Fish oil increases cholesterol storage in white adipose tissue with concomitant decreases in inflammation, hepatic steatosis, and atherosclerosis in mice

Although fish oil has hypolipidemic and antiatherosclerotic properties, the potential for white adipose tissue (WAT) to mediate these effects has not been studied. LDL-receptor deficient (LDLR-/-) mice were fed high fat, olive oil-containing diets supplemented with additional olive oil or with fish oil for 12 wk. Fish oil feeding significantly reduced plasma lipid levels. In contrast, lipid storage in WAT was increased in fish oil-fed mice as evidenced by increased total fat (P < 0.05) and perigonadal WAT mass (P < 0.05), increased cholesterol storage (P < 0.001), and adipocyte hypertrophy. Despite increased adipose tissue mass, WAT-specific inflammation and insulin sensitivity were improved (P < 0.05), concomitant with reduced macrophage infiltration. Furthermore, fish oil increased WAT and plasma levels of adiponectin. In addition, fish oil feeding decreased the formation of proinflammatory F2- isoprostanes, markers of oxidative stress (P < 0.05). The increased WAT lipid storage in fish oil-fed mice was associated with reduced lipid accumulation in liver (P < 0.05) and decreased atherosclerotic lesion area (P < 0.05). Taken together, these data highlight the specific role of WAT in regulating dietary fish oil-mediated improvement in systemic lipid homeostasis and atherosclerosis.     

葡萄糖酸铬、鱼油对肥胖大鼠胰岛素抵抗和瘦素抵抗的影响

为探讨在大鼠肥胖形成的过程中 ,葡萄糖酸铬、鱼油对胰岛素抵抗和瘦素抵抗的影响。选取雄性Wistar大鼠 5 0只按体重随机分为 5组。基础对照组 :喂基础饲料同时灌胃水 5ml kgBW。高脂对照组 :喂高脂饲料同时灌胃豆油 5ml kgBW。高脂加鱼油组 :喂高脂饲料同时灌胃鱼油 5ml kgBW。高脂加铬组 :喂高脂饲料同时灌胃葡萄糖酸铬 3mg kgBW(以铬计 )。高脂加鱼油加铬组 :喂含铬高脂饲料同时灌胃鱼油 5ml kgBW。喂养五周 ,于每周末称重、采尾血测定血糖、胰岛素和瘦素。结果高脂饲料诱导的肥胖组体重、血糖、胰岛素和瘦素均高于基础对照组 ,提示铬和鱼油有降血糖、降低胰岛素、瘦素的作用 ,而且能改善胰岛素抵抗和瘦素抵抗作用。     

Long-term effect of fish oil diet on basal and stimulated plasma glucose and insulin levels in ob/ob mice

In this study, the ob/ob mouse model was used to investigate epidemiological evidence linking fish intake to relative reduction in incidence of Type 2 diabetes mellitus and glucose. We have investigated, in comparison to low and high fat diets, the effect of a fish oil diet on basal and stimulated plasma glucose and insulin levels in male and female ob/ob mice. Mice were fed for 12 months with a saturated fat diet containing 25% lard, with a low fat diet containing 5% soybean oil, with a polyunsaturated fat diet containing 25% safflower seed oil (n-6) or with polyunsaturated fat diet containing 23% fish oil (n-3). Total body weight increased to approximately 100 g at the end of the experiment, with the highest increase in the order of lard > safflower oil > fish oil > soybean oil diet. Intercurrent deaths were found especially in the fish oil diet group. Compared to the other diet groups, plasma insulin levels of the fish oil diet group were significantly increased 3 months after the start of the diet and remained higher for another 3 months. Thereafter, the level declined to those of the other diet groups. Glucose-tolerance tests at 3, 6, 8 and 10 months showed a tendency of more efficient tissue glucose uptake in the fish oil group compared to the other groups, which was in accordance with a higher plasma insulin levels. At 12 months, microscopy revealed an increased severity of hepatic brown pigment accumulation and extramedullary haematopoiesis in the spleen of mice fed with fish oil. We conclude that fish oil diet in ob/ob mice reduced the body weight gain and increased the glucose-induced insulin secretion. Fish oil diet also increased intercurrent mortality. However, a consistent course of death could not be established using morphological parameters.     

