Influence of Prevastein, an isoflavone-rich soy product, on mammary gland development and tumorigenesis in Tg.NK (MMTV/c-neu) mice

We investigated spontaneous mammary tumor development and mammary gland morphogenesis in female Tg.NK mice postnatally exposed to dietary soy isoflavones (0, 11, 39, and 130 mg aglycones/kg diet) added to a Western-style diet. Instead of preventing mammary tumorigenesis, the highest dose of isoflavones was associated with a small but significant increase in the number and size of tumors as compared to mice administered a Western-style control diet (P < 0.05). At postnatal Week 6, dynamic activity (measured as apoptotic density) at the highest dose and the degree of branching of the mammary tree in all isoflavone-exposed groups was increased as compared to controls (P < 0.05). At adulthood, the epithelium appeared more quiescent in the medium- and high-dose groups evident by reduced apoptotic density and a reduction in the percentage of terminal end buds (TEBs), respectively, as compared to controls (P < 0.05). The number of actively dividing cells within the TEBs was unaffected by isoflavone exposure as was the activity of drug-metabolizing and antioxidant enzymes. In conclusion, isoflavones may augment mammary gland and mammary tumor development.     

Soy isoflavones increase latency of spontaneous mammary tumors in mice

Soy protein, with and without isoflavones, is being added to foods by manufacturers in response to the Food and Drug Administration (FDA)-approved health claim for cardiovascular protection. Furthermore, soy isoflavones are increasingly consumed by women in the United States as an alternative to hormone replacement therapy. The role of these phytoestrogens in breast cancer is controversial. Although exposure of rodents to soy isoflavones during the perinatal period appears to reduce mammary cancer formation, exposure in utero or during adulthood may increase tumor growth. The mouse mammary tumor virus (MMTV)-neu mouse spontaneously develops mammary tumors due to overexpression of the ErbB-2/neu/HER2 oncogene. This model is comparable with human breast cancer because overexpression of the neu oncogene occurs in 20-40% of human breast cancers. We fed MMTV-neu mice AIN-93G diets containing no isoflavones, 250 mg/kg genistein, 250 mg/kg daidzein or an isoflavone mixture (NovaSoy, equivalent to 250 mg genistein/kg) from 7 wk of age. Mammary tumor latency was significantly delayed in mice fed isoflavones compared with the control. Once tumors formed, however, the isoflavones did not reduce the number or size of tumors such that at 34 wk of age there were no differences in tumor burden among the treatment groups. Hence, in the MMTV-neu mouse, soy isoflavones delayed mammary tumorigenesis. Further studies are warranted to define the cellular mechanisms through which these compounds affect mammary tumorigenesis in this model.     

Consumption of a low-carbohydrate and high-fat diet (the ketogenic diet) exaggerates biotin deficiency in mice

ObjectiveBiotin is a water-soluble vitamin that acts as a cofactor for several carboxylases. The ketogenic diet, a low-carbohydrate, high-fat diet, is used to treat drug-resistant epilepsy and promote weight loss. In Japan, the infant version of the ketogenic diet is known as the “ketone formula.” However, as the special infant formulas used in Japan, including the ketone formula, do not contain sufficient amounts of biotin, biotin deficiency can develop in infants who consume the ketone formula. Therefore, the aim of this study was to evaluate the effects of the ketogenic diet on biotin status in mice.MethodsMale mice (N = 32) were divided into the following groups: control diet group, biotin-deficient (BD) diet group, ketogenic control diet group, and ketogenic biotin-deficient (KBD) diet group. Eight mice were used in each group.ResultsAt 9 wk, the typical symptoms of biotin deficiency such as hair loss and dermatitis had only developed in the KBD diet group. The total protein expression level of biotin-dependent carboxylases and the total tissue biotin content were significantly decreased in the KBD and BD diet groups. However, these changes were more severe in the KBD diet group.ConclusionThese findings demonstrated that the ketogenic diet increases biotin bioavailability and consumption, and hence, promotes energy production by gluconeogenesis and branched-chain amino acid metabolism, which results in exaggerated biotin deficiency in biotin-deficient mice. Therefore, biotin supplementation is important for mice that consume the ketogenic diet. It is suggested that individuals that consume the ketogenic diet have an increased biotin requirement.     

