饮食诱导肥胖抵抗和肥胖大鼠血中激素水平的比较

目的　研究饮食诱导肥胖抵抗 (DIO R)和肥胖 (DIO)大鼠血中胰岛素、瘦素 (leptin)和神经肽Y(NPY)水平的差别。方法　采用 5 0只健康雄性SD大鼠 ,随机分为基础组和高脂组 ,分别用基础饲料和高脂饲料喂养 13周 ,然后根据体重筛选出DIO R和DIO组 ,观察体重、摄食量和体脂含量的变化 ,放免法测血清胰岛素、leptin和血浆NPY含量。结果　DIO R大鼠体重、摄食量和体脂含量均明显低于DIO大鼠 (P <0 0 5 ) ;血清胰岛素、血浆NPY含量显著低于DIO大鼠 (P <0 0 5 ) ;高脂饲料使大鼠血清leptin水平明显增加 (P <0 0 5 ) ,但DIO R与DIO大鼠间无明显差别 (P >0 0 5 )。结论　高脂饲料能够诱导SD大鼠发生肥胖和肥胖抵抗 ,胰岛素 leptin NPY反馈环的平衡在肥胖抵抗的发生中起重要作用。     

A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations

BACKGROUND: Ad libitum, low-carbohydrate diets decrease caloric intake and cause weight loss. It is unclear whether these effects are due to the reduced carbohydrate content of such diets or to their associated increase in protein intake. OBJECTIVE: We tested the hypothesis that increasing the protein content while maintaining the carbohydrate content of the diet lowers body weight by decreasing appetite and spontaneous caloric intake. DESIGN: Appetite, caloric intake, body weight, and fat mass were measured in 19 subjects placed sequentially on the following diets: a weight-maintaining diet (15% protein, 35% fat, and 50% carbohydrate) for 2 wk, an isocaloric diet (30% protein, 20% fat, and 50% carbohydrate) for 2 wk, and an ad libitum diet (30% protein, 20% fat, and 50% carbohydrate) for 12 wk. Blood was sampled frequently at the end of each diet phase to measure the area under the plasma concentration versus time curve (AUC) for insulin, leptin, and ghrelin. RESULTS: Satiety was markedly increased with the isocaloric high-protein diet despite an unchanged leptin AUC. Mean (+/-SE) spontaneous energy intake decreased by 441 +/- 63 kcal/d, body weight decreased by 4.9 +/- 0.5 kg, and fat mass decreased by 3.7 +/- 0.4 kg with the ad libitum, high-protein diet, despite a significantly decreased leptin AUC and increased ghrelin AUC. CONCLUSIONS: An increase in dietary protein from 15% to 30% of energy at a constant carbohydrate intake produces a sustained decrease in ad libitum caloric intake that may be mediated by increased central nervous system leptin sensitivity and results in significant weight loss. This anorexic effect of protein may contribute to the weight loss produced by low-carbohydrate diets.     

The role of high-fat diets and physical activity in the regulation of body weight

The prevalence of obesity is increasing in westernized societies. In the USA the age-adjusted prevalence of BMI > 30 kg/m2 increased between 1960 and 1994 from 13% to 23% for people over 20 years of age. This increase in the prevalence of obesity has been attributed to an increased fat intake and a decreased physical activity. However, the role of the impact of the level of dietary fat intake on human obesity has been challenged. High-fat diets, due to their high energy density, stimulate voluntary energy intake. An increased fat intake does not stimulate its own oxidation but the fat is stored in the human body. When diet composition is isoenergetically switched from low to high fat, fat oxidation only slowly increases, resulting in positive fat balances on the short term. Together with a diminished fat oxidation capacity in pre-obese subjects, high-fat diets can therefore be considered to be fattening. Another environmental factor which could explain the increasing prevalence of obesity is a decrease in physical activity. The percentage of body fat is negatively associated with physical activity and exercise has pronounced effects on energy expenditure and substrate oxidation. High-intensity exercise, due to a lowering of glycogen stores, can lead to a rapid increase in fat oxidation, which could compensate for the consumption of high-fat diets in westernized societies. Although the consumption of high-fat diets and low physical activity will easily lead to the development of obesity, there is still considerable inter-individual variability in body composition in individuals on similar diets. This can be attributed to the genetic background, and some candidate genes have been discovered recently. Both leptin and uncoupling protein have been suggested to play a role in the prevention of diet-induced obesity. Indeed, leptin levels are increased on a high-fat diet but this effect can be attributed to the increased fat mass observed on the high-fat diet. No effect of a high-fat diet per se on leptin levels is observed. Uncoupling proteins are increased by high-fat diets in rats but no data are available in human subjects yet. In conclusion, the increased intake of dietary fat and a decreasing physical activity level are the most important environmental factors explaining the increased prevalence of obesity in westernized societies.     

