硫胺素、核黄素和烟酰胺对大鼠体重增长及脂代谢影响的实验研究(英文)

目的:B族维生素以辅酶的形式参与糖、脂肪和蛋白质代谢,本文观察硫胺素、核黄素和烟酰胺补充对高脂饲料诱导大鼠肥胖的影响。方法:采用预防肥胖模型法,2×2×2析因设计分为8组:高脂对照组(F0组),高脂+硫胺素(F1组),高脂+核黄素(F2组),高脂+烟酰胺(F3组),高脂+硫胺素+核黄素(F4组),高脂+硫胺素+烟酰胺(F5组),高脂+核黄素+烟酰胺(F6组),高脂+硫胺素+核黄素+烟酰胺(F7组),每组12只大鼠,给予高脂饲料喂养,同时硫胺素(100 mg/kg bw/d)、核黄素(100mg/kg bw/d)、烟酰胺(250 mg/kg bw/d)灌胃,另设正常对照组(C组)12只,普通饲料喂养,自来水灌胃,15周后,分析其体重、摄食量、体脂重量、血脂等实验前后的变化情况及各组动物之间的差别。结果:经过15周喂养后,高脂喂养大鼠体重比正常对照组平均增加了15.7%;而补充烟酰胺(F3)及联合硫胺素(F5)或核黄素(F6)以及三者联合补充(F7)组高脂喂养大鼠与高脂对照组(F0)相比,体重分别降低了35.0%,30.0%,30.1%和30.6%(P值均小于0.05);甚至比正常对照组大鼠平均体重分别下降了22.8%,17.0%,17.0%和17.7%(P值均小于0.05);而补充核黄素或和硫胺素组大鼠体重没有明显增加或降低(P值均大于0.05)。血脂分析结果显示高脂喂养并联合补充核黄素或/和烟酰胺和/或硫胺素组大鼠血清CHOL和LDL水平明显低于高脂对照组;而高脂喂养并联合补充烟酰胺(F3)及联合硫胺素(F5)或核黄素(F6)以及三者联合补充(F7)组大鼠LDL/HDL比值分别0.29、0.26、0.25和0.26,明显低于F0组的0.37(P值均小于0.05)。结论:大剂量烟酰胺可有效地调节血脂水平和控制肥胖大鼠的体重增长,而核黄素及硫胺素对控制肥胖大鼠体重增长的作用不明显,尚待进一步研究;核黄素只能够降低血脂水平,提示大剂量烟酰胺可通过增加机体的能量代谢来控制体重的增长。     

食物温度对大鼠体重、血糖、血脂及抗氧化作用的影响

目的：观察食物温度对大鼠体重、血糖、血脂及抗氧化作用的影响。方法：将40只Wistar大鼠随机分为4组（A组、B组、C组、D组）,分别喂食不同温度（10～15℃、22～32℃、42～52℃、52～62℃）的食物和饮水,饲养35d后测量体重,测定血糖（G）、总胆固醇（TC）、甘油三脂（TG）,测定血清中超氧化物歧化酶（SOD）活性、谷光甘肽过氧化物酶（GSH-Px）活力及丙二醛（MDA）和蛋白含量。结果：采用不同温度的饮食喂养35d后,各组大鼠的体重、血糖、血脂无显著差异（P〉0．05）;C组大鼠的血浆SOD和GSH-Px活性明显高于A组（P〈0．05）,MDA和蛋白含量显著低于A组（P〈0．05）。结论：不同温度的饮食对代谢的影响不明显．42～52℃饮食组大鼠的生化指标较为稳定,有较强的抗氧化作用,过低温度的饮食使机体处于应急状态。     

硫胺素水平对团头鲂幼鱼生长、肝组织沉积量及血液生化指标的影响

为研究硫胺素对团头鲂幼鱼生长、组织沉积量和血液生化指标的影响,试验采用单因素浓度梯度设计,配制了6组等氮等能的半纯合饲料,各组硫胺素含量分别为0、0.51、0.98、1.59、2.13和2.68 mg/kg。选取团头鲂幼鱼720尾[初重为（0.30±0.01）g],按随机原则分为6组,每组4重复,各重复30尾,日投饵3次,饲喂8周后采集样品。结果表明,与对照组相比,0.98、1.59、2.13、和2.68 mg/kg添加组的增重率和特定生长率均显著提高（P < 0.05）。1.59和2.13 mg/kg硫胺素添加组的成活率显著高于对照组（P < 0.05）。随着饲料中硫胺素含量的升高,血浆葡萄糖含量呈现先下降后上升的趋势,血浆葡萄糖水平在1.59 mg/kg时为最小值（P < 0.05）。对照组与0.51 mg/kg硫胺素组相比血浆中丙酮酸含量差异不显著,但显著高于其他试验组（P < 0.05）。以团头鲂幼鱼的增重率和肝脏硫胺素沉积量为评价指标,进行双折线回归分析,饲料中硫胺素适宜添加水平分别为1.48和1.84 mg/kg。     