Effects of a high-fat diet and bamboo extract supplement on anxiety- and depression-like neurobehaviours in mice

High-fat diet is a major causative factor of overweight and obesity, which are associated with an increased risk of neuropsychiatric diseases, such as anxiety and depression. In the present study, we investigated the protective effects of bamboo extract (BEX) on anxiety- and depression-like neurobehaviours in mice treated with a high-fat diet. Male mice with CD-1 genetic background were treated for 2 months with either a standard or a high-fat diet (10 or 45?% energy from fat, respectively), with or without the BEX supplement (11?g dry mass per 17?MJ). The anxiety levels of mice were evaluated using open-field and hole-board tests, and depression was measured using the force-swimming test. The anxiety responses of the animals were found significantly increased after the high-fat diet treatment, and this elevation was effectively abolished by the BEX supplement. The high-fat diet seemed to have an anti-depressive effect in mice at the tested time point, but the effect of the BEX supplement on the depression level of the animals was not conclusive. The high-fat diet significantly decreased total glutathione content in the blood while the BEX supplement increased glutathione oxidation. In summary, the present study shows that decreased total glutathione concentration in the blood co-occurred with a high-fat treatment, high anxiety level and low depression level in mice, and when supplemented in a high-fat diet, BEX had an anxiolytic effect in mice.     

Lysophospholipid profile in serum and liver by high-fat diet and tumor induction in obesity-resistant BALB/c mice

ObjectiveOur previous study revealed that chronic consumption of a high-fat diet (HFD) stimulates colon cancer progression in obesity-resistant BALB/c mice. The aim of the present study was to investigate the significant alteration of metabolites caused by tumor progression and an HFD in the serum and liver in the same mouse model.MethodsMale BALB/c mice were fed either a control diet or a HFD for 20.5 wk. The syngeneic CT26 colon carcinoma cells were injected into the right rear flank of mice after 16 wk of feeding. Metabolites in serum and liver samples were analyzed by ultra-performance liquid chromatography-quadrupole-time-of-flight-mass spectrometry-based metabolomics.ResultsHFD feeding and tumor injection induced changes in the choline-containing phospholipids, namely, phosphatidylcholines and lysophosphatidylcholines (lysoPCs), and lysophosphatidylethanolamines in the serum and liver. The majority of these metabolite changes were due to HFD feeding (11 in sera and 5 in livers) rather than tumors (3 in sera and 1 in livers).ConclusionThe HFD- and tumor-related metabolite alterations of phospholipids, especially lysoPCs, in the liver and serum of obesity-resistant mice, suggesting that the lysoPCs are potential biomarkers for the chronic consumption of HFD in nonobese individuals.     

大豆异黄酮持续暴露对小鼠卵巢发育影响

目的探讨大豆异黄酮对未成年小鼠卵巢发育影响,为雌性生殖发育毒性研究提供实验依据。方法21 d ICR 小鼠48只, 按体重随机分为对照组, 低、中、高剂量大豆异黄酮组(50、100、200 ㎎/㎏), 每日灌胃1次, 持续5周, 干预结束后测定血清性激素水平, 观察阴门开放时间, 计算卵巢脏器系数及各级卵泡构成比。结果高剂量大豆异黄酮组小鼠卵巢系数[(0.436±0.120) mg/g]低于对照组[(0.987±0.420)mg/g](P<0.05); 高剂量大豆异黄酮组小鼠雌二醇水平[(32.96±12.83)pg/mL]明显低于对照组[(53.76±16.44)pg/mL](P<0.05), 而孕酮在各组间差异无统计学意义;与对照组小鼠阴门开放时间[(33.50±2.68)d]比较, 中剂量大豆异黄酮组小鼠阴门开放时间[(31.14±1.21)d]提前, 差异有统计学意义(P<0.05);大豆异黄酮组小鼠成熟卵泡比例随着剂量增加呈下降趋势, 而闭锁卵泡比例呈上升趋势, 与对照组比较, 高剂量大豆异黄酮组小鼠成熟卵泡比例下降, 闭锁卵泡比例上升, 差异有统计学意义(P<0.05)。结论断乳至性成熟期持续暴露大豆异黄酮, 可干扰未成年小鼠卵巢发育。     