Increasing the protein:carbohydrate ratio in a high-fat diet delays the development of adiposity and improves glucose homeostasis in mice

Dietary fat is considered an important contributing factor in the obesity epidemic, and high-fat diets are used widely to induce obesity and diabetes-related traits in susceptible rodent strains. Little attention, however, is usually paid to the interaction of fat with the other macronutrients. The aim of this study, therefore, was to investigate the effects of high-fat, isoenergetic diets with different protein:carbohydrate (CHO) ratios on obesity, energy metabolism, and glucose homeostasis in mice. Male adult C57BL/6J mice consumed ad libitum for 10 wk a control diet (41:42:17 ratio of CHO:protein:fat, 15.5 kJ/g) or 2 different high-fat diets: high carbohydrate (HC; 41:16:43, 17.7 kJ/g) or low carbohydrate (LC; 11:45:44, 17.5 kJ/g). Body weight and fat gains were rapid and were greater in HC mice than in other groups due to an initial pronounced hyperphagia and subsequent passive overconsumption. Weight and fat gains were less in LC mice but still greater than in controls. Energy expenditure was not affected by the diets, and total energy intake explained 84% of the variation in final body weight. The respiratory quotient was lower in LC mice than in other groups, indicating high fat oxidation rates due to the LC diet. Blood glucose was lower and insulin sensitivity greater in LC mice than in HC mice. We conclude that increasing the protein:CHO ratio in a high-fat diet delays but does not prevent the development of adiposity. However, glucose homeostasis was improved in LC mice, indicating that a combination of high fat and high CHO is responsible for the development of metabolic syndrome-related traits in mice.     

饮食诱导肥胖抵抗和饮食诱导肥胖大鼠的对比研究

目的 探讨饮食诱导肥胖抵抗(DIO—R)大鼠和饮食诱导肥胖(DIO)大鼠的肥胖相关指标的变化。方法 采用50只健康雄性别大鼠，随机分为对照组和高脂组，分别用基础饲料和高脂饲料喂养13周，然后根据体重筛选出DIO—R和DIO组，观察能量摄入和体脂含量的变化；试纸法测定血糖；应用酶法测定大鼠总胆固醇(CHO)、甘油三脂(TG)、高密度胆固醇(HDL—C)；放免法测血清瘦素(1eptin)含量。结果 在前5周时，DIO—R大鼠与DIO大鼠摄入的总能量无显性差异；在实验终期，DIO—R大鼠明显低于DIO大鼠(P＜0．05)。DIO—R大鼠体脂含员、血糖、TG、CHO均明显低于DIO大鼠(P＜0．05)，DIO—R和DIO大鼠的HDL—C无明显差别。高脂饲料使大鼠血清(1eptin)水平明显增加(P＜0．05)，但DIO—R与DIO大鼠间无明显差别。结论 高脂饲料能够诱导别大鼠发生肥胖和肥胖抵抗，血清leptin水平增加在大鼠肥胖抵抗的发生中起部分作用。     

A mixture of the Salacia reticulata (Kotala himbutu) aqueous extract and cyclodextrin reduces the accumulation of visceral fat mass in mice and rats with high-fat diet-induced obesity

