Hospitalization of patients with nutritional anemia in the United States in 2020.

Background: Nutritional anemia is highly prevalent and has triggered a globally recognized public health concern worldwide. Objective: To better understand the prevalence of anemia and the state of nutritional health in developed countries to inform global nutritional health and better manage the disease. Method: We employed the Healthcare Cost and Utilization Project (HCUP)-2020 National Inpatient Health Care Data (NIS), administered by The Agency for Healthcare Research and Quality. Nutritional anemia was diagnosed according to the International Classification of Diseases, 10th Revision (ICD-10). Matching analysis and multivariate regression were used to adjust for patient and hospital characteristics. Controls were obtained by stratifying and matching for age and sex. Results: The 2020 HCUP-NIS database encompassed a survey over 6.4 million hospitalized patients, among which 1,745,350 patients diagnosed with anemia, representing approximately 26.97% of the hospitalized population, over 310,000 were diagnosed with nutritional anemia, and 13,150 patients were hospitalized for nutritional anemia as primary diagnosis. Hospitalization rate for nutritional anemia exhibited an increased age-dependent increase nationwide, especially among females, who displayed 1.87 times higher than males. Notably, in comparison to the control group, individuals of the Black race exhibit a higher prevalence of nutritional anemia (case group: 21.7%, control group: 13.0%, p < 0.001). In addition, hospitalization rates were higher among low-income populations, with lower rates of private insurance (case group: 18.7%, control group: 23.5%, p < 0.001) and higher rates of Medicaid insurance (case group: 15.4%, control group: 13.9%, p < 0.001). In areas characterized by larger urban centers and advanced economic conditions within the urban-rural distribution, there was an observed increase in the frequency of patient hospitalizations. Iron deficiency anemia emerged as the predominant subtype of nutritional anemia, accounting for 12,214 (92.88%). Secondary diagnosis among patients hospitalized for nutritional anemia revealed that a significant number faced concurrent major conditions like hypertension and renal failure. Conclusion: In economically prosperous areas, greater attention should be given to the health of low-income individuals and the older adult. Our findings hold valuable insights for shaping targeted public health policies to effectively address the prevalence and consequences of nutritional anemia based on a overall population health.

Association between phthalate exposure and obesity risk: A meta-analysis of observational studies.

According to epidemiological studies, phthalate exposure is associated with an increased risk of obesity in children and adults; however, these observations remain debatable. Therefore, we performed a systematic review and meta-analysis of the current literature to explore the effects of phthalate exposure on obesity. A systematic search was performed from inception to July 2022 in PubMed, EMBASE, Scopus, and Web of Science. Quality assessment was completed using criteria modified from Newcastle-Ottawa Scale (NOS) for the included studies. Meta-analysis showed that childhood exposure to MnBP, MBP, MEP, MiBP, and MECPP was positively correlated with obesity. In adults, MMP, MEP, and MiBP were positively correlated with adult abdominal obesity, while MEHHP, MECPP, and MCOP were positively correlated with adult general obesity. Subgroup analysis revealed that the positive correlation was particularly significant in women, as well as in Europe and the United States. Overall, a substantial association exists between phthalate exposure and obesity in children and adults. Sex and study site may provide limited sources of heterogeneity.

Di(2-ethylhexyl) phthalate disturbs cholesterol metabolism through oxidative stress in rat liver.

Di(2-ethylhexyl) phthalate (DEHP) is widely used and has been implicated in hepatotoxicity, although the mechanism is unclear. Here, we investigated the effect of DEHP on hepatic cholesterol metabolism in SD rats exposed to 0 and 300 mg/kg/day DEHP for 12 weeks. An RNA-Seq analysis was performed to describe the hepatic responses to long-term DEHP exposure in combination with serological and oxidative stress parameter measurements. DEHP increased the serum levels of total cholesterol (TC), high-density lipoprotein (HDL), and alanine transaminase (ALT). Moreover, DEHP increased the content of malondialdehyde (MDA) and decreased antioxidant enzyme activities in the liver. Transcriptomic results revealed that DEHP dramatically changed the cholesterol metabolism pathway and oxidation-reduction process and depressed gene expression involved in cholesterol efflux and monooxygenase activity. Total antioxidant capacity (T-AOC) positively correlated with Abcg5 and Abcg8. Overall, this study showed the mechanisms underlying hepatotoxicity caused by DEHP, providing new insights into understanding DEHP poisoning.