Norepinephrine- and epinephrine-deficient mice gain weight normally on a high-fat diet

OBJECTIVE: Signaling through adrenergic receptors (ARs) by norepinephrine (NE) and epinephrine (Epi) regulates weight gain when mice are fed a high-fat diet (HFD) by controlling diet-induced thermogenesis. Thus, one would predict that mice unable to make NE/Epi because of inactivation of the dopamine beta-hydroxylase gene (Dbh-null mice) would have a propensity to become obese. We characterized the response of Dbh-null and control mice to a HFD. RESEARCH METHODS AND PROCEDURES: Dbh-null and control mice were fed an HFD or a regular diet (RD) for 2 months. Body weight, adiposity, muscle triglyceride levels, and adipocyte size were measured, as were circulating leptin, adiponectin, triglyceride, glucose, and insulin levels. A glucose tolerance test was also preformed. RESULTS: Dbh-null mice gain weight normally on an HFD and have the same adiposity. Their serum triglyceride and leptin levels are normal, but adipocytes are approximately 30% smaller than controls. Dbh-null mice maintain low blood glucose levels and glucose tolerance when exposed to the HFD in contrast to controls. DISCUSSION: Complete lack of NE/Epi does not predispose to obesity. Because mice lacking all three betaARs become obese on an HFD, an imbalance of signaling through alpha- and betaARs seems to be responsible for obesity. Surprisingly, Dbh-null mice maintain glucose tolerance.     

Characterization of an integrated,endogenous mouse mammary tumor virus-like (MMTV) betaretrovirus genome in a black Syrian hamster (Mesocricetus auratus)

Retroviruses (family Retroviridae) are important agents of humans and animals. This study reports the detection and complete genome characterization of a novel endogenous retrovirus from the black Syrian hamster (Mesocricetus auratus) with a squamous cell skin tumor. The proviral genome, tentatively named black Syrian hamster retrovirus (BSHRV/2013/HUN, MK304634), was 8784 nucleotide in length with typical full-length betaretrovirus genome organization of 5’LTR-gag-pro-pol-env-3’LTR and with a characteristic mouse mammary tumor virus-like (MMTV) betaretrovirus dUTPase domain but without a sag gene. The BSHRV gag (534aa), pro/pol (~1099aa) and env (672aa) proteins had 56%/63%/50% aa identity to the corresponding proteins of MMTV (AF228552). The proviral DNA is detectable in tumor as well as in tumor-free cells by conventional PCR and qPCR but only visible in the tumor cells by in situ hybridization. Low level retroviral RNA expression was found only in the DNase-treated RNA tumor samples using RT/nested PCR. BSHRV/2013/HUN-like betaretrovirus DNA was also identified from a faecal and tissue samples from 1 of the further 3 tested individuals by nested-PCR and qPCR. Further research is needed to investigate the distribution, activity and etiological role of this novel MMTV-like betaretrovirus species in hamster.     