The effects of a mixture of the Salacia reticulata (Kotala himbutu) aqueous extract and cyclodextrin (SRCD) on the development of obesity were examined. We studied the effects of SRCD on the elevation of plasma triacylglycerol levels induced by oral administration of a high-fat (HF) liquid diet to male Sprague-Dawley rats. The plasma triacylglycerol concentration was significantly lower in the SRCD-treated rats than in the control rats 4 h after HF diet administration (P<0.05). In a study of female C57BL/6 mice that consumed a solid HF diet containing 0, 0.2 or 0.5% SRCD ad libitum for 8 wk, the increases in body weight and visceral fat mass were less in those fed the diet supplemented with 0.5% SRCD than in those fed the HF diet (P<0.05). In male Sprague-Dawley rats fed a solid HF diet with or without 0.2% SRCD and restricted in energy intake to that of rats fed a normal diet for 35 d, the increases in body weight and visceral fat mass were smaller in the SRCD-supplemented rats (P<0.05). In addition, the energy efficiency and the plasma leptin and adiponectin concentrations were lower in the mice and rats that were administered SRCD than in those fed the HF diet alone (P<0.05). The inhibitory effects of SRCD on HF diet-induced obesity may be attributable to the inhibition of carbohydrate and lipid absorption from the small intestine. Therefore, SRCD may suppress the accumulation of visceral fat and the glucose intolerance that accompany this type of obesity.     

Diet-induced changes in stearoyl-CoA desaturase 1 expression in obesity-prone and -resistant mice

OBJECTIVE: To investigate stearoyl-coenzyme A desaturase (SCD) 1 expression in obesity-prone C57BL/6 mice and in obesity-resistant FVB mice to explore the relationship of SCD1 expression and susceptibility to diet-induced obesity. RESEARCH METHODS AND PROCEDURES: Nine-week-old C57BL/6 and FVB mice were fed either a high- or low-fat diet for 8 weeks. Body weight and body composition were measured before and at weeks 4 and 8 of the study. Energy expenditure was measured at weeks 1 and 5 of the study. Hepatic SCD1 mRNA was measured at 72 hours and at the end of study. Plasma leptin and insulin concentrations were measured at the end of study. RESULTS: When C57BL/6 mice were switched to a calorie-dense high-fat diet, animals gained significantly more body weight than those maintained on a low-calorie density diet primarily due to increased fat mass accretion. Fat mass continued to accrue throughout 8 weeks of study. Increased calorie intake did not account for all weight gain. On the high-fat diet, C57BL/6 mice decreased their energy expenditure when compared with mice fed a low-fat diet. In response to 8 weeks of a high-fat diet, SCD1 gene expression in liver increased >2-fold. In contrast, feeding a high-fat diet did not change body weight, energy expenditure, or SCD1 expression in FVB mice. DISCUSSION: Our study showed that a high-fat hypercaloric diet increased body adiposity first by producing hyperphagia and then by decreasing energy expenditure of mice susceptible to diet-induced obesity. Consumption of a high-fat diet in species predisposed to obesity selectively increased SCD1 gene expression in liver.     

Fat intake affects adiposity,comorbidity factors,and energy metabolism of sprague-dawley rats

OBJECTIVE: Childhood obesity is an emerging health problem. This study assesses the effects of three levels of dietary fat (10%, 32%, and 45% measured by kilocalories) on weight gain, body composition, energy metabolism, and comorbidity factors in rats from weaning through maturation. RESEARCH METHODS AND PROCEDURES: The role of dietary fat on the susceptibility to obesity was assessed by feeding diets containing three levels of dietary fat to rats from weaning through 7 months of age. Body composition was analyzed by DXA after 6 and 12 weeks of dietary treatment. Energy metabolism was measured by indirect calorimetry. RESULTS: Energy intake, weight gain, fat mass, and plasma glucose, cholesterol, triglyceride, free fatty acid, leptin, and insulin levels increased dose-dependently with increased dietary fat. No difference in absolute lean mass among the three groups was observed. Therefore, the differences in weight gain are accounted for primarily by increased fat accretion. Compared with rats that were relatively resistant to obesity when on a 45% fat diet, diet-induced obesity-prone rats were in positive energy balance and had an elevated respiratory quotient, indicating a switch in energy substrate use from fat to carbohydrate, which promotes body-fat accretion. DISCUSSION: Our data support the hypothesis that administration of increasing amount of dietary fat to very young rats enhances susceptibility to diet-induced obesity and its comorbidities.     