蒙古旱獭体重和体长增长的研究

1985和1986年对647只蒙古旱獭体重、体长的增长规律进行了研究。体重体长随年龄增加而增长,但体重和体长的增长特点不同,体重随年龄增加而直线上升,体长则呈抛物线形上升。根据这一规律,将体长的增长划为突增期、稳增期和停滞期三个时期。并根据体重和体长分布呈二元正态分布之特点,以直线回归方程Y=30.78+0.004X表示体重(X)与体长(Y)的相关关系,相关系数r=0.9602(p<0.01)。     

硫胺素对Arthrobacter sp.A302环磷酸腺苷发酵的影响

研究在培养基中加入硫胺素（V B1）对cAMP发酵的影响。结果表明：V B1的最适添加量为0.5 g/L,与对照组相比,环磷酸腺苷（cAMP）产量和细胞干质量分别提高了36.4%和41.8%,达到7.5和7.8 g/L。琥珀酸和α-酮戊二酸的含量有明显的提高,平均提高了43.59%和40.77%;同时,主要副产物乙酸的含量没有明显变化。在发酵过程中,V B1的加入对ATP的含量及与cAMP合成密切相关的几种酶的活性也有显著的影响。     

孕中期营养指导对妊娠糖尿病孕妇体重增长及妊娠结局的影响研究

目的：研究营养指导对孕妇体重增长及妊娠结局的影响。方法：选择2012年7月—2012年8月在卫生部北京医院产科常规查体的164例孕妇为研究对象,于孕中期建档日开始进行个体化饮食指导,于孕22～24w糖筛后对妊娠糖尿病（GDM）孕妇进行饮食控制并跟踪整个孕期。分别记录血糖正常组和GDM组孕妇孕24w体重及产前体重,记录新生儿体重、身长、胎盘重、巨大儿及剖宫产人数等指标。结果：孕24w体重增长值：GDM组为7.53±2.80kg、血糖正常组为6.66±3.68kg（P=0.35）;产前体重增长值：GDM组为15.25±3.54kg;血糖正常组为17.21±4.85kg（P=0.12）;巨大儿发生率：GDM组为25%、血糖正常组为6.4%（P=0.04）;剖宫产率：GDM组为68.8%、血糖正常组为35%（P=0.01）。结论：个体化饮食指导有利于孕妇的合理体重增长,但是并未显著改变巨大儿发生率的增加,建议针对高危孕妇进行早期营养干预。     

成人脂肪肝与体重指数和血脂水平的关系研究

目的:研究成人脂肪肝与体重指数(BMI)和血脂水平的关系。方法:选取2012年1月到2014年11月我社区成年人800例,检测所有入选者的体重和身高,并计算BMI,检测入选者的血脂水平和脂肪肝情况,应用Logistic回归分析来分析脂肪肝与BMI和血脂之间的关系。结果:共检测出脂肪肝376例,占47.0%,肥胖者532例,占66.5%;肥胖者伴随脂肪肝的发生率64.7%,显著高于非肥胖者脂肪肝的发生率11.9%,两者比较差异具有统计学意义(P0.05);脂肪肝者总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)显著高于非脂肪肝者,而高密度脂蛋白(HDL-C)显著低于非脂肪肝者,两者比较差异具有统计学意义(P0.05);Logistic回归分析显示:脂肪肝与BMI和血脂之间存在相关关系(P0.05)。结论:BMI和血脂水平与成人脂肪肝存在较大关系,应该注意控制体重,进而降低脂肪肝的发生率,改善脂肪肝的情况。     

密度因素对布氏田鼠体重增长及免疫功能的影响

为了研究种群密度对布氏田鼠(Microtus brandti)免疫功能的影响，我们以分别取自稳定的同性别饲养群的成年布氏田鼠为对象，测定了雌性和雄性个体在低(1只／笼)、中(4只／笼)、高(8只／笼)3个饲养密度梯度下的生长及免疫指标，包括体重、睾丸重、脾脏重、血清抗体及皮质醇含量等。结果发现：(1)随着密度的升高，布氏田鼠的体重和雄性睾丸的重量有所降低；(2)中密度和高密度饲养条件下雌性的免疫水平高于低密度个体，但密度对雄性个体的免疫状况影响不大；(3)不同密度饲养条件下布氏田鼠血清中的皮质醇含量没有显著差异。这些结果表明，和睦稳定的种内关系未必对布氏田鼠造成社群压力，但密度能够影响布氏田鼠的生长、繁殖和免疫状况，而且这些影响存在着性别差异。     