Integrated metabolomics and transcriptomics reveal di(2-ethylhexyl) phthalate-induced mitochondrial dysfunction and glucose metabolism disorder through oxidative stress in rat liver.

Di(2-ethylhexyl) phthalate (DEHP) is a ubiquitous pollutant that results in hepatotoxicity. However, an understanding of the systematic mechanism of hepatic injury caused by DEHP remains limited. Here, we performed a comprehensive metabolomics and transcriptomics analyses to describe hepatic responses of rats to long-term DEHP exposure and, together with pathology and functional injury of liver, systematically analyzed the pathogenesis and mechanisms of liver damage. SD rats were exposed to 0 and 600 mg/kg/day DEHP for 12 weeks. Thereafter, biochemical indicators and histopathological changes regarding liver function were detected. Metabolomics and transcriptomics profiles of rat liver samples were analyzed using a UPLC-MS/MS system and Illumina Hiseq 4000, respectively. DEHP induced hepatocyte structural alterations and edema, depressed monooxygenase activity, decreased antioxidant activities, aggravated oxidative damage, blocked the tricarboxylic acid cycle and respiratory chain, and disturbed glucose homeostasis in the liver. These findings indicate that reactive oxygen species play a major role in these events. Overall, this study systematically depicts the comprehensive mechanisms of long-term DEHP exposure to liver injury and highlights the power of metabolomics and transcriptomics platforms in the mechanistic understanding of xenobiotic hepatotoxicity.

Novel insights into di­(2­ethylhexyl)phthalate activation: Implications for the hypothalamus­pituitary­thyroid axis.

Di (2­ethylhexyl) phthalate (DEHP), an environmental pollutant, is widely used as a plasticizer and causes serious pollution in the ecological environment. As previously reported, exposure to DEHP may cause thyroid dysfunction of the hypothalamic­pituitary­thyroid (HPT) axis. However, the underlying role of DEHP remains to be elucidated. The present study performed intragastrical administration of DEHP (150, 300 and 600 mg/kg) once a day for 90 consecutive days. DEHP­stimulated oxidative stress increased the thyroid follicular cavity diameter and caused thyrocyte oedema. Furthermore, DEHP exposure altered mRNA and protein levels. Thus, DEHP may perturb TH homeostasis by affecting biosynthesis, biotransformation, bio­transportation, receptor levels and metabolism through disruption of the HPT axis and activation of the thyroid­stimulating hormone (TSH)/TSH receptor signaling pathway. These results identified the formerly unappreciated endocrine­disrupting activities of phthalates and the molecular mechanisms of DEHP­induced thyrotoxicity.

Rosmarinic acid alleviates di-2-ethylhexyl phthalate (DEHP) -induced thyroid dysfunction via multiple inflammasomes activation.

DEHP (di-2-ethylhexyl phthalate), an environmental endocrine disruptor, is widely used in industrial products, particularly as plasticizers and softeners which could disrupt the function of the hypothalamic-pituitary-thyroid (HPT) axis. Rosmarinic acid (RA) possesses potential antioxidant and anti-inflammatory capacities in disease models. Nevertheless, evidence on the association between DEHP-induced thyroid dysfunction and inflammation, as well as the molecular mechanism underlying the protective effects of RA-mitigated DEHP-induced thyroid injury remains inconclusive. Male Sprague Dawley (SD) rats were intragastrically administered DEHP (150 mg/kg, 300 mg/kg, 600 mg/kg) once a day for 90 consecutive days. Also, FRTL-5 cells were treated with a wide range of DEHP concentrations (10-8, 10-7, 10-6, 10-5, 10-4, 10-3, 10-2 M) for 24 hr. Subsequently, RA (50 µM) was administered for 24 hr before 10-4 M DEHP challenge. We found that DEHP induced thyroid damage and inflammatory infiltration in vivo. In addition, we showed that DEHP triggered inflammatory cell death, which is mediated by multiple inflammasomes. Moreover, RA, pyroptosis inhibitor (Ac-YVAD-cmk) and antioxidant inhibitor (NAC) treatment significantly alleviated DEHP-induced thyrocyte death, suppressing pro-inflammatory cytokine production, inhibiting multiple inflammasomes activation and attenuating thyrocyte death, respectively. Collectively, our results reveal that a critical role of inflammasomes activation in DEHP-induced thyroid injury, and suggest that RA confers protection against DEHP-induced thyroid inflammation, and facilitating control of the effects of DEHP after given pyroptosis inhibitor or antioxidant inhibitor. These results indicate that it should be possible to provide novel insights into toxicologically and pharmacologically targeting this molecule to DEHP-induced inflammation.