Long term effects of high fat and sucrose diets on obesity and lymphocyte proliferation in mice

Objective  To clarify the effect of prolonged feeding of a high-fat and sucrose, and to clarify the effect of sucrose instead of other carbohydrate on obesity and immunity in C57BL/6J mice. Methods  We investigated the development of obesity and immune cell function in four groups of mice fed high-fat, high-fat plus high-sucrose, high-sucrose, and control diet for 7 months. Results  Mice fed high-fat and high-fat plus high-sucrose groups developed severe obesity. Body weight, adipose tissue weight, serum leptin, blood glucose, and insulin were significantly higher, while the level of serum soluble leptin receptor was significantly lower in mice fed high-fat and high-fat plus high-sucrose diets than in mice fed the control or high-sucrose diets. Splenocyte proliferation stimulated by T-cell mitogen (PHA, ConA, and anti-CD 3 antibody) and B-cell mitogen (LPS) was significantly lower in both obese, high-fat and high-fat plus high-sucrose groups than in control and high-sucrose groups. However, these parameters did not differ between high-fat and high-fat plus high-sucrose groups. Conclusions  Long-term feeding of high-fat diet and high-fat plus high-sucrose diet similarly induced severe obesity in C57BL/6J mice. Not only T-cell, but also B-cell function may be impaired in mice made severely obese by the high-fat or high-fat plus high-sucrose diets.     

Dietary intervention with vitamin D,calcium, and whey protein reduced fat mass and increased lean mass in rats

The aim of the current study was to determine the effects and the mechanisms of inclusion of dietary whey protein, high calcium, and high vitamin D intake with either a high-sucrose or high-fat base diets on body composition of rodents. Male Wistar rats were assigned to either no whey protein, suboptimal calcium (0.25%), and vitamin D (400 IU/kg) diet (LD), or a diet containing whey protein, high calcium (1.5%), and vitamin D (10 000 IU/kg) diet (HD), and either high-fat (40% of energy) or high-sucrose (60%) base diets for 13 weeks. Liver tissue homogenates were used to determine [¹⁴C]glucose and [¹⁴C]palmitate oxidation. mRNA expression of enzymes related to energy metabolism in liver, adipose, and muscle, as well as regulators of muscle mass and insulin receptor was assessed. The results demonstrated that there was reduced accumulation of body fat mass (P = .01) and greater lean mass (P = .03) for the HD- compared to LD-fed group regardless of the background diet. There were no consistent differences between the LD and HD groups across background diets in substrate oxidation and mRNA expression for enzymes measured that regulate energy metabolism, myostatin, or muscle vascular endothelial growth factor. However, there was an increase in insulin receptor mRNA expression in muscle in the HD compared to the LD groups. In conclusion, elevated whey protein, calcium, and vitamin D intake resulted in reduced accumulation of body fat mass and increased lean mass, with a commensurate increase in insulin receptor expression, regardless of the level of calories from fat or sucrose.     

Effect of palatable hyperlipidic diet on lipid metabolism of sedentary and exercised rats

OBJECTIVE: The present study was designed to examine 1) whether continuous feeding with a palatable hyperlipidic diet and cycling this diet with chow diet would affect lipid and carbohydrate metabolism in a similar way; and 2) whether the effect of chronic exercise on lipid and carbohydrate metabolism would be modified by these diet regimens. METHODS: Male 25-d-old Wistar rats were assigned to one of six groups: sedentary rats fed with chow diet; exercised (swimming 90 min/d, 5 d/wk) rats fed with chow diet; sedentary rats fed with a palatable hyperlipidic diet; exercised rats fed with the palatable hyperlipidic diet; sedentary rats fed with food cycles (four cycles alternating the chow and hyperlipidic diets weekly); and exercised rats fed with food cycles. After 8 wk of treatment, the animals were killed 24 h after the last exercise session. RESULTS: The hyperlipidic diet and food cycles schedules caused similar increases in body weight gain, carcass lipogenesis rate and adiposity, lipid content of the liver and gastrocnemius muscle, and serum total lipid, triacylglycerol, insulin, and leptin levels. The exercise attenuated body weight gain, adipose tissue mass, and serum triacylglycerol, insulin, and leptin levels similarly in the hyperlipidic and food cycles groups. Carcass lipogenesis rate was not affected by exercise in any of the three groups. CONCLUSIONS: The data showed that the continuous intake of a hyperlipidic palatable diet for 8 wk and the alternation of the high-fat intake with periods of chow intake cause obesity and affected lipid metabolism in a similar way. Chronic exercise attenuated body weight gain and adiposity and improved serum lipid concentrations in both high-fat feeding regimens.     