高脂饮食及罗格列酮对C57BL／6小鼠肝脏AGFmRNA表达的影响

目的探讨小鼠肝脏组织血管生成素相关生长因子（Angiopietin—related growth factor,AGF）mRNA表达水平的变化与胰岛素抵抗的关系。方法将雄性C57BIM6小鼠以高脂饮食喂养10周,建立胰岛素抵抗模型,再以罗格列酮灌胃8周;实验结束时以口服糖耐量试验、HOMA评分评价实验小鼠血糖、胰岛素抵抗水平,用RT-PCR技术检测这三组小鼠肝脏组织AGFmRNA的表达,并进行统计学分析。结果高脂饮食组小鼠肝脏AGFmRNA的表达低于对照组,差异具有统计学意义（P〈0．05）,罗格列酮组灌胃后小鼠肝脏AGFmRNA的表达增加（P〈0．01）;相关分析显示小鼠肝脏AGFmRNA表达与血浆胰岛素水平呈负相关（r=-0．516,P〈0．05）。结论高脂饮食诱导小鼠血浆葡萄糖及胰岛素水平增高,肝脏AGFmRNA表达降低,当胰岛素抵抗程度得到改善时,AGF的表达随之增加。     

Diet-induced obesity and mammary tumor development in MMTV-neu female mice

Obesity is a risk factor for postmenopausal breast cancer and is associated with shortened latency and/or increased mammary tumor (MT) incidence in animals. Elevated body weight is usually associated with hormone-responsive tumors. In agreement with these data we previously showed that latency of hormone-responsive MTs in MMTV-TGF-alpha mice with diet-induced obesity was significantly shortened. Here, we used the same protocol to determine the impact of diet-induced obesity on estrogen receptor-negative MT development in MMTV-neu (strain 202) mice. Mice were fed a low-fat diet (n=20) or a high-fat diet (n=54) from 10 wk of age. Body weight at 19 wk of age was used to assign high-fat mice to obesity-prone, overweight, and obesity-resistant groups. Mice were euthanized due to MT size or at 85 wk of age. Final body weights of obesity-prone mice were heaviest, and those of obesity-resistant and low-fat groups were similar. Fat pad weights were heaviest in obesity-prone mice followed by overweight and obesity-resistant groups, and lightest in low-fat mice. Serum IGF-I levels were similar for low-fat and high-fat mice, whereas leptin was higher in high-fat mice (P <0.0001). MT latency, incidence, metastasis, and burden were similar for all groups. These findings support that obesity is not a risk factor for development of estrogen-negative breast cancer.     

Effects of natural raw meal (NRM) on high-fat diet and dextran sulfate sodium (DSS)-induced ulcerative colitis in C57BL/6J mice

BACKGROUND/OBJECTIVESColitis is a serious health problem, and chronic obesity is associated with the progression of colitis. The aim of this study was to determine the effects of natural raw meal (NRM) on high-fat diet (HFD, 45%) and dextran sulfate sodium (DSS, 2% w/v)-induced colitis in C57BL/6J mice.MATERIALS/METHODSBody weight, colon length, and colon weight-to-length ratio, were measured directly. Serum levels of obesity-related biomarkers, triglyceride (TG), total cholesterol (TC), low density lipoprotein (LDL), high density lipoprotein (HDL), insulin, leptin, and adiponectin were determined using commercial kits. Serum levels of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 were detected using a commercial ELISA kit. Histological study was performed using a hematoxylin and eosin (H&E) staining assay. Colonic mRNA expressions of TNF-α, IL-1β, IL-6, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) were determined by RT-PCR assay.RESULTSBody weight and obesity-related biomarkers (TG, TC, LDL, HDL, insulin, leptin, and adiponectin) were regulated and obesity was prevented in NRM treated mice. NRM significantly suppressed colon shortening and reduced colon weight-to-length ratio in HFD+DSS induced colitis in C57BL/6J mice (P < 0.05). Histological observations suggested that NRM reduced edema, mucosal damage, and the loss of crypts induced by HFD and DSS. In addition, NRM decreased the serum levels of pro-inflammatory cytokines, TNF-α, IL-1β, and IL-6 and inhibited the mRNA expressions of these cytokines, and iNOS and COX-2 in colon mucosa (P < 0.05).CONCLUSIONThe results suggest that NRM has an anti-inflammatory effect against HFD and DSS-induced colitis in mice, and that these effects are due to the amelioration of HFD and/or DSS-induced inflammatory reactions.     