Effect of Ambient PM2.5-Bound BbFA and DahA on Small Airway Dysfunction of Primary Schoolchildren in Northeast China.

Given the lack of research on the schoolchildren exposure to PM2.5-bound PHAs in northeast China, we investigated the effects of exposure to ambient benzo[b]fluoranthene (BbFA) and dibenz[a,h]anthracene (DahA) bound to PM2.5 on pulmonary ventilation dysfunction (PVD) and small airway dysfunction (SAD). PM2.5 samples at two schools (A and B) were collected, and the concentrations of PM2.5-bound 4-6-ring PAHs were analyzed. PVD and SAD were evaluated by pulmonary function tests in 306 students while urinary MDA and CRP levels were measured. The results confirmed that ambient PM2.5-bound 4-6-ring PHA levels were significantly higher and the PVD and SAD incidence in schools A and B were increased during the heating season. We found that PM2.5-bound BbFA, BkFA, BaP, and DahA levels were only correlated with SAD in schoolchildren; the correlation coefficients of BbFA and DahA were the highest effect estimates, possibly due to altered MDA levels. Therefore, this research enables us to better understand the effects of exposure to ambient PM2.5-bound PHAs on pulmonary function parameters. Our results also showed that identification of hazardous PM2.5-bound BbFA and DahA to health is crucial for preventing the respiratory-related diseases.

Biomarker Identification of Maternal Genistein Exposure Induced Obesity by Metabonomics Analysis.

The objective of this study was to confirm the effect of maternal genistein exposure on body weight of male offspring and the metabolic alterations associated with maternal genistein-induced obesity. Pregnant female Sprague-Dawley (SD) rats were supplemented with 300 mg/kg diet of genistein (GEN) or no genistein (CON) throughout pregnancy and lactation. The growth of male offspring was investigated until 12 week age and the mechanism of obesity was studied using metabonomics by ultra performance liquid chromatography and quadrupole time-of-flight (UPLC Q-TOF) MS with electrospray ionization in positive ESI mode (ESI+). Compared with the CON group, body weight, fat pad and food intake of male offspring in GEN group were increased significantly at the age of weeks 10 to 12 (p<0.05). Ten urine principal metabolites contributing to the clusters were identified, including increased 8-Isoprostaglandin F2a, and decreased L-Proline, Betaine, L-Acetylcarnitine, Norsalsolinol, Indoleacrylic acid, L-Tryptophan, Lysophosphatidylcholines (LysoPC) (20 : 4), Lysophosphatidylethanolamines (LysoPE) (18 : 1) and LysoPC (O-18 : 0). Our results confirmed weight-increasing effects of maternal genistein exposure, accompanied by favorable changes in metabolites in the male offspring' urine. Therefore, this research enables us to better understand obesity and predict risk of obesity-related disease by studying metabolites present in the urine.

Transcriptomics and metabonomics analyses of maternal DEHP exposure on male offspring.

The objectives of this study were to evaluate the effect of maternal Di-2-ethylhexyl phthalate (DEHP) exposure on male offspring and to explore the mechanism of changes with the metabolic alterations and differential genes. Pregnant female Sprague-Dawley (SD) rats were intragastrically administered with 600 mg/kg body weight of DEHP or corn oil (CON) throughout pregnancy and lactation. The growth of male offspring was investigated until 14 weeks old, the indices of blood were detected, and mechanism was studied using metabonomics and transcriptomics. Compared with the CON group, body weight, body length, food intake, body fat weight, Lee's index, organ coefficient, blood lipids, and oral glucose tolerance test (OGTT) of male offspring were not significantly changed in maternal DEHP group. However, serum biochemical indexes such as alanine transaminase (ALT), total protein (TP), albumin (ALB), blood urea nitrogen (BUN), and creatinine (CREA) were markedly reduced in maternal DEHP group (p < 0.05). In addition, insulin level was elevated and catalase (CAT) level was decreased notably in maternal DEHP group compared with the CON group (p < 0.05). Furthermore, thyroxine (T4) level was lower and thyroid stimulating hormone (TSH) level was higher in maternal DEHP group (p < 0.05). Metabonomics revealed seven principal metabolites were identified, including increased L-allothreonine, creatine, uric acid, retinyl ester, L-palmitoylcarnitine, and decreased glycocholic acid and LysoPC (18:3). Transcriptomics displayed 35 differential genes were involved in the mechanism of maternal DEHP exposure. Therefore, this research confirms the effect of a certain dose of maternal DEHP exposure on male offspring and understands exactly the mechanism of these changes with metabonomics and transcriptomics.