Leptin expression in hypothalamic PVN reverses dietary obesity and hyperinsulinemia but stimulates ghrelin

OBJECTIVE: In order to circumvent the multiple peripheral effects of hyperleptinemia and leptin resistance, the efficacy of leptin transgene expression in the hypothalamic paraventricular nucleus (PVN) to reinstate the central energy homeostasis in obesity was examined. RESEARCH METHODS AND PROCEDURES: A recombinant adeno-associated viral vector encoding either leptin (rAAV-lep) or green fluorescent protein (rAAV-GFP) was microinjected into the PVN of obesity-prone rats consuming a high-fat diet (HFD). RESULTS: rAAV-lep, and not rAAV-GFP, microinjection significantly reduced energy intake and enhanced energy expenditure, thereby resulting in normalization of weight and blood levels of leptin, insulin, free fatty acids, and glucose concomitant with enhanced ghrelin secretion during the extended period of observation. DISCUSSION: Thus, we show, for the first time, that amelioration of leptin insufficiency with enhanced localized leptin availability in the PVN alone can reverse dietary obesity and the attendant hyperinsulinemia and concurrently block the central stimulatory effects of elevated endogenous ghrelin on food intake and adiposity.     

Honey promotes lower weight gain, adiposity, and triglycerides than sucrose in rats

Various dietary carbohydrates have been linked to obesity and altered adipose metabolism; however, the influences of honey vs common sweeteners have not been fully explored. We hypothesized that in comparison with sucrose, a honey-based diet would promote lower weight gain, adiposity, and related biomarkers (leptin, insulin, and adiponectin) as well as a better blood lipid profile. Thirty-six male Sprague-Dawley rats (228.1 ± 12.5 g) were equally divided by weight into 2 groups (n = 18) and provided free access to 1 of 2 diets of equal energy densities differing only in a portion of the carbohydrate. Diets contained 20% carbohydrate (by weight of total diet) from either clover honey or sucrose. After 33 days, epididymal fat pads were excised and weighed, and blood was collected for analyses of serum concentrations of lipids, glucose, and markers of adiposity and inflammation. Body weight gain was 14.7% lower (P ≤ .05) for rats fed honey, corresponding to a 13.3% lower (P ≤ .05) consumption of food/energy, whereas food efficiency ratios were nearly identical. Epididymal fat weight was 20.1% lower (P ≤ .05) for rats fed honey. Serum concentrations of triglycerides and leptin were lower (P ≤ .05) by 29.6% and 21.6%, respectively, and non-high-density lipoprotein cholesterol was higher (P ≤ .05) by 16.8% for honey-fed rats. No significant differences in serum total cholesterol, high-density lipoprotein cholesterol, adiponectin, C-reactive protein, monocyte chemoattractant protein-1, glucose, or insulin were detected. These results suggest that in comparison with sucrose, honey may reduce weight gain and adiposity, presumably due to lower food intake, and promote lower serum triglycerides but higher non-high-density lipoprotein cholesterol concentrations.     