A high oxidised frying oil content diet is less adipogenic, but induces glucose intolerance in rodents

Oxidised frying oil (OFO) and fish oil have been shown to be peroxisome proliferator-activated receptor (PPAR)alpha activators and their ingestion results in pleotropic peroxisome proliferator responses in rats. To examine the effect of dietary OFO on adiposity, four groups of weanling Sprague-Dawley rats were fed isoenergetically with, respectively, a low fat basal diet containing 5 g/100 g of fresh soybean oil (LSB) or a high fat diet containing 20 g/100 g of fresh soybean oil (HSB), OFO (HO) or fish oil (HF). The tissue mass, cell size and lipid/DNA ratio in the retroperitoneal fat pad and serum leptin levels were lowest in the HO group (P < 0.05), indicating that dietary OFO has a greater anti-adipogenic action than dietary fish oil. However, a tendency to hyperglycaemia was observed in the HO group (P = 0.0528). To examine the effect of dietary OFO on glucose tolerance, three groups of rats and three groups of mice were fed, respectively, the LSB, HSB or HO diet, and an oral glucose tolerance test was performed. After oral glucose load, the area under the curve for blood glucose (AUCglu) over 2 h was significantly higher, and that for serum insulin (AUCins) over 90 min was significantly lower, in the HO group than in the other two groups (P < 0.05). These results demonstrate that, in rats and mice, a high OFO diet is less adipogenic, but induces glucose intolerance.     

Increasing the amount of fat in a conjugated linoleic acid-supplemented diet reduces lipodystrophy in mice

Conjugated linoleic acid (CLA) is a naturally occurring group of dienoic derivatives of linoleic acid found in beef and dairy products. However, when 1 g CLA/100 g diet was given to mice in a low fat diet (4 g fat/100 g diet), they showed a marked decrease in fat mass, but demonstrated symptoms of lipoatrophic diabetes, i.e., marked hepatomegaly and insulin resistance. In this study, to determine whether the decrease in adipose tissue was responsible for these adverse effects, mice were fed different doses of CLA and dietary fat. In Experiment 1, mice were fed different doses of CLA (0, 0.1 and 1 g CLA/100 g diet) in a fixed 4 g fat/100 g diet; in those fed 0.1 g CLA, subcutaneous white adipose tissue (WAT) weight was 48% lower than in mice fed 0 g CLA. The mice fed 0.1 g CLA did not exhibit hepatomegaly and insulin resistance. In Experiment 2, mice were fed for 5 mo different amounts of dietary fat (4, 13 and 34 g fat/100 g diet) in 0 or 1 g CLA/100 g diet; in mice fed 1 g CLA with 34 g fat, retroperitoneal and subcutaneous WAT weights were 76 and 79% lower, respectively, than those of mice fed 0 g CLA with 34 g fat. Mice fed 1 g CLA in the diet with 34 g fat had normal plasma insulin concentrations and a 45% greater liver weight. These data suggested that the percentage of CLA in dietary fat might be a determinant of CLA-mediated lipodystrophy.     

The major green tea polyphenol, (-)-epigallocatechin-3-gallate, inhibits obesity, metabolic syndrome, and fatty liver disease in high-fat-fed mice

