Effects of vitamin D deficiency on chronic alcoholic liver injury.

Vitamin D deficiency (VDD) has been found among alcoholics. However, little is known about the effect of VDD on alcoholic liver disease and the molecular mechanisms remain unclear. The aim of the current study was to evaluate whether vitamin D was deficient among patients with alcoholic fatty liver disease (AFLD) and the effect of VDD on chronic alcoholic liver injury and possible molecular mechanisms in mice. Our results found that lower 25-hydroxyvitamin D [25(OH)D] concentrations in patients with AFLD. And further analysis found that 25(OH)D is a protective factor in patients with AFLD. Mice experiments indicated that VDD can alter the composition of gut microbiota, down-regulate the protein levels of intestinal tight junction protein Occludin and E-cadherin, up-regulate the expression of inflammatory cytokines (tnf-α, il-1ß, il-6, il-8, ccl2, il-10) in liver and colon tissue. And further exacerbated the protein levels of p65,P-IκB,P-p65 in alcoholic liver injury mice. In conclusion, VDD aggravates chronic alcoholic liver injury by activating NF-κB signaling pathway.

Effects of different dietary patterns during pregnancy on birth outcomes and glucose parameters in women with gestational diabetes mellitus: A systematic review and meta-analysis.

PURPOSE: Dietary interventions are the cornerstone of gestational diabetes mellitus (GDM) treatment. This study aimed to evaluate the effects of dietary patterns during pregnancy on birth outcomes and glucose parameters in women with GDM. METHODS: PubMed, Embase, and The CoChrane Library were searched from the time of database creation to November 30, 2021, along with manual searches. Data analyses were performed using Stata 15.4 software. RESULTS: From 2461 studies, 27 RCTs involving 1923 women were eligible. The pooled results showed that dietary pattern interventions during pregnancy reduced birth weight (WMD: -0.14 kg; 95% CI: -0.24, -0.00), hemoglobin A1 C (HbA1 C) (WMD: -0.19, 95% CI: -0.34, -0.05), and macrosomia incidence (RR 0.65 [95% CI 0.48, 0.88]). Low glycemic index (GI) diet reduced macrosomia incidence (RR 0.31 [95% CI 0.11, 0.93]) and fasting plasma glucose (FPG) levels (WMD: -0.10 mmol/L; 95% CI: -0.14, -0.05); a low carbohydrate (CHO) diet reduced large for gestational age (LGA) incidence (RR 0.33 [95% CI 0.13, 0.82]) and HbA1 C (WMD: -0.32; 95% CI: -0.51, -0.14); dietary approaches to stop hypertension (DASH) diet reduced birth weight (WMD:-0.59 kg; 95% CI: -0.64, -0.55), insulin use (RR 0.31 [95% CI 0.18, 0.56), macrosomia incidence (RR 0.12 [95% CI 0.03, 0.50]), and cesarean sections incidence (RR 0.57 [95% CI 0.40, 0.82]). CONCLUSION: Dietary patterns during pregnancy can improve certain birth outcomes and glycemic parameters. Due to limitations in the quality and number of included studies, the above findings still need to be validated by further randomized controlled trials with high quality and large samples.

Docosahexaenoic acid protects against lipopolysaccharide-induced fetal growth restriction via inducing the ubiquitination and degradation of NF-κB p65 in placental trophoblasts.

