereas Vdr overexpression strengthened the down-regulation effects. Hairless protein did express in brown adipocyte and was localized in cell nuclei. 1,25(OH)2D3 increased Hairless protein expression in the cell nuclei. Hairless (Hr) silencing notably elevated Ucps expression in activated condition induced by ISO and T3. Moreover, immunoprecipitation results revealed that Vdr could interact with Hairless, which might contribute to decreasing expression of Vdr target gene Ucps. These data suggest that vitamin D suppresses expression of Ucps in brown adipocyte in a Vdr-dependent manner and the corepressor Hairless protein probably plays a role in the down-regulation.

Vitamin D Deficiency Aggravates Hepatic Oxidative Stress and Inflammation during Chronic Alcohol-Induced Liver Injury in Mice.

Vitamin D deficiency has been reported in alcoholics. This study is aimed at evaluating the effects of vitamin D deficiency on chronic alcohol-induced liver injury in mice. Mice were fed with modified Lieber-DeCarli liquid diets for 6 weeks to establish an animal model of chronic alcohol-induced liver injury. In the VDD+EtOH group, mice were fed with modified diets, in which vitamin D was depleted. Vitamin D deficiency aggravated alcohol-induced liver injury. Furthermore, vitamin D deficiency aggravated hepatocyte apoptosis during alcohol-induced liver injury. Although it has a little effect on hepatic TG content, vitamin D deficiency promoted alcohol-induced hepatic GSH depletion and lipid peroxidation. Further analysis showed that vitamin D deficiency further increased alcohol-induced upregulation of hepatic inducible nitric oxide synthase (inos), two NADPH oxidase subunits p47phox and gp91phox, and heme oxygenase- (HO-) 1. By contrast, vitamin D deficiency attenuated alcohol-induced upregulation of hepatic antioxidant enzyme genes, such as superoxide dismutase (sod) 1 and gshpx. In addition, vitamin D deficiency significantly elevated alcohol-induced upregulation of hepatic proinflammatory cytokines and chemokines. Taken together, these results suggest that vitamin D deficiency aggravates hepatic oxidative stress and inflammation during chronic alcohol-induced liver injury.

Vitamin D Deficiency Attenuates Acute Alcohol-Induced Hepatic Lipid Accumulation in Mice.

Vitamin D deficiency has been frequently reported in chronic liver disease. However, its influence on hepatic lipid accumulation in alcoholic liver disease remains unclear. The present study investigated the effects of vitamin D deficiency on acute alcohol-induced hepatic lipid metabolism in mice. Mice were fed with vitamin D deficient diet, in which vitamin D was depleted for 12 weeks to establish an animal model of vitamin D deficiency. Some mice were administered a single gavage of alcohol (4 g/kg bodyweight) before they were euthanized. Results show that feeding mice with vitamin D deficient diet did not induce hepatic lipid accumulation. In contrast, vitamin D deficiency markedly reduced alcohol-induced triacylglycerol (TAG) content and prevented hepatic lipid accumulation. Moreover, vitamin D deficiency significantly attenuated alcohol-induced sterol-regulated element-binding protein (SREBP)-1c activation, which regulates genes for hepatic fatty acid (FA) and TAG synthesis, and the expression of its target genes fatty acid synthase (Fasn) and acetyl-coenzyme- A carboxylase (Acc). In addition, vitamin D deficiency alleviated alcohol-induced downregulation of hepatic nuclear peroxisome proliferator-activated receptor (PPAR)α, which governs FA transport and ß-oxidation, and the expression of Carnitine palmitoyltransferase (Cpt)-1α, cytochrome P450, family 4, subfamily a, polypeptide (Cyp4a)10, and Cyp4a14, which are key enzymes for hepatic fatty acids ß-oxidation and ω-oxidation. Taken together, these results suggest that vitamin D deficiency is not a direct risk factor for hepatic lipid accumulation. Vitamin D deficiency alleviates acute alcohol-induced hepatic lipid accumulation through inhibiting hepatic de novo fatty acid syntheses and promoting fatty acid ß-oxidation and ω-oxidation.

Vitamin d deficiency attenuates high-fat diet-induced hyperinsulinemia and hepatic lipid accumulation in male mice.

It is increasingly recognized that vitamin D deficiency is associated with increased risks of metabolic disorders among overweight children. A recent study showed that vitamin D deficiency exacerbated inflammation in nonalcoholic fatty liver disease through activating toll-like receptor 4 in a high-fat diet (HFD) rat model. The present study aimed to further investigate the effects of vitamin D deficiency on HFD-induced insulin resistance and hepatic lipid accumulation. Male ICR mice (35 d old) were randomly assigned into 4 groups as follows. In control diet and vitamin D deficiency diet (VDD) groups, mice were fed with purified diets. In HFD and VDD+HFD groups, mice were fed with HFD. In VDD and VDD+HFD groups, vitamin D in feed was depleted. Feeding mice with vitamin D deficiency diet did not induce obesity, insulin resistance, and hepatic lipid accumulation. By contrary, vitamin D deficiency markedly alleviated HFD-induced overweight, hyperinsulinemia, and hepatic lipid accumulation. Moreover, vitamin D deficiency significantly attenuated HFD-induced up-regulation of hepatic peroxisome proliferator-activated receptor γ, which promoted hepatic lipid uptake and lipid droplet formation, and its target gene cluster of differentiation 36. In addition, vitamin D deficiency up-regulated carnitine palmitoyltrans 2, the key enzyme for fatty acid ß-oxidation, and uncoupling protein 3, which separated oxidative phosphorylation from ATP production, in adipose tissue. These data suggest that vitamin D deficiency is not a direct risk factor for obesity, insulin resistance, and hepatic lipid accumulation. Vitamin D deficiency alleviates HFD-induced overweight, hyperinsulinemia, and hepatic lipid accumulation through promoting fatty acid ß-oxidation and elevating energy expenditure in adipose tissue.

Effects of maternal LPS exposure during pregnancy on metabolic phenotypes in female offspring.

It is increasingly recognized that intra-uterine growth restriction (IUGR) is associated with an increased risk of metabolic disorders in late life. Previous studies showed that mice exposed to LPS in late gestation induced fetal IUGR. The present study investigated the effects of maternal LPS exposure during pregnancy on metabolic phenotypes in female adult offspring. Pregnant mice were intraperitoneally injected with LPS (50 µg/kg) daily from gestational day (GD)15 to GD17. After lactation, female pups were fed with standard-chow diets (SD) or high-fat diets (HFD). Glucose tolerance test (GTT) and insulin tolerance test (ITT) were assessed 8 and 12 weeks after diet intervention. Hepatic triglyceride content was examined 12 weeks after diet intervention. As expected, maternal LPS exposure during pregnancy resulted in fetal IUGR. Although there was an increasing trend on fat mass in female offspring whose dams were exposed to LPS during pregnancy, maternal LPS exposure during pregnancy did not elevate the levels of fasting blood glucose and serum insulin and hepatic triglyceride content in female adult offspring. Moreover, maternal LPS exposure during pregnancy did not alter insulin sensitivity in adipose tissue and liver in female adult offspring. Further analysis showed that maternal LPS exposure during pregnancy did not exacerbate HFD-induced glucose tolerance and insulin resistance in female adult offspring. In addition, maternal LPS exposure during pregnancy did not aggravate HFD-induced elevation of hepatic triglyceride content in female adult offspring. In conclusion, LPS-induced IUGR does not alter metabolic phenotypes in adulthood.