In this study, we investigated the effects of the major green tea polyphenol, (-)-epigallocatechin-3-gallate (EGCG), on high-fat-induced obesity, symptoms of the metabolic syndrome, and fatty liver in mice. In mice fed a high-fat diet (60% energy as fat), supplementation with dietary EGCG treatment (3.2 g/kg diet) for 16 wk reduced body weight (BW) gain, percent body fat, and visceral fat weight (P < 0.05) compared with mice without EGCG treatment. The BW decrease was associated with increased fecal lipids in the high-fat-fed groups (r(2) = 0.521; P < 0.05). EGCG treatment attenuated insulin resistance, plasma cholesterol, and monocyte chemoattractant protein concentrations in high-fat-fed mice (P < 0.05). EGCG treatment also decreased liver weight, liver triglycerides, and plasma alanine aminotransferase concentrations in high-fat-fed mice (P < 0.05). Histological analyses of liver samples revealed decreased lipid accumulation in hepatocytes in mice treated with EGCG compared with high-fat diet-fed mice without EGCG treatment. In another experiment, 3-mo-old high-fat-induced obese mice receiving short-term EGCG treatment (3.2 g/kg diet, 4 wk) had decreased mesenteric fat weight and blood glucose compared with high-fat-fed control mice (P < 0.05). Our results indicate that long-term EGCG treatment attenuated the development of obesity, symptoms associated with the metabolic syndrome, and fatty liver. Short-term EGCG treatment appeared to reverse preexisting high-fat-induced metabolic pathologies in obese mice. These effects may be mediated by decreased lipid absorption, decreased inflammation, and other mechanisms.     

Influence of moderate energy restriction and seafood consumption on bone turnover in overweight young adults

BACKGROUND: Overweight and obesity are increasing in young adults. However, moderate energy restriction aimed at lowering body weight may promote bone turnover and bone loss. Inclusion of fish or fish oils in a weight-loss diet may attenuate these adverse skeletal effects. OBJECTIVE: We examined the effects of incorporating fish or fish oil into an energy-restricted diet on bone turnover markers in young overweight adults. DESIGN: While following a strict hypoenergetic (-30% relative to estimated requirements) diet for 8 wk, 276 overweight men and women [body mass index (in kg/m(2)): 27.5-32.5; age: 20-40 y) were randomly assigned to 1 of 4 dietary groups: sunflower-oil capsules (3 g/d; control), cod (3 x 150 g/wk), salmon (3 x 150 g/wk), and fish-oil capsules (3 g/d). Body weight, bone biomarkers, and 25-hydroxyvitamin D were measured at baseline and endpoint. Data were analyzed with repeated-measures analysis of variance and general linear models. RESULTS: The mean (+/-SD) weight loss was 5.14 +/- 3.0 kg (5.8% +/- 3.2% body weight) during the 8 wk in the 4 dietary groups combined. Urinary N-telopeptides of type I collagen and serum C-terminal telopeptide of type I collagen increased (P < 0.05), whereas serum osteocalcin (but not bone-specific alkaline phosphatase) decreased (P < 0.05) from baseline to endpoint. Increased fish or fish-oil consumption had no effect (P > 0.1) on the changes in bone markers induced by weight loss. In contrast, increased salmon consumption increased serum 25-hydroxyvitamin D (P < 0.01). CONCLUSIONS: A nutritionally adequate but energy-restricted diet, with different contents of n-3 fatty acids, which resulted in modest weight loss, unfavorably altered bone turnover markers in young overweight adults. Such changes were not prevented by increased fish or fish-oil consumption.     

Adaptive changes in adipocyte gene expression differ in AKR/J and SWR/J mice during diet-induced obesity

Obesity-prone (AKR/J) and obesity-resistant (SWR/J) mice were weaned onto low (LF) or high fat (HF) diets to identify adaptive changes in adipocyte gene expression that are associated with differences between the strains in fat deposition. Food consumption was monitored at weekly intervals and all mice were evaluated after consuming their respective diets for 4 wk for analysis of mRNA levels of selected metabolic genes. Despite similar food consumption, body weight and fat deposition were significantly greater in AKR/J than in SWR/J mice, and this difference was greatly accentuated by the HF diet. The HF diet produced distinct differences between strains in gene expression patterns among fat depots. In AKR/J mice, UCP1 mRNA was decreased 10-fold in interscapular brown adipose tissue (BAT) and four- to fivefold in retroperitoneal and inguinal white adipose tissue (WAT). The HF diet also decreased PGC-1 and beta(3)-adrenergic receptor mRNA by two- and ninefold in BAT from AKR/J mice. In contrast, the HF diet either increased uncoupling protein (UCP)1 in BAT or had no effect on expression of these genes in adipose tissues from SWR/J mice. UCP2 mRNA was fourfold higher in WAT from AKR/J compared with SWR/J mice and increased by an additional twofold in WAT from AKR/J mice fed the HF diet. UCP2 was unaffected by diet in SWR/J mice. These studies show that the diet-induced obesity of AKR/J mice is characterized by increased metabolic efficiency and is associated with changes in adipocyte gene expression that limit the adaptive thermogenic response to increased energy density.     