Effects of diet on norepinephrine turnover in obese (ob/ob) mice

Effects of energy restriction and of supplemental sucrose or fat on norepinephrine (NE) turnover in brown adipose tissue (BAT) and heart of female obese (ob/ob) and lean mice were examined. Rates of NE turnover in BAT of control female obese mice (8 weeks old) were 39% lower than in control lean mice; no differences were evident in hearts of these mice. Energy intake of 6-week-old ob/ob mice was restricted to the intake of lean mice for 2 weeks. This restriction decreased intake by 41% and reduced rates of NE turnover in heart (-15%), but not in BAT, of obese mice. Next, 7 1/2-week-old lean and obese mice were given access to stock diet and a 30% sucrose solution for 3-4 days. Intake of stock diet decreased by more than 50%. Total energy intake increased in lean mice (+18%), but decreased (-19%) in obese mice. When a 10% sucrose solution was offered intake of stock diet still decreased, but total energy intake was unchanged in lean and obese mice. Oxygen consumption increased in lean mice (+19 to +24%), but not in obese mice, when fed either 30 or 10% sucrose solutions, or a fat-supplemented diet where fat isocalorically replaced the sucrose consumed from 30% sucrose solution. Rates of NE turnover were not significantly increased in lean mice fed the 30% sucrose solution, but were increased in BAT (+34%) and heart (+25%) in lean mice fed the fat-supplemented diet.(ABSTRACT TRUNCATED AT 250 WORDS)     

长期抗生素暴露对高脂饮食负荷小鼠糖代谢和肠道菌群的影响

目的 探究长期抗生素暴露对高脂饮食负荷小鼠糖代谢和肠道菌群的影响。方法 45只新生BALB/c小鼠随机分为对照组、高脂饮食组和高脂饮食抗生素联合组（n=15）,联合组小鼠出生后以头孢曲松（100mg/kg）灌胃15周,第21d起,高脂组和联合组以高脂饲料,对照组以普通饲料喂养12周。实验结束后,对小鼠进行口服糖耐量实验并采集小鼠内脏、脂肪、血清和粪便,测定小鼠脏器系数、脂体比、血糖、胰岛素和瘦素及肠道菌群。结果 高脂饮食引起小鼠肝脏系数、总脂体比、胰岛素抵抗指数、空腹血糖和血糖曲线下面积显著升高（P均<0.05）。与对照组和高脂组比较,联合组alpha多样性指数显著降低（P<0.05）;主坐标分析显示三组组间群落组成具有明显差异。门水平上,与高脂组比较,联合组厚壁菌门相对丰度显著升高（P<0.05）,拟杆菌门相对丰度显著降低（P<0.05）,高脂组变形菌门相对丰度显著高于对照组和联合组（P均<0.05）。属水平上,高脂饮食诱导厚壁菌门布劳特氏菌属（Blautia）相对丰度增加,降低了拟杆菌门另枝菌属（Alistipes）相对丰度,联合组厚壁菌门肠球菌属（Enterococcus）和葡萄球菌属（Staphylococcus）相对丰度明显升高,其他菌属相对丰度均降低。结论 长期抗生素暴露可能通过改变肠道中细菌生长从而调节肠道菌群,在一定程度上抵抗高脂饮食负荷小鼠的糖代谢失调,表明肠道细菌和宿主代谢功能间存在密切的关联,肠道细菌有望成为改善膳食营养调节的机体能量代谢的重要靶点。     