Urinary metabolomic profiling in rats exposed to dietary di(2-ethylhexyl) phthalate (DEHP) using ultra-performance liquid chromatography quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF-MS).

Di(2-ethylhexyl) phthalate (DEHP) is an omnipresent environmental chemical with widespread nonoccupational human exposure through multiple ways. Although considerable efforts have been invested to investigate mechanisms of DEHP toxicity, the key metabolic biomarkers of DEHP toxicity remain to be identified. The aim of this study was to assess the urinary metabonomics of dietary DEHP in rats using the technique of ultra-performance liquid chromatography quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF-MS). Fourteen female Wistar rats were divided into two groups and given increasing dietary doses of DEHP for 30 consecutive days. The urinary metabolite profile was studied using ultra-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry. Principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA) enabled clusters to be clearly separated. Eleven principal urinary metabolites were identified as contributing to the clusters. The clusters in the positive electrospray ionization (ESI) mode were xanthurenic acid, kynurenic acid, nonate, N6-methyladenosine, and L-isoleucyl-L-proline. The clusters in the negative ESI mode were hippuric acid, tetrahydrocortisol, citric acid, phenylpropionylglycine, cPA(18:2(9Z, 12Z)/0:0), and LysoPC(14:1(9Z)). The urinary metabonomic changes indicated that exposure to dietary DEHP can affect energy-related metabolism, liver and renal function, fatty acid metabolism, and cause DNA damage in rats. The findings of this study on the urinary metabolites and metabolic pathways of DEHP may form the basis for future studies on the mechanisms of toxicity of this commonly found environmental chemical.

Effects of Long-Term In Vivo Exposure to Di-2-Ethylhexylphthalate on Thyroid Hormones and the TSH/TSHR Signaling Pathways in Wistar Rats.

Di-(2-ethylhexyl)phthalate (DEHP) was a widely used chemical with human toxicity. Recent in vivo and in vitro studies suggested that DEHP-exposure may be associated with altered serum thyroid hormones (THs) levels, but the underlying molecular mechanisms were largely unknown. To explore the possible molecular mechanisms, 128 Wistar rats were dosed with DEHP by gavage at 0, 150, 300, and 600 mg/kg/day for 3 months (M) and 6 M, respectively. After exposure, expression of genes and proteins in the thyroid, pituitary, and hypothalamus tissues of rats were analyzed by Q-PCR and western blot, while the sera and urine samples were assayed by radioimmunoassay and ELISA. Results showed that serum THs levels were suppressed by DEHP on the whole. DEHP treatment influenced the levels of rats' thyrotropin releasing hormone receptor (TRHr), Deiodinases 1 (D1), thyroid stimulating hormone beta (TSHß), sodium iodide symporter (NIS), thyroid stimulating hormone receptor (TSHr), thyroperoxidase (TPO), thyroid transcription factor 1 (TTF-1), and thyroglobulin (TG) mRNA/protein expression in the hypothalamus-pituitary-thyroid (HPT) axis and decreased urine iodine. Taken together, observed findings indicate that DEHP could reduce thyroid hormones via disturbing the HPT axis, and the activated TSH/TSHR pathway is required to regulate thyroid function via altering TRHr, TSHß, NIS, TSHr, TPO, TTF-1 and TG mRNA/protein expression of the HPT axis.

Bioelectricity generation and dewatered sludge degradation in microbial capacitive desalination cell.