Effect of dietary carbohydrate source on the development of obesity in agouti transgenic mice

OBJECTIVES: Our objective was to evaluate the effects of a qualitative change in dietary carbohydrate source on body weight and adiposity in a rodent model of diet-induced obesity. RESEARCH METHODS AND PROCEDURES: We evaluated the effects of high-fat diets (basal) varying in carbohydrate source in aP2-agouti transgenic mice. In the ad libitum study, animals were given free access to the basal diet or one of four test diets for 6 weeks. In two of the diets, dietary carbohydrate was derived from a single source: mung bean noodles (MUNG) or rolled oats (ROLL). The remaining diets were designed to mimic commercially available instant oatmeal with added sugar (IO-S) or flavored instant oatmeal (IO-F). In the energy-restricted study, animals were given ad libitum access to the basal diet for 6 weeks. Subsequently, animals were assigned to one of six treatment groups for 6 weeks. One group was continued on the basal diet ad libitum. The remaining groups were maintained with energy restriction (70% ad libitum) on either the basal, MUNG, ROLL, IO-S, or IO-F diet. RESULTS: Subcutaneous fat pad mass was significantly higher (p<0.05) in the energy-restricted basal and IO-S groups compared with the energy-restricted ROLL diet. Similarly, visceral fat pad mass was significantly lower with ROLL and MUNG diets (p<0.05 for both) compared with basal and IO-S diets, and the insulin:glucose ratio was reduced (by 23% to 34%, p<0.05) in these two diets compared with all others. In ad libitum-fed animals, liver fatty acid synthase expression was 43% to 62% lower (p<0.05) with ROLL and MUNG diets compared with all others. DISCUSSION: These data suggest that a qualitative change in dietary carbohydrate source modulates body weight and adiposity.     

Effect of dairy supplementation on body composition and insulin resistance in mice

OBJECTIVE: This study examined whether yogurt supplementation attenuated the weight gain and insulin resistance in mice fed a moderate-fat diet. METHODS: Nine-week-old male mice (F1 BTBR x C57Bl6/J) were housed individually for the duration of the study. After initial measurements of body weight and composition, mice were randomly assigned to receive one of two isocaloric diets (19.4% kcal protein, 45.5% kcal carbohydrate, and 35.1% kcal fat). One diet was supplemented with dried yogurt powder (10.75 g/100 g of diet). In the first experiment, mice received the diets for 4 wk, after which body weight and body composition were reassessed. In the second experiment, an insulin tolerance test was performed at week 4 and glucose uptake in gonadal fat was assessed at week 5. RESULTS: Baseline body weight was not significantly different between control and yogurt mice (P = 0.85). Body weight and fat mass increased significantly over time (P < 0.001) and there was a significant effect of diet on the increase in body weight (P < 0.05) and fat mass (P < 0.001), with the yogurt mice gaining less weight and fat than the control mice. Food intake was not significantly affected by the yogurt supplementation (P = 0.906). Digestive efficiency was significantly lower in the yogurt mice (P < 0.05) due to greater fecal production (P < 0.01). There was no significant effect of diet on the glucose area under the curve during the insulin tolerance test (P = 0.24). Glucose uptake in the gonadal fat was significantly higher in the yogurt mice than in controls under basal (P < 0.05) and insulin-stimulated (P < 0.05) conditions. CONCLUSION: Yogurt supplementation resulted in less weight and fat gain in mice fed isocaloric diets due to a decrease in digestive efficiency. Yogurt also enhanced the uptake of glucose in fat but did not significantly improve insulin sensitivity.     