Lipopolysaccharide (LPS) could induce adverse birth outcomes by evoking inflammation. We investigated the effect and mechanism of docosahexaenoic acid (DHA) on LPS-induced placental inflammation and fetal growth restriction (FGR). In vivo, pregnant CD-1 mice were divided into four groups: Ctrl, DHA, LPS and DHA+LPS group. We found that DHA pretreatment reduced the incidence of FGR induced by LPS and activated the expression of peroxisome proliferators-activated receptor gamma (PPARγ) in placental tissue. Moreover, the LPS-induced increase of mRNA levels of Tnf-α, Il-6, Il-1ß, Mip-2 and Kc in placental tissue was significantly attenuated by DHA pretreatment. A similar effect of DHA was observed in serum of pregnant mice and amniotic fluid. In contrast, the levels of the IL-10 were significantly increased after DHA pretreatment. In vitro, we clarified that DHA antagonized the activation of the NF-κB signaling pathway induced by LPS, which was dependent on PPARγ. Subsequently, CHX (translation inhibitor) was used to indicated that PPARγ significantly increased the degradation rate of p65, an effect that was inhibited by MG132 (proteasome inhibitor) treatment. Finally, it was confirmed that the activation of PPARγ could significantly promote the ubiquitination and degradation of p65. Our results suggested that DHA alleviated LPS-induced inflammatory responses and FGR by activating PPARγ expression, leading to p65 ubiquitination and degradation.

Higher dietary insulinaemic potential is associated with increased risk of liver steatosis and fibrosis.

BACKGROUND AND AIMS: Hyperinsulinaemia and insulin resistance play a central role in the progression of hepatic steatosis and fibrosis, and diet can modulate insulin response. We thus hypothesised that diet with higher insulinaemic potential is associated with an increased risk of these conditions. METHODS: Two empirically dietary indices for hyperinsulinaemia (EDIH) and insulin resistance (EDIR) were derived to identify food groups most predictive of fasting concentrations of C-peptide and insulin and homeostatic model assessment for insulin resistance respectively. Hepatic steatosis and fibrosis were defined by controlled attenuation parameter and liver stiffness measurement using transient elastography (TE). Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by logistic regression. RESULTS: Of the 4171 participants with TE examination, 1436 (age-standardised prevalence, 33.8%) were diagnosed with steatosis, 255 (5.6%) with advanced fibrosis and 101 (2.2%) with cirrhosis. The multivariable-adjusted ORs for participants comparing the highest to the lowest EDIH tertile were 1.17 (95% CI: 0.99-1.39, Ptrend  = .005) for steatosis, 1.74 (95% CI: 1.24-2.44, Ptrend  = .001) for advanced fibrosis and 2.05 (95% CI: 1.21-3.46, Ptrend  = .004) for cirrhosis. Similar associations were observed for EDIR with ORs of 1.32 (95% CI: 1.11-1.55, Ptrend  < .001) for steatosis and 1.43 (95% CI: 1.03-1.99, Ptrend  = .006) for advance fibrosis. These positive associations remained among never drinkers and individuals who were free of hepatitis B and/or C. CONCLUSIONS: Our findings suggest that hyperinsulinaemia and insulin resistance may partially underlie the influence of diet on hepatic steatosis and fibrosis, and highlight the importance of reducing or avoiding insulinaemic dietary pattern.

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.

The effect of Chinese famine exposure in early life on dietary patterns and chronic diseases of adults.

OBJECTIVE: To assess the effect of famine exposure during early life on dietary patterns, chronic diseases, and the interaction effect between famine exposure and dietary patterns on chronic diseases in adulthood. DESIGN: Cross-sectional study. Dietary patterns were derived by factor analysis. Multivariate quantile regression and log-binomial regression were used to evaluate the impact of famine exposure on dietary patterns, chronic diseases and the interaction effect between famine exposure and dietary patterns on chronic diseases, respectively. SETTING: Hefei, China. PARTICIPANTS: Adults aged 45-60 years (n 939). RESULTS: 'Healthy', 'high-fat and high-salt', 'Western' and 'traditional Chinese' dietary patterns were identified. Early-childhood and mid-childhood famine exposure were remarkably correlated with high intake of the traditional Chinese dietary pattern. Compared with the non-exposed group (prevalence ratio (PR); 95 % CI), early-childhood (3·13; 1·43, 6·84) and mid-childhood (2·37; 1·05, 5·36) exposed groups showed an increased PR for diabetes, and the early-childhood (2·07; 1·01, 4·25) exposed group showed an increased PR for hypercholesterolaemia. Additionally, relative to the combination of non-exposed group and low-dichotomous high-fat and high-salt dietary pattern, the combination of famine exposure in early life and high-dichotomous high-fat and high-salt dietary pattern in adulthood had higher PR for diabetes (4·95; 1·66, 9·05) and hypercholesterolaemia (3·71; 1·73, 7·60), and significant additive interactions were observed. CONCLUSIONS: Having suffered the Chinese famine in childhood might affect an individual's dietary habits and health status, and the joint effect between famine and harmful dietary pattern could have serious consequences on later-life health outcomes.