金属离子对酵母胞内核黄素产量的影响

研究了金属离子对脆壁酵母 (Saccharomycesefragilis)RY 5胞内核黄素积累的影响 ,运用均匀设计方法进行了培养基优化。结果表明 :Mg2 + ,Zn2 + ,Fe2 + 对RY 5的核黄素产量有着显著影响 ,培养基中金属离子的最佳浓度为 :MgSO4·7H2 O 1 .1g/L ;CoSO4·7H2 O 2 8mg/L ;CuSO4·5H2 O 0 .0 1mg/L ;MnCl2 0 .0 2mg/L ;ZnSO4·7H2 O 3 4mg/L ;FeSO4·7H2 O 1 4mg/L ,RY 5的核黄素产量可达 1 40mg/kg。     

血糖水平对缺氧缺血新生大鼠体重和脑重的影响观察

目的　观察不同血糖水平及缺氧缺血 (hypoxicischemia ,HI)前后血糖对缺氧缺血新生大鼠体重和脑重的影响。方法　通过制备缺氧缺血新生大鼠合并高低血糖模型 ,分别在脑HI后 2、2 4、48、72h和 7d共 5个时段 ,分别在断头前测体重和断头后取脑称脑重 ,并辅以免疫组化分析HI后 2 4h时段各组脑内葡萄糖转运蛋白 1(GLUT1)及葡萄糖转运蛋白 3 (GLUT3 )合成量的变化。结果　 2 4h时段HI组、HI前低血糖组、HI后低血糖组体重呈显著意义 ,低于正常组 ;2 4h时段缺氧缺血前后低血糖脑重均呈显著意义 ,低于其他各组 ,7d时段I前重高血糖组脑重高于HI组及HI前低血糖组。HI前重高血糖组HI后 2 4h在皮质部位GLUT1的合成量显著高于其他各组。HI前低血糖组HI后 2 4h在皮质部位GLUT3的合成量显著低于其他各组。结论　HI前低血糖对新生大鼠体重、脑重增长不利 ,HI前重高血糖有可能缓解HI引起的体重、脑重的减轻而显示一定的保护作用     

Time-Dependent Effects of Progressive Gamma -Linolenate Feeding on Hyperphagia,Weight Gain,and Erythrocyte Fatty Acid Composition During Growth of Zucker Obese Rats

Obese Zucker rats (fa/fa) have low levels of arachidonic acid (AA) in liver phospholipids (PL). We have previously shown that a 70% gamma-linolenate concentrate (GLA; an AA intermediate) fed at a fixed dose (0.07 g/day) normalized hepatic PL AA and reduced weight gain selectively in the obese animals. In a follow-up study, 16 obese (fa/fa) and 16 lean (Fa/Fa) 4-week-old male rats were randomized into 4 groups of 8 each and gavaged daily with soybean oil (SOY) containing 55% 18:2ω6 (an AA precursor) or GLA, using a progressive dose (≤ 5% of total calories) based on body weight. A defined diet with 11% of energy as SOY was fed ad libitum for 60 days. GLA obese had lower body weight (p<0.0001) and 60-day cumulative food intake (p<0.05) compared to SOY obese, but neither parameter differed between the lean groups. For the last twenty days cumulative food intake was identical for GLA obese and SOY lean, whereas SOY obese consumed 18% more (p<0.05). Thus the progressive dose of GLA selectively suppressed hyperphagia in obese Zucker rats. Erythrocytes collected at 15-day intervals showed parallel increases in AA in both genotypes over time, suggesting normal AA availability during rapid growth. Thus, the reduced PL AA in the livers from the obese rats probably reflects impaired distribution in selected tissues rather than reduced hepatic production. Due to the potential health risks of enriching tissue lipids with AA, great caution is advised in considering GLA as therapy for human obesity.     