Effects of fish oil and safflower oil emulsions on diet-induced hepatic steatosis in rats receiving total parenteral nutrition

This study was conducted to investigate the effects of fish oil and safflower oil emulsions in total parenteral nutrition (TPN) solutions on diet-induced hepatic steatosis. Rats were divided into a control group (C, n = 6) and four experimental groups (A, B, S, F, n = 11 approximately 14). The control group was fed a chow diet whereas the experimental groups received a high fat (15%, w/w) diet containing 0.1% (w/w) cholesterol. Group A received the high fat diet for 4 weeks, and was killed at the end of the fourth week to ensure that hepatic steatosis had occurred. Groups S and group F received TPN with safflower oil or fish oil emulsions, respectively, for 1 week following experimental diet feeding for 4 weeks. Group B was fed a limited amount of the high fat diet, without cholesterol, for 1 week following 4 weeks of experimental diet in order to maintain the same body weight and cholesterol intake as the TPN groups. Diet-induced hepatic steatosis was observed in the experimental groups. Fat deposition was reversed when the total caloric and cholesterol intake was reduced. Fish oil infusion ameliorated the severity of hepatic steatosis, whereas safflower oil had no effect on liver fat deposition. These results suggest that TPN with fish oil emulsions may be beneficial to patients with diet-induced hepatic steatosis.     

Reduction of body weight by dietary garlic is associated with an increase in uncoupling protein mRNA expression and activation of AMP-activated protein kinase in diet-induced obese mice

This study investigated the antiobesity effect of garlic in diet-induced obese mice. Male C57BL/6J mice were fed a high-fat diet (45% fat) for 8 wk to induce obesity. Subsequently, they were fed a high-fat control diet, high-fat diets supplemented with 2%, or 5% garlic (wt:wt) for another 7 wk. Dietary garlic reduced body weight and the mass of various white adipose tissue deposits and also ameliorated the high-fat diet-induced abnormal plasma and liver lipid profiles. Garlic supplementation significantly decreased the mRNA levels of adipogenic genes in white adipose tissues (WAT). However, consumption of garlic increased the expression of mRNA for uncoupling proteins in brown adipose tissue (BAT), liver, WAT, and skeletal muscle. Mice treated with garlic maintained a significantly higher body temperature than untreated mice during a 6-h, 4°C cold challenge and, notably, AMP-activated protein kinase (AMPK) activity was stimulated in BAT, liver, WAT, and skeletal muscle. These results suggest that the antiobesity effects of garlic were at least partially mediated via activation of AMPK, increased thermogenesis, and decreased expression of multiple genes involved in adipogenesis.     

Baseline plasma C-reactive protein concentrations influence lipid and lipoprotein responses to low-fat and high monounsaturated fatty acid diets in healthy men

To date, no studies have compared the effects of consuming a low-fat diet and a high monounsaturated fatty acid (MUFA) diet, under unrestricted energy intake conditions, on plasma C-reactive protein (CRP) concentrations. Men [n = 61; 37.5 +/- 11.5 y old (mean +/- SD), mean BMI 29.0 +/- 5.0 kg/m2] were randomly assigned to consume ad libitum a moderately low-fat diet (25.8% of energy intake from fat) or a high-fat diet rich in MUFA (40.1% of energy intake from fat, 22.5% from MUFA) for 6-7 wk. Plasma CRP concentrations were measured using a highly sensitive assay. Neither diet affected the plasma CRP concentration. However, baseline CRP concentrations predicted lipoprotein/lipid responsiveness to the experimental diets. After intake of the low-fat diet, plasma total and VLDL-triglyceride (TG) concentrations were increased in the subgroup with high CRP concentrations (P < 0.05 and P < 0.01, respectively) whereas they were reduced in the subgroup with low CRP concentrations at baseline (P < 0.01 for both). The high-MUFA diet reduced plasma TG, VLDL-TG, and VLDL cholesterol only in the subgroup with low CRP at baseline (P < 0.0001). In conclusion, the low-fat diet and the high-MUFA diet did not affect plasma CRP concentrations. However, baseline plasma CRP concentrations may modulate the diet-induced changes in plasma lipid and lipoprotein concentrations.     