高脂、高蛋白饮食对幼年大鼠氧化应激的影响

目的:探讨高脂、高蛋白饮食对幼年大鼠氧化应激的影响。方法:5~6周龄雄性Wistar大鼠随机分为对照组、高脂组和高蛋白组,分别用基础饲料、高脂饲料和高蛋白饲料喂养12周。于第6周和第12周测定血清总超氧化物歧化酶(T-SOD)、过氧化氢酶(CAT)、丙二醛(MDA)和谷胱甘肽(GSH)水平。结果:与对照组比较,第6周和第12周时,高脂组和高蛋白组大鼠体脂含量明显增加(P<0.05),血清CAT活性明显下降(P<0.01)。结论:短期和长期高脂或高蛋白饮食能增加幼年大鼠体脂含量,并增加机体氧化应激水平。     

高脂饲料诱导对大鼠血脂的影响

目的比较分析两种不同高脂饲料对大鼠血脂的影响,为建立合理而实用的高脂血症动物模型提供依据。方法 Wistar大鼠30只,按体重随机分为对照组(喂饲基础饲料),高脂配方1组和高脂配方2组,每组各10只,实验期间每周记录一次大鼠体重,每两周检测一次血脂,实验周期为6周。结果高脂饲料诱导6周后,高脂配方1组大鼠的血清总胆固醇(TC)和低密度脂蛋白胆固醇(LDL-C)分别比对照组升高了1.4倍和2.2倍(P<0.01),血清高密度脂蛋白胆固醇(HDL-C)水平比对照组降低了22.2%(P<0.01),血清甘油三酯(TG)水平与对照组无显著差异(P>0.05);高脂配方2组大鼠的血清TC和LDL-C分别比对照组升高了11.5倍和5.7倍(P<0.01),血清TG和HDL-C水平分别比对照组降低了39.7%和34.6%(P<0.01)。结论两种高脂饲料诱导均可建立大鼠高胆固醇血症模型,但均不能显著升高大鼠血清TG水平。     

Effects of a high-fat diet and strain on hypothalamic gene expression in rats

OBJECTIVE: This study was designed to investigate whether dietary fat and genetic background might differentially alter the expression of hypothalamic genes involved in food intake. RESEARCH METHODS AND PROCEDURES: Three-month-old Osborne-Mendel (OM) and S5B/Pl rats were fed either a high-fat or a low-fat diet for 14 days. mRNA for neuropeptide Y (NPY), corticotrophin-releasing hormone, NPY Y-1 receptor and Y-5 receptor, and serotonin 2c (5-HT2c) receptors were measured using Northern blotting or ribonuclease protection assays. RESULTS: OM rats showed an increased expression of NPY and corticotrophin-releasing hormone compared with S5B/Pl rats. The expression of NPY-Y1 and -Y5 receptor mRNA was significantly higher in the hypothalamus of OM rats compared with S5B/Pl rats. The expression of 5HT-2c receptor mRNA was significantly reduced in both strains of rats eating a high-fat diet when compared with the animals eating the low-fat diet. DISCUSSION: These data suggest that over activity of the NPY system may contribute to the development of obesity in OM rats and that expression of the 5HT-2c receptor gene may be modulated by dietary fat.     

原花青素对高脂饮食小鼠脂质代谢的影响

目的探讨原花青素(Oligomeric proanthocyanidin,OPC)干预对高脂饮食小鼠脂质代谢的影响。方法雄性C57BL/6小鼠48只按体重随机分为4组:A:对照组(Control);B:Con+OPC组;C:高脂组(High fat,HF);D:HF+OPC组,其中B和D组给予OPC(100 mg/kg/d)干预10周。测定血清总胆固醇(Total cholesterol,TC)、甘油三酯(Triglyceride,TG),丙氨酸氨基转氨酶(Alanine aminotransferase,ALT)、天门冬氨酸氨基转移酶(Aspartate aminotransferase,AST)以及肝脏TC和TG的水平,通过实时定量PCR法检测肝脏脂质代谢关键基因mRNA的表达水平。结果 HF组小鼠血清TG、TC、ALT以及肝脏TG的含量显著高于对照组(P0.05);OPC干预显著降低HF组小鼠血清TC水平、ALT活性以及肝脏TC和TG含量(P0.05),提高HF组小鼠肝脏三磷酸腺苷结合盒转运体A1(ATP-binding cassette transporter-1,ABCA1)mRNA的表达水平(P0.05)。结论 OPC干预能够有效改善高脂饮食小鼠血清和肝脏脂质代谢紊乱的情况。     

Maintenance energy requirements, energy retention and heat production of young obese (ob/ob) and lean mice fed a high-fat or a high-carbohydrate diet.