Microbial desalination cell (MDC) is a new approach for the synergy in bioelectricity generation, desalination and organic waste treatment without additional power input. However, current MDC systems cause salt accumulation in anodic wastewater and sludge. A microbial capacitive desalination cell (MCDC) with dewatered sludge as anodic substrate was developed to address the salt migration problem and improve the sludge recycling value by special designed-membrane assemblies, which consisted of cation exchange membranes (CEMs), layers of activated carbon cloth (ACC), and nickel foam. Experimental results indicated that the maximum power output of 2.06 W/m3 with open circuit voltage (OCV) of 0.942 V was produced in 42 days. When initial NaCl concentration was 2 g/L, the desalinization rate was about 15.5 mg/(L·h) in the first 24 h, indicating that the MCDC reactor was suitable to desalinize the low concentration salt solution rapidly. The conductivity of the anodic substrate decreased during the 42-day operation; the CEM/ACC/Ni assemblies could effectively restrict the salt accumulation in MCDC anode and promote dewatered sludge effective use by optimizing the dewatered sludge properties, such as organic matter, C/N, pH value, and electric conductivity (EC).

Aniline Induces Oxidative Stress and Apoptosis of Primary Cultured Hepatocytes.

The toxicity and carcinogenicity of aniline in humans and animals have been well documented. However, the molecular mechanism involved in aniline-induced liver toxicity and carcinogenesis remains unclear. In our research, primary cultured hepatocytes were exposed to aniline (0, 1.25, 2.50, 5.0 and 10.0 µg/mL) for 24 h in the presence or absence of N-acetyl-l-cysteine (NAC). Levels of reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH), activities of superoxide dismutase (SOD) and catalase (CAT), mitochondrial membrane potential, DNA damage, cell viability, and apoptosis were detected. Levels of ROS and MDA were significantly increased and levels of GSH and CAT, activity of SOD, and mitochondrial membrane potential in hepatocytes were significantly decreased by aniline compared with the negative control group. The tail moment and DNA content of the tail in exposed groups were significantly higher than those in the negative control group. Cell viability was reduced and apoptotic death was induced by aniline in a concentration-dependent manner. The phenomena of ROS generation, oxidative damage, loss of mitochondrial membrane potential, DNA damage and apoptosis could be prevented if ROS inhibitor NAC was added. ROS generation is involved in the loss of mitochondrial membrane potential and DNA injury, which may play a role in aniline-induced apoptosis in hepatocytes. Our study provides insight into the mechanism of aniline-induced toxicity and apoptosis of hepatocytes.

Interaction Effects between Organochlorine Pesticides and Isoflavones In Vitro and In Vivo.

Organochlorine pesticides (OCPs) have caused increasing global concern due to their high toxicity, persistence, bioaccumulation, and significant adverse effects on human health. This study was to explore the interaction effects between OCPs and isoflavones. Six kinds of OCPs and 2 kinds of isoflavones-genistein and daidzein were included to study their effect on MCF-7 cells in vitro. Eighty-one female Sprague-Dawley rats were randomized to 9 groups according to factorial design to study the interaction effect between isoflavones and γ-HCH. Compared to organochlorine pesticides alone group, proliferation rate of MCF-7 cells was lower in 100 µmol/L genistein + organochlorine pesticides and 100 µmol/L daidzein + organochlorine pesticides group (p < 0.05). In vivo study showed that there are interaction effects on kidney weight and liver weight when treated with isoflavones and γ-HCH. The changes in uterine morphology and positive expression of ERα showed inhibition effects between isoflavones and γ-HCH. In conclusion, the data suggests that there are interactions between isoflavones and OCPs in vitro and in vivo.

Soy isoflavone supplementation could reduce body weight and improve glucose metabolism in non-Asian postmenopausal women--a meta-analysis.