The relationship between famine exposure during early life and body mass index in adulthood: A systematic review and meta-analysis.

BACKGROUND: Previous epidemiologic studies have reported famine exposure during early life association with overweight or obesity in adulthood, but a consistent perspective has not been established to date. PURPOSE: To determine, by conducting a systematic review and meta-analysis, whether exposure to famine could increase body mass index (BMI) in adult or not, and assess the association between famine exposure and the risk of overweight or obesity. METHODS: Published articles were systematically searched (until August, 2017) from PubMed, ScienceDirect, Cochrane, and China National Knowledge Infrastructure. Initially, comparing differences in BMI between exposed and non-exposed groups that weight mean difference (WMD) were used. Subsequently, the effect of famine exposure on overweight or obesity risk, which pooled relative risks (RRs), odds ratios (ORs) or hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using a random-effects model. RESULT: Twenty studies were included in this systematic review and meta-analysis. Compared with non-exposed group, famine exposure group significantly increased the risk of overweight (OR = 1.10, 95% CI: 1.04-1.16) and obesity (OR = 1.15, 95% CI: 1.05-1.24). Sensitivity analyses revealed no significant change in the famine exposure and BMI, the risk of overweight and obesity study when any one study was excluded. Subgroup analyses showed that age, gender, exposure type, study type, continent, famine cause and paper publication date were associated with BMI, the risk of overweight and obesity. Meta-regression analyses suggested that continent, famine cause could partially explain heterogeneity for famine exposure and BMI studies. CONCLUSION: The systematic review and meta-analysis indicates that famine exposure during early life may increase BMI, the risk of overweight and obesity, especially for female, fetal famine exposure or subject age less than 50. Furthermore, famine exposure group the risk of overweight and obesity in cross-sectional studies, Asian studies, famine cause by natural disaster or paper published from 2015 to the present studies are higher than that of non-exposed group.

Maternal and cord blood fatty acid patterns with excessive gestational weight gain and neonatal macrosomia.

BACKGROUND AND OBJECTIVES: This study evaluated the association of maternal excessive gestational weight gain with saturated and polyunsaturated fatty acid concentrations in maternal and cord serum. METHODS AND STUDY DESIGN: We included 77 pairs of women and their newborns and classified them into three groups as follows: mothers with normal gestational weight gain and their babies with normal birth weight in group I (30 pairs), mothers with excessive gestational weight gain and their babies with normal birth weight in group II (30 pairs), and mothers with excessive gestational weight gain and their macrosomic babies in group III (17 pairs). Serum fatty acid concentrations were determined through gas chromatography-mass spectrometry. RESULTS: No remarkable difference in maternal dietary intake was observed among the three groups. C16:0, C18:0, eicosapentaenoic acid, and docosahexaenoic acid concentrations were significantly higher in group III mothers than in group I mothers. Compared with group I neonates, total saturated and polyunsaturated fatty acid concentrations were significantly lower but total n-3 polyunsaturated fatty acid and docosahexaenoic acid concentrations were significantly higher in group II neonates (p<0.05). The n-6: n-3 ratio in maternal and cord serum was approximately 10:1 and 1.5:1, respectively. CONCLUSION: Women with excessive gestational weight gain who deliver a macrocosmic neonate tend to have higher total saturated fatty acid concentrations but lower docosahexaenoic acid concentrations in their neonate cord serum. Fatty acid concentrations in maternal and cord serum are not associated with maternal dietary pattern.

Physiological and behavioral responses in offspring mice following maternal exposure to sulfamonomethoxine during pregnancy.