Female obese (ob/ob) and lean mice were weaned at 21 days of age, placed in wire-mesh cages maintained at 25 to 30 degrees, and fed a high-fat or a high-carbohydrate diet for 21 days. The body energy balance procedure was utilized to determine the maintenance energy requirements, and the efficiency of dietary energy utilization, above maintenance, in these mice. Heat production of each mouse was measured weekly in a gradient-layer calorimeter. Regressions of changes in body energy per kg3/4 on metabolizable energy intake per kg3/4 indicated that the maintenance energy requirement averaged 72 kcal/kg3/4/day for obese mice and 124 kcal/kg3/4/day for lean mice. Diet composition did not influence the maintenance energy requirements, but utilization of energy, above maintenance, in obese mice fed the high-fat diet was 41% more efficient than observed in obese mice fed the high-carbohydrate diet and 38 to 71% more efficient than observed in lean mice. Heat production, per unit body weight was lower in obese mice than in lean mice. The lowest heat production was observed in obese mice fed the high-fat diet. The 40% lower maintenance energy requirement of the obese mice is a major factor contributing to the high efficiency of energy retention in these mice. Consumption of a high-fat diet further improved the ability of the obese mice to retain dietary energy.     

Effects of high-fat diet on plasma lipids, adiposity, and inflammatory markers in ovariectomized C57BL/6 mice

ObjectiveWe hypothesized that a high-fat (HF) diet aggravates ovariectomy-related complications. To test this hypothesis, ovariectomized (OVX) mice were fed a HF diet, and we investigated the lipid metabolism, adipose tissue remodeling, adipokines, and inflammatory cytokines.MethodsTo investigate the situation in a mouse model of ovariectomy, OVX and SHAM C57BL/6 mice fed a HF diet (60% fat) or standard chow (SC, 10% fat) were monitored for 18 wk. We evaluated daily food intake and weekly body weight. Mice were killed at 30 wk of age. Blood samples and adipose tissue were collected for biochemical, histologic, and molecular analysis.ResultsOVX groups showed atrophied uterus compared to the SHAM groups, ensuring the success of surgically induced menopause. Despite lower food intake, OVX-HF mice gained about 52% more weight and had heavier total body fats, especially in relation to ovarian fat pad (372%)—a visceral fat which is associated with increased pathogenicity in obesity, and showed larger adipocytes (30%) when compared to OVX-SC mice. Biochemical analysis showed that the OVX-HF mice had increased levels of serum total cholesterol (51%), greater serum triglycerides (158%), lower serum adiponectin (40%), and higher plasma leptin (323%) than OVX-SC mice. The obese group (OVX-HF) also had higher IL-6 levels than both SHAM-HF (241%) and OVX-SC mice (870%).ConclusionOVX C57BL/6 mice fed HF diet had greater adipose fat pad, larger adipocytes, and increased inflammatory markers, reinforcing the idea that a HF diet aggravates the complications of ovariectomy-associated inflammation.     

Effects of long term exposure to beer on the genesis and development of spontaneous mammary adenocarcinoma and prolactin levels in female virgin C3H/St mice.

The exposure of female inbred virgin C3H/St mice infected with the Bittner particle to a commercial brand of beer increases body weight but has no significant effects on survival, the incidence of spontaneous mammary adenocarcinoma, tumor latency, or growth even on continuous administration of beer in place of drinking water over the entire postweaning lifespan of the animals. Prolactin excretion in young beer-group mice was slightly elevated but not significantly different from the prolactin levels observed in normally maintained control animals.