下丘脑Orexin 对肥胖大鼠能量代谢的影响

目的:探讨下丘脑注射OXR-1选择性受体拮抗剂ACT-335827对肥胖大鼠代谢的效果。方法:通过高脂饮食建立肥胖大鼠模型,采用CODA 8通道高通量非侵入性血压系统(EMKA)测量血压;所有脂类都使用商品酶试剂盒和TOSHIBA-40FR全自动分析仪测量;空腹血糖采用葡萄糖氧化酶法;空腹胰岛素采用放射免疫法测定。肥胖大鼠出现代谢紊乱后,给予ACT-335827处理,检测大鼠体重、血压、脂肪、甘油三酯、总胆固醇、高密度脂蛋白、低密度脂蛋白、游离脂肪酸(NEFA)、瘦素、空腹血糖及空腹胰岛素等的变化。结果:与普通饮食组相比,经过10周高脂饮食,高脂饮食组大鼠体重显著升高(P0.05),给予ACT-335827处理后,普通大鼠的体重、血压、脂肪含量、脂代谢等均无明显变化;与高脂饮食和高脂饮食加生理盐水处理组大鼠比较,高脂饮食加ACT-335827处理组肥胖大鼠的体重显著下降(P0.05),腹部和附睾脂肪含量下降(P0.05),低密度脂蛋白、甘油三酯、总胆固醇、瘦素水平下降(P0.05),空腹血糖及空腹胰岛素也显著降低(P0.05),但血压、肠系膜脂肪和肩胛棕色脂肪、高密度脂蛋白和NEFA无明显变化(P0.05)。结论:ACT-335827对肥胖大鼠的代谢紊乱具有改善作用,对肥胖大鼠有一定的减肥作用。     

Oral Administration of Lycopene Reverses Cadmium-suppressed Body Weight Loss and Lipid Peroxidation in Rats

Cadmium (Cd) exposure has been recognized to result in a wide variety of cellular responses, including oxidative stress and body weight loss. The aim of the present study was to examine the effect of lycopene supplementation on the antioxidant defense system, lipid peroxidation (LPO) level, nitric oxide (NO), tumor necrosis factor alpha (TNF-α) production, and body weight in Cd-exposed rats. Animals were divided into four groups (n = 7): control, Cd-treated, Cd plus lycopene-treated, and lycopene-treated. Cadmium (as CdCl₂) was administrated orally for 20 days (6.6 mg kg⁻¹ day⁻¹), and lycopene (10 mg kg⁻¹ day⁻¹) was similarly administered. Lycopene administration significantly suppressed Cd-induced LPO in plasma and kidney homogenates. Lycopene also reversed Cd-decreased body weight compared to the control. Cadmium treatment had diverse effects on the antioxidant enzyme activities. Although antioxidant superoxide dismutase activity was unchanged, glutathione peroxidase activity was decreased, and catalase activity was elevated in kidney homogenates of Cd-administrated group. However, lycopene treatment reversed Cd-changed enzyme activities to the control level. Xanthine oxidase activity and TNF-α concentration were not altered by Cd administration, indicating that superoxide anion production and inflammation were not stimulated. Cadmium did not change NO levels in kidney homogenates but decreased those in plasma, and this effect was not prevented by lycopene supplementation. The result suggests that consumption of adequate levels of lycopene may be useful to prevent heavy-metal-induced LPO and body weight loss.     

S 23521 Decreases Food Intake and Body Weight Gain in Diet‐Induced Obese Rats

Objective: To investigate the effect of S 23521, a new glucagon‐like peptide‐1‐(7‐36) amide analogue, on food intake and body weight gain in obese rats, as well as on gene expression of several proteins involved in energy homeostasis. Research Methods and Procedures: Lean and diet‐induced obese rats were treated with either S 23521 or vehicle. S 23521 was given either intraperitoneally (10 or 100 μg/kg) or subcutaneously (100 μg/kg) for 14 and 20 days, respectively. Because the low‐dose treatment did not affect food intake and body weight, the subcutaneous treatment at high dose was selected to test the effect on selected end‐points. Results: Treated obese rats significantly decreased their cumulative energy intake in relation to vehicle‐treated counterparts (3401 ± 65 vs. 3898 ± 72 kcal/kg per 20 days; p < 0.05). Moreover, their body weight gain was reduced by 110%, adiposity was reduced by 20%, and plasma triglyceride levels were reduced by 38%. The treatment also improved glucose tolerance and insulin sensitivity of obese rats. Regarding gene expression, no changes in uncoupling protein‐1, uncoupling protein‐3, leptin, resistin, and peroxisome proliferator‐activated receptor (PPAR)‐γ were observed. Discussion: S 23521 is an effective glucagon‐like peptide‐1‐(7‐36) amide analogue, which induced a decrease in energy intake, body weight, and adiposity in a rat model of diet‐induced obesity. In addition, the treatment also improved glucose tolerance and insulin sensitivity of obese rats. These results strongly support S 23521 as a putative molecule for the treatment of obesity.     