Sulfamonomethoxine (SMM), a veterinary antibiotic, is widely used in China. However, the impacts of maternal SMM exposure on neurobehavioral development in early life remain little known. In this study, we investigated the effects of maternal SMM exposure during pregnancy on behavioral and physiological responses in offspring mice. Pregnant mice were randomly divided into three SMM-treated groups, namely low-(10mg/kg/day), medium-(50mg/kg/day), and high-dose (200mg/kg/day), and a control group. The pregnant mice in the SMM-treated groups received SMM by gavage daily from gestational day 1-18, whereas those in the control received normal saline. On postnatal day (PND) 50, spatial memory was assessed using the Morris water maze test, and anxiety was measured using the elevated plus-maze and open field tests. The results showed significantly increased blood glucose in pups whose mothers received a high SMM dose. In addition, maternal SMM exposure increased anxiety-related activities among the offspring; spatial learning and memory were impaired more severely in the male offspring. The contents of tetrahydrobiopterin (BH4) and brain-derived neurotrophic factors (BDNF) on PND 22 were significantly reduced in the male offspring of the high-dose group compared with the controls. These findings indicate that SMM may be identified as a risk factor for cognitive and behavioral development on the basis of gender and that it may be associated with diminished BH4 and BDNF levels early in life.

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.

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.

[Impact of oral vitamin D supplementation in early life on diabetic mice induced by streptozotocin].

OBJECTIVE: To evaluate the effect of oral vitamin D supplementation in early life on blood glucose, insulin content, diabetes incidence, and histomorphology in pancreatic islet induced by streptozotocin. METHODS: Three-week-old C57BL/6 mice were given either control diet (American Institute of Nutrition [AIN]-93G), or three different dose of vitamin D-supplemented diet. Nine weeks after dietary intervention, C57BL/6 mice were treated with streptozotocin i.p. for 5 consecutive days. After injection of STZ, The fasting blood glucose and diabetes incidence was tested once a week. The insulin content, histomorphology in pancreatic islets was conducted at the end of experiments. RESULTS: (1) Vitamin D supplementation in early life can decrease the fasting blood glucose values induced by STZ, and the decreases effect of high dose vitamin D-supplemented group is the most significant (P<0.01). (2) Vitamin D supplementation in early life can prevent diabetes incidence, and the decreases effect of high dose vitamin D-supplemented group is the most significant, fully suppress the onset of diabetes about four weeks later after injected by STZ (P<0.01). (3) As compared to the control group, insulin content in medium and high dose vitamin D-supplemented groups were significantly up-regulated after injection of STZ (P<0.05), and the effect of high dose vitamin D-supplemented group is the most significant. (4) The damage of pancreatic islets induced by STZ was clearly restored in medium and high dose vitamin D-supplemented groups, and effect of high dose vitamin D-supplemented group is the most significant. CONCLUSION: Oral vitamin D supplementation in early life can decrease the fasting blood glucose values, prevent diabetes incidence, up-regulate insulin content, restored the damage of pancreatic islets induced by STZ, and effects of high dose vitamin D-supplementde group are all the most significant.

A potential practical approach to reduce Ara h 6 allergenicity by gamma irradiation.

Peanut allergen Ara h 6 was isolated and irradiated at 1, 3, 5, or 10 kGy, and a whole peanut protein extract (WPPE) was also treated by irradiation. Alteration in structure of Ara h 6 was characterised by circular dichroism (CD) spectroscopy, ultraviolet (UV) absorption spectroscopy, fluorescence spectroscopy and SDS-PAGE, and antigenicity was evaluated by immunoblotting and indirect ELISA with anti-Ara h 6 polyclonal antibody. Irradiation induced significant changes in the secondary and tertiary structures of Ara h 6, and the antigenicity of both purified Ara h 6 and WPPE were reduced upon increasing the irradiation doses. Moreover, a good correlation between the loss in α-helix and IgG binding to Ara h 6 was observed. This indicated that irradiation might be an efficient approach to reduce or eliminate peanut allergenicity.

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.