肥胖抵抗大鼠的食欲调节

目的　探讨肥胖抵抗大鼠摄食量减少的原因。方法　采用 50只健康雄性SD大鼠,分为对照组 10只和高脂组 40只,分别用基础饲料和高脂饲料喂养 13周,然后根据体重和能量摄入量筛选出饮食诱导肥胖抵抗(DIO-R)大鼠 9只和饮食诱导肥胖(DIO)大鼠 10只,观察总摄食量的变化,放免法测定血清瘦素和血浆神经肽Y水平,免疫印迹法测定大鼠脑组织中黑色素皮质激素受体 4(MCR- 4)蛋白含量。结果　DIO- R大鼠总摄食量为(1 679 .1±146. 8)g,明显低于DIO大鼠的总摄食量(1 818 .4±148 .9)g;DIO R大鼠血浆神经肽Y含量为 ( 795. 24±83 .59 )ng/L,显著低于DIO大鼠(1 007. 14±172. 83)ng/L;基础组大鼠血清瘦素含量为 ( 4 .80±0. 75 )μg/L,DIO R组为 ( 9 .17±1 .19)μg/L,DIO组为(9 .32±1 .04)μg/L,提示高脂饲料使大鼠血清瘦素水平明显增加,但DIO- R与DIO大鼠间无明显差别;基础组大鼠脑组织中MCR 4含量峰面积分析表明基础组为(342±31)mm2,DIO R组为(455±33)mm2,DIO组为(355±30)mm2,说明高脂饲料使DIO R大鼠脑组织中MCR- 4含量增加。结论　DIO- R大鼠通过增加ob基因的表达降低神经肽Y途径活性并激活MCR 4途径来减少进食量,从而抑制体重的增加。     

Flaxseed lignan attenuates high-fat diet-induced fat accumulation and induces adiponectin expression in mice

Flaxseed lignan secoisolariciresinol diglucoside (SDG) has been reported to prevent and alleviate lifestyle-related diseases including diabetes and hypercholesterolaemic atherosclerosis. This study assesses the effect of SDG on the development of diet-induced obesity in mice and the effect of the SDG metabolite enterodiol (END) on adipogenesis in 3T3-L1 adipocytes. We compared body weight, visceral fat weight, liver fat content, serum parameters, mRNA levels of lipid metabolism-related enzymes and adiponectin in mice fed either a low-fat diet (5 % TAG), high-fat diet (30 % TAG) or high-fat diet containing 0.5 and 1.0 % (w/w) SDG for 4 weeks. Administration of SDG to mice significantly reduced high-fat diet-induced visceral and liver fat accumulation, hyperlipaemia, hypercholesterolaemia, hyperinsulinaemia and hyperleptinaemia. SDG also suppressed sterol regulatory element binding protein 1c mRNA level in the liver and induced increases in the adiponectin mRNA level in the white adipose tissue and carnitine palmitoyltransferase I mRNA level in the skeletal muscle. Differentiated 3T3-L1 adipocytes were treated with 0, 5, 10 and 20 mumol/l END and then assayed for mRNA expression of adipogenesis-related genes and DNA binding activity of PPARgamma to the PPAR response element consensus sequence. END induced adipogenesis-related gene mRNA expression including adiponectin, leptin, glucose transporter 4 and PPARgamma, and induced PPARgamma DNA binding activity in 3T3-L1 adipocytes. In conclusion, SDG induced adiponectin mRNA expression and showed beneficial effects on lipid metabolism in diet-induced obesity in mice. Flaxseed lignans are suggested to regulate adipogenesis-related gene expressions through an increase in PPARgamma DNA binding activity.     

解偶联蛋白在肥胖抵抗中的作用

目的探讨解偶联蛋白在大鼠抵抗饮食诱导肥胖中的作用.方法将50只健康雄性SD大鼠随机分为对照组和高脂组,分别用基础饲料和高脂饲料喂养13周,然后根据体重和能量摄入量筛选出饮食诱导肥胖抵抗(dietinduced obesity resistance,DIO-R)和饮食诱导肥胖(diet-induced obesity,DIO)组,观察体重的变化;RT-PCR法测定大鼠褐色脂肪、白色脂肪及骨骼肌中解偶联蛋白mRNA水平.结果DIO-R大鼠体重明显低于DIO大鼠(P＜0.05);高脂饲料可增加DIO-R大鼠褐色脂肪解联偶蛋白(UCP)mRNA、白色脂肪UCP2 mRNA及骨骼肌UCP3 mR-NA水平.结论解偶联蛋白表达增加在肥胖抵抗大鼠的能量消耗中起重要作用,是大鼠抵抗肥胖发生的部分原因.     