Effects of Parenteral Lipid Infusion on DNA Damage in Very Low Birth Weight Infants

Very low birth weight (VLBW) infants are known to have poorly developed antioxidant system and may be at increased risk for radical damage. Previous studies have reported higher levels of lipid peroxide products in lipid emulsion used for parenteral nutrition. To examine the direct effects of parenteral lipid infusion on DNA damage in VLBW infants, we measured urinary 8-hydroxydeoxyguanosine (8-OHdG) levels in VLBW infants before, during, and after the parenteral lipid infusion. In both the lipid-infused and lipid-free groups, urinary 8-OHdG excretion levels at 14 days old were significantly ( p <0.01) lower than those at 2 and 7 days old. However, there were no significant differences in urinary 8-OHdG excretion levels between the lipid-infused and lipid-free groups at 2, 7, and 14 days old. Our results suggest that parenteral lipid infusion does not cause oxidative DNA damage, but irrespective of the infusion DNA damage during the first week of life is enhanced when compared with 14 days after birth in VLBW infants.     

Birth Weight,Adulthood BMI,and Subsequent Weight Gain in Relation to Leptin Levels in Swedish Women

LISSNER, LAUREN, CECILIA KARLSSON, ANNA KARIN LINDROOS, LARS SJOSTROM, BJORN CARLSSON, LENA CARLSSON, AND CALLE BENGTSSON. Birth weight, adulthood BMI, and subsequent weight gain in relation to leptin levels in Swedish women. Obes Res. Objective Leptin seems to be involved in the regulation of energy balance, although little is known about the epidemiology of leptin with respect to prediction of weight gain and incidence of obesity-related diseases. The dual aim of this study is to document characteristics of leptin after long-term storage, and to describe its relation to body weight, from birth to old age, in an ongoing prospective study. Research Methods and Procedures A population-based sample of Swedish women was first examined at the ages of 38 to 60 and re-examined 24 years later. This study used 1358 frozen serum samples that had been stored 29 years for analysis of leptin concentrations and their relation to body weight history. Results Leptin values obtained from stored samples showed the same correlation with relative weight as that seen in a contemporary sample with similar demographic characteristics. Lower self-reported birth weight was associated with higher leptin levels in adulthood (p = 0.01), controlling for age and adult BMI. Prospective analyses revealed that high leptin in 38 to 46-year-olds predicted subsequent long-term weight gain (p = 0.003), although no significant associations were seen in women initially aged 50 or older. Discussion: It is feasible to use frozen serum for studying leptin in relation to obesity and related developments many years later. High leptin level was a risk factor for subsequent weight gain in 38- and 46-year-old women. Retrospective analyses involving birth weight suggest that leptin resistance in adulthood might have fetal origins.     

Serum Leptin Concentrations and Weight Gain in Postobese,Postmenopausal Women

Objective : This study was designed to determine if serum leptin concentrations (adjusted for fat mass) after weight loss on a low-calorie diet predict subsequent weight gain. Research Methods and Procedures : Body composition and serum leptin concentrations were determined on 14 moderately obese, postmenopausal, nondiabetic women with a familial predisposition to obesity. Assessments were obtained under tightly controlled metabolic ward conditions of macronutrient intake and weight maintenance both before (obese state) and after a mean weight loss of 12.0 kg to normal body weight (postobese state). Four years later, without intervention, body weight and body composition were reassessed. Results : Weight loss resulted in significant decreases in fat mass (29.7 ± 5.4 vs. 20.3 ± 4.7; kg), body mass index (27.7 ± 1.6 vs. 23.0 ± 1.5; kg/m2), percent body fat (40.7 ± 4.3 vs. 33.1 ± 5.0), and serum leptin concentrations (31.8 ± 16.0 vs. 11.5 ± 5.4; ng/mL). Serum leptin concentrations were positively correlated (p<<0.05) with fat mass in both the obese and postobese states (r = 0.67 and r = 0.56, respectively). However, residual serum leptin concentrations (adjusted for fat mass) in the obese and postobese states were not related to changes in body weight (p<= 0.61 and 0.52), fat mass (p = 0.72 and 0.42), body mass index (p = 0.59 and 0.33), or percent body fat (p = 0.84 and 0.46) over the follow-up period. Discussion : These finding do not support the hypothesis that relatively low concentrations of leptin predict weight regain after weight loss. However, because the number of subjects in this study was limited, further studies are warranted.