OBJECTIVE: The objective of this study was to conduct a systematic review and a meta-analysis to confirm the effects of soy isoflavone supplementation on body weight, fasting glucose, and insulin level in non-Asian postmenopausal women. METHODS: We searched the PubMed, EMBASE, and Cochrane databases up to October 2010 for randomized controlled trials regarding the effects of isoflavone supplementation on body weight, fasting glucose, and insulin level. Pooled estimates and 95% confidence intervals (CIs) were calculated by the fixed-and-random-effects model. RESULTS: Nine studies with 528 participants for body weight, 11 studies with 1182 participants for fasting glucose, and 11 studies with 1142 participants for fasting insulin were included, respectively. Significant reductions were found in body weight [weighted mean difference (WMD), -0.515; 95%CI: -0.895 to -0.134; P = 0.008), glucose level (WMD, -0.189; 95%CI: -0.344 to -0.033), and fasting insulin level (WMD, -0.940; 95%CI: -1.721 to -0.159) with soy isoflavone supplementation compared with placebo control group in non-Asian postmenopausal women after adjusted by unpublished studies. Furthermore, isoflavone supplementation in shorter duration (<6 mo) could significantly reduce body weight (WMD, -0.506; 95%CI: -0.888 to -0.124; P = 0.009) and longer duration (≥ 6 mo) could significantly reduce blood glucose in postmenopausal women (WMD, -0.270; 95%CI: -0.430 to -0.110; P = 0.001). Meanwhile, more reduction in body weight was observed in the lower dose subgroup (dose < 100 mg). Moreover, it is more effective to reduce body weight and fasting insulin level with soy isoflavone supplementation in normal weight (body mass index < 30) than obese (body mass index ≥ 30) women. CONCLUSIONS: This meta-analysis showed soy isoflavone supplementation could be beneficial for body weight reduction, glucose, and insulin control in plasma. Large and well-designed studies are recommended to confirm this conclusion.

Soy isoflavone and its effect to regulate hypothalamus and peripheral orexigenic gene expression in ovariectomized rats fed on a high-fat diet.

OBJECTIVE: To explore the effect of soy isoflavone on obesity in the light of hypothalamus and peripheral orexigenic gene regulation. METHODS: Fifty-four female rats were randomly assigned to 6 groups: one sham-operated group (SHAM), one ovariectomized (OVX) control group, three OVX groups fed with 400 ppm (L-SI), 1200 ppm (M-SI) and 3600 ppm (H-SI) isoflavone respectively, and one OVX group receiving 0.45 ppm diethylstilbestrol (EC). All rats were allowed to take high-fat diet for 4 weeks. Some neuropeptides were measured by RT-PCR. These neuropeptides included NPY, pro-opiomelanocortin (POMC), cocaine and amphetamine regulated transcript (CART), orexin, melanin-concentrating hormone (MCH), melanin-concentrating hormone precursor (P-MCH), ghrelin, and leptin. RESULTS: Compared with the OVX control group, the body weight and food intake in the H-SI group were reduced significantly and there was a significant dose-dependent manner in the 3 isoflavone groups. The results of RT-PCR showed that the NPY level in the 3 isoflavone groups was significantly increased and the POMC/CART gene expression decreased significantly in rats' hypothalamus compared with that in the OVX control group. However, the expression of orexin, MCH and P-MCH had no change. The peripheral grelin mRNA expression was higher in the 3 isoflavone groups, while leptin gene expression in the fat was not consistent. CONCLUSIONS: This research showed that isoflavone could prevent obesity induced by high-fat diet and ovariectomy through regulating hypothalamus and peripheral orexigenic gene expressions associated with food intake.

Isoflavone reduces body weight by decreasing food intake in ovariectomized rats.

BACKGROUND/AIMS: The primary objective of this study was to further determine the mechanisms by which isoflavone prevents obesity induced by ovariectomy. METHODS: Female 8-week-old Wistar rats were randomly assigned to 6 groups: a sham-operated group; an ovariectomized (OVX) control group; 3 OVX groups orally administered 400 ppm (L-SI), 1,200 ppm (M-SI) and 3,600 ppm (H-SI) of an isoflavone preparation, respectively, and an OVX group receiving 0.45 ppm of diethylstilbestrol. All animals were allowed free access to a high-fat diet and water for 4 weeks. Some neuropeptides, including ghrelin, neuropeptide Y (NPY), alpha-melanocyte-stimulating hormone (alpha-MSH), cholecystokinin (CCK), peptide YY (PYY), insulin and estradiol (E2), were measured by radioimmunoassay. RESULTS: Compared with the OVX control group, body weight, total abdominal fat, food intake and food availability of the M-SI and H-SI groups were significantly reduced. The results also showed that isoflavone and diethylstilbestrol could decrease ghrelin and NPY levels and increase CCK, PYY and E2 levels. The level of alpha-MSH was not changed. CONCLUSIONS: These findings showed that isoflavone could reduce obesity by decreasing food intake, possibly by (1) reducing ghrelin and NPY levels, thereby decreasing food intake, and (2) increasing CCK and PYY levels, which can induce satiety by irritating the vagal center.