n-3多不饱和脂肪酸对肥胖小鼠肠道菌群的影响

目的 探讨n-3多不饱和脂肪酸(n-3 polyunsaturated fatty acids,n-3 PUFAs)对饮食诱导肥胖小鼠肠道菌群的影响。方法 将30只3～4 周龄C57BL/ 6J雄性小鼠,随机分为3组(10只/组),分别给予高脂饲料、鱼油n-3 PUFAs高脂饲料(脂肪含量均为34.9%,供能比均为60%)以及正常脂饲料(脂肪来源于猪油和葵花籽油,脂肪含量为4.3%,供能比为10%)喂养16周。然后采集粪便,采用16sDNA-实时荧光定量PCR方法检测肠道菌群变化;取结肠组织,采用实时荧光定量PCR方法检测白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)、肿瘤坏死因子-α(TNF-α)以及单核细胞趋化蛋白-1(monocyte chemoattractant protein-1,MCP-1)的mRNA表达水平。结果 与正常脂饲料喂养对照组小鼠相比,高脂饲料诱导肥胖小鼠粪便中厚壁菌门及乳杆菌属的数量显著增多,而拟杆菌门、放线菌门、变形菌门以及双歧杆菌属的数量则显著减少(P<0.05)。两组肥胖小鼠相比,鱼油n-3 PUFAs高脂组肥胖小鼠的粪便双歧杆菌属数量明显增加,而乳杆菌属数量显著减少(P<0.05)。对结肠炎性因子mRNA表达水平检测显示,高脂饲料组肥胖小鼠的IL-1β、IL-6、TNF-α及MCP-1表达量较正常脂饲料组小鼠均明显升高(P<0.05),而IL-10的表达量无变化;鱼油n-3 PUFAs高脂饲料组肥胖小鼠的IL-1β、TNF-α较高脂饲料组肥胖小鼠有显著性的降低(P<0.05)。结论 鱼油n-3 PUFAs可以改善肥胖状态下的肠道菌群紊乱及肠道炎症状态。     

Long-term weight maintenance and cardiovascular risk factors are not different following weight loss on carbohydrate-restricted diets high in either monounsaturated fat or protein in obese hyperinsulinaemic men and women

The aim of this study was to determine after 52 weeks whether advice to follow a lower carbohydrate diet, either high in monounsaturated fat or low fat, high in protein had differential effects in a free-living community setting. Following weight loss on either a high monounsaturated fat, standard protein (HMF; 50 % fat, 20 % protein (67 g/d), 30 % carbohydrate) or a high protein, moderate fat (HP) (40 % protein (136 g/d), 30 % fat, 30 % carbohydrate) energy-restricted diet (6000 kJ/d) subjects were asked to maintain the same dietary pattern without intensive dietary counselling for the following 36 weeks. Overall weight loss was 6.2 (SD 7.3) kg (P < 0.01 for time with no diet effect, 7.6 (SD 8.1) kg, HMF v. 4.8 (SD 6.6) kg, HP). In a multivariate regression model predictors of weight loss at the end of the study were sex, age and reported percentage energy from protein (R2 0.22, P < 0.05 for the whole model). Fasting plasma insulin decreased (P < 0.01, with no difference between diets), 13.9 (SD 4.6) to 10.2 (SD 5.2) mIU/l, but fasting plasma glucose was not reduced. Neither total cholesterol nor LDL-cholesterol were different but HDL was higher, 1.19 (SD 0.26) v. 1.04 (SD 0.29) (P < 0.001 for time, no diet effect), while TAG was lower, 1.87 (SD 1.23) v. 2.22 (SD 1.15) mmol/l (P < 0.05 for time, no diet effect). C-reactive protein decreased (3.97 (SD 2.84) to 2.43 (SD 2.29) mg/l, P < 0.01). Food records showed that compliance to the prescribed dietary patterns was poor. After 1 year there remained a clinically significant weight loss and improvement in cardiovascular risk factors with no adverse effects of a high monounsaturated fat diet.     

