High-fat diets: healthy or unhealthy?

In the current dietary recommendations for the treatment and prevention of Type 2 diabetes and its related complications, there is flexibility in the proportion of energy derived from monounsaturated fat and carbohydrate as a replacement for saturated fat. Over the last few years, several population studies have shown that subjects eating a lot of refined grains and processed foods have a much larger increase in waist circumference than those following a diet higher in monounsaturated fat, protein and carbohydrates rich in fibre and whole grain. In the present issue of Clinical Science, Sinitskaya and co-workers have demonstrated that, in normal-weight rodents categorized into groups of high-fat and medium-carbohydrate [53%/30% of energy as fat/carbohydrate; 19.66 kJ/g (4.7 kcal/g)], high-fat and low-carbohydrate [67%/9% of energy as fat/carbohydrate; 21.76 kJ/g (5.2 kcal/g)] and high-fat and carbohydrate-free [75%/0% of energy as fat/carbohydrate; 24.69 kJ/g (5.9 kcal/g)] diets, the high-fat diets containing carbohydrates were both obesogenic and diabetogenic, whereas the very-high-fat and carbohydrate-free diet was not obesogenic but led to insulin resistance and higher risk of cardiovascular disease. This finding may indicate that high-fat diets could easily give rise to an unhealthy diet when combined with carbohydrates, highlighting the significance of macronutrient composition, rather than caloric content, in high-fat diets.     

外周血Th17/Treg平衡变化与Crohn病患者病情程度的关联性及临床意义

目的:探讨外周血Th17/Treg平衡变化与克罗恩病(Crohn病)患者病情程度的关联性及动态监测临床意义.方法:选取2018年1月～2020年6月我院Crohn病患者103例作为观察组,其中轻度活动期29例,中度活动期23例,重度活动期21例,缓解期30例,另选同期健康体检者41例作为对照组.对比两组及观察组不同病情...     

不同高脂饲料对小鼠肥胖和胰岛素抵抗模型制备情况的效果比较

目的:探讨两种不同的高脂饲料在C57/BL6J小鼠肥胖和胰岛素抵抗(IR)模型制备过程中的效果差别,以期为更好的制备C57/BL6J小鼠肥胖和IR模型提供理论指导.方法:以雄性C57/BL6小鼠为实验材料,随机分为三组,分别为基础组,喂食国内A公司啮齿动物基础饲料;模型1组,喂食国内A公司生产的啮齿动物高脂饲料(HFD...     

The immunologic outcome of enhanced function of mouse liver lymphocytes and Kupffer cells by high-fat and high-cholesterol diet

Dietary lipids/cholesterol may modulate liver immune function. We have recently found that mouse F4/80 Kupffer cells are classified into phagocytic CD68 Kupffer cells and cytokine-producing CD11b Kupffer cells. We here investigate how a high-fat and/or high-cholesterol diet affects innate immune liver mononuclear cells. For 4 weeks, C57BL/6 mice were fed a high-fat and high-cholesterol diet (HFCD), a high-cholesterol diet (HCD), a high-fat diet (HFD), or a control diet (CD). High-fat and high-cholesterol diet and HCD increased liver cholesterol levels; serum cholesterol levels increased in HFCD and HFD mice but not in HCD mice. The increased proportion of natural killer (NK) cells, downregulated NK1.1 expression of natural killer T cells, and enhanced CD69 and IL-12 receptor β mRNA expression of liver lymphocytes indicate the activation of them by HFCD. IL-12 production from Kupffer cells and interferon γ production from NK/natural killer T cells activated by LPS and/or IL-12 both increased. IL-12 pretreatment more effectively improved the survival of HFCD mice relative to the survival of CD mice upon injections of liver metastatic EL-4 cells. In contrast, HFCD mouse survival decreased after LPS injection and generalized Shwartzman reaction. Consistently in HFCD mice, Toll-like receptor 4 mRNA expression of whole Kupffer cells was upregulated, and CD11b Kupffer cells proportionally increased. Although the proportion of CD68 Kupffer cells decreased in HFCD mice, phagocytic activity of them was enhanced. Mice fed with HCD rather than those fed with HFD showed features closer to HFCD mice. Thus, enhanced function of mouse liver mononuclear cells is likely dependent on the liver cholesterol level, rather than the liver triglyceride level.     

Effects of a Mediterranean-inspired diet on blood lipids, vascular function and oxidative stress in