Isoflavone regulates lipid metabolism via expression of related genes in OVX rats fed on a high-fat diet.

OBJECTIVE: To investigate the effects of isoflavone on body weight, fat mass, and gene expression in relation to lipid metabolism. METHODS: Thirty-six female SD rats were ovariectomized or sham-operated and fed on a high-fat diet. Two months later, abdominal incision was made, blood was collected to separate serum, and the liver and adipose tissue were immediately collected and weighed. Some portions of these tissues were frozen in liquid nitrogen and stored at -80 degrees C. RESULTS: Ovariectomy (OVX) with a high-fat diet could induce obesity in rats, while treatment with isoflavone significantly inhibited the increase in body weight and fat mass in abdomen. Serum total cholesterol and leptin were significantly decreased in isoflavone group, compared with the OVX group. The mRNA expression of liver fatty acid synthase (FAS) in the OVX group was significantly higher than that in sham-operated group, while this difference was not observed in the isoflavone group. The mRNA expression of liver hormone-sensitive lipase (HSL) in the OVX rats tended to be lower than that in the sham-operated rats. Furthermore, a large amount of isoflavone maintained the mRNA expression at a sham level. CONCLUSION: Isoflavone may prevent obesity induced by ovariectomy with a high-fat diet, in part by modulating gene expression related to lipid metabolism.

[Effects of soybean isoflavone on body weight and food utilization rate in ovariectomized rats].

OBJECTIVE: To investigate the inhibitory action of phytoestrogen soybean isoflavone on body weight increasing in ovariectomized rats that imitated postmenopausal women and the effect of decreasing food availability. METHODS: Four-month-old Wistar rats were sham-operated or ovariectomized by abdominal cavity operation and divided into Sham, Ovx, estrogen group(EC) and three isoflavone group and feed 16 weeks. The diet was prepared by ourselves and some contained diethylstilbestrol or different concentration of isoflavone. During the experiment, the rats weight and food intake were recorded. The food utilization rates of each group were calculated. RESULTS: The result showed that high dosage of soybean isoflavone (187.4 mg/kg bw x d) can significantly inhibited OVX induced weight gain and inhibitory action decreased with the dose reduce. Compared with Sham and Ovx group, the food intake of isoflavone group decreased significantly but no different in 3 dosage group and higher than EC group. Compared with Ovx group, the food utilization rates of high isoflavone group decreased significantly but higher than EC group. Isoflavone not influenced the growth and organ/body rates of rats. CONCLUSION: High dosage of isoflavone (187.4mg/kg bw x d) decreased OVX rat's weight gain significantly through reducing food utilization rate.

Blocking effects of genistein on cell proliferation and possible mechanism in human gastric carcinoma.

AIM: To study the blocking effects of genistein on cell proliferation cycle in human gastric carcinoma cells (SGC-7901) and the possible mechanism. METHODS: MTT assay was applied in the detection of the inhibitory effects of genistein on cell proliferation. Flow cytometry was used to analyze the cell cycle distribution. Immunocytochemical technique and Western blotting were performed to detect the protein expression of cyclin D1, cyclin B1 and p21(waf1/cip1). RESULTS: Genistein significantly inhibited the growth and proliferation of human gastric carcinoma cells (SGC-7901). Seven days after treatment with different concentrations of genistein (2.5, 5.0, 10.0, 20.0 microg/mL), the growth inhibitory rates were 11.2%, 28.8%, 55.3%, 84.7% respectively and cell cycles were arrested at the G(2)/ M phase. Genistein decreased cyclin D1 protein expression and enhanced cyclin B1 and p21(waf/cip1) protein expression in a concentration-dependent manner. CONCLUSION: The growth and proliferation of SGC-7901 cells can be inhibited by genistein via blocking the cell cycle, with reduced expression of cyclin D1 and enhanced expression of cyclin B1 and p21(waf/cip1) protein in the concentration range of 0-20 microg/mL.