茶色素对单纯性肥胖大鼠胰岛素抵抗的影响

目的探讨茶色素对单纯性肥胖大鼠胰岛素抵抗的影响。方法50只清洁级SD大鼠随机分成对照组、高脂组和低中高剂量茶色素干预组。高脂组和茶色素干预组以高脂饲料饲喂8周诱发肥胖致胰岛素抵抗模型，茶色素干预组再给予低中高剂量茶色素灌胃8周，实验结束后采血测定血糖，血胰岛素及血TG、TCH、LDL和FFA，并剖杀动物测睾周和肾周脂体比。结果（1）高脂组空腹胰岛素、TG、TC和FFA明显高于对照组（P〈0．05），而空腹血糖、LDL和HDL无显著性差异；（2）中高剂量茶色素干预组空腹胰岛素、TG和FFA低于高脂组；（3）高脂组睾周脂体比、肾周脂体比和内脏脂体比均高于对照组（P〈0.05）。经茶色素干预后，中、高剂量睾周脂体比、肾周脂体比和脂体比均较高脂组低（P〈0．05）。结论茶色素可降低单纯性肥胖大鼠的空腹胰岛素，调节血脂，提高胰岛素敏感性，改善胰岛素抵抗。     

铬、鱼油对肥胖模型大鼠瘦素和胰岛素的影响

目的铬、鱼油参与并调节糖、脂肪代谢,选择铬、鱼油作为影响因素,观察其对饮食诱导肥胖大鼠的影响。方法将肥胖模型大鼠按体重随机分为4组,每组8只。分别为肥胖组、鱼油组、鱼油+铬组和铬组,另设基础对照组。在实验的第0周和第6周空腹采尾血,测定血清瘦素和胰岛素水平。结果3个实验组的胰岛素和瘦素水平在第0周时,与肥胖组差异无显著性(P>0.05),第6周时,显著低于肥胖组(P<0.05)。结论结果提示铬、鱼油有缓解肥胖大鼠高胰岛素和高瘦素水平的作用。     

D-核糖对高脂喂饲小鼠胰岛素抵抗的影响

目的观察D-核糖对高脂喂饲的C57BL/6小鼠血糖、血脂及胰岛素等的影响,探讨D-核糖对改善高脂膳食引起的糖耐量异常和胰岛素抵抗的可能性。方法 8 w龄C57BL/6雄性小鼠36只,随机分成正常对照、高脂对照、低剂量的D-核糖+高脂组(高脂+2.5%核糖)和高剂量的D-核糖+高脂组(高脂+5%核糖),喂饲12 w,记录摄食量和体重变化。11w进行葡萄糖耐量试验(OGTT),并计算葡萄糖曲线下面积(AUC)。干预12w处死,进行血生化指标及胰岛素检测。结果高脂+5%核糖组小鼠的血糖水平低于高脂对照组(P<0.05);高脂+2.5%核糖和高脂+5%核糖组糖耐量曲线下面积(P<0.01)、血清胰岛素水平(P<0.05)及胰岛素抵抗指数HOMA-IR(P<0.01)均显著低于高脂对照组。血清胆固醇(CHO)、高密度脂蛋白胆固醇(HDL-C)在核糖干预后的变化并不明显(P>0.05);高脂+5%核糖组血清低密度脂蛋白胆固醇(LDL-C)、血清甘油三酯(TG)及游离脂肪酸(FFA)低于高脂对照组(P<0.05)。结论 D-核糖可以改善高脂饲料喂饲小鼠的糖耐量异常和胰岛素抵抗。[营养学报,2013,35(2):142-145]