Ameliorative effect of myricetin on insulin resistance in mice fed a high-fat,high-sucrose diet

BACKGROUND/OBJECTIVES

Obesity-associated insulin resistance is a strong risk factor for type 2 diabetes mellitus. The aim of this study was to investigate the effect of myricetin on adiposity, insulin resistance, and inflammatory markers in mice with diet-induced insulin resistance.

MATERIALS/METHODS

Five-week-old male C57BL/6J mice were fed a basal diet, a high-fat, high-sucrose (HFHS) diet, or the HFHS diet containing 0.06% myricetin or 0.12% myricetin for 12 weeks after a 1-week adaptation, and body weight and food intake were monitored. After sacrifice, serum lipid profiles, glucose, insulin, adipocyte-derived hormones, and proinflammatory cytokines were measured. The homeostasis model assessment for insulin resistance (HOMA-IR) was determined.

RESULTS

Myricetin given at 0.12% of the total diet significantly reduced body weight, weight gain, and epidydimal white adipose tissue weight, and improved hypertriglyceridemia and hypercholesterolemia without a significant influence on food intake in mice fed the HFHS diet. Serum glucose and insulin levels, as well as HOMA-IR values, decreased significantly by 0.12% myricetin supplementation in mice fed the HFHS diet. Myricetin given at 0.12% of the total diet significantly reduced serum levels of leptin, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in mice fed the HFHS diet.

CONCLUSIONS

These findings suggest that myricetin may have a protective effect against diet-induced obesity and insulin resistance in mice fed HFHS diet, and that alleviation of insulin resistance could partly occur by improving obesity and reducing serum proinflammatory cytokine levels.     

增食因子在肥胖抵抗大鼠食欲调节中的作用

目的　探讨增食因子A和B在肥胖抵抗大鼠食欲调节中的作用。方法　 5 0只健康雄性SD大鼠 ,随机分为对照组和高脂组 ,分别用基础饲料和高脂饲料喂养 13周 ,然后根据体重和能量摄入量筛选出饮食诱导肥胖抵抗(diet -inducedobesityresistance ,DIO -R)和饮食诱导肥胖 (diet-inducedobesity ,DIO)组 ,观察摄食量的变化 ,Western Blot法测定大鼠脑组织中增食因子A和B的蛋白含量。结果　DIO -R大鼠总摄食量明显低于DIO大鼠 (P <0 0 5 ) ;高脂饲料可增加大鼠脑组织中增食因子A和B的含量 ,但DIO -R大鼠和DIO大鼠间无显著性差异。结论　DIO -R大鼠体内增食因子A(orexinA)和B(orexinB)的增食作用可能被其它抑制食欲因素的作用所掩盖。因而 ,orexinA和orexinB在肥胖抵抗大鼠的食欲调节中作用较弱     

断乳后不同饲料构成对高脂膳食大鼠肥胖发生的影响

目的研究断乳后不同饲料构成对高脂膳食大鼠肥胖发生的影响。方法雄性Wistar大鼠出生后24天断乳,按体重随机分为A、B、C三组,分别给予高碳水化合物供能的基础饲料、高蛋白质供能饲料和高不饱和脂肪供能饲料。3周后均转为基础饲料。2周后再按体重将A组分为A1、A2两组,A1组继续基础饲料,A2、B、C组则转为以猪油为主的高脂膳食,6周后结束实验。分别在不同处理期末每组随机处死8只动物,称重、留取脂肪组织,计算脂体比,采血检测血糖、血脂和激素指标。结果断乳后喂饲高不饱和脂肪饲料可以显著降低高脂膳食大鼠的体重、体脂肪含量和脂体比(P<0.05),显著降低胰岛素水平、提高胰岛素敏感性(P<0.05),显著增加胰高血糖素、甲状腺激素等促脂解激素的水平(P<0.05),增加瘦素敏感性(P<0.05),改善高脂膳食大鼠的瘦素抵抗。早期喂饲高蛋白质饲料也有一定的降低体重、体脂肪含量和促脂解作用趋势,但是该组的血糖值高于A2组。结论断乳后给予高不饱和脂肪饲料可以显著抑制高脂膳食大鼠的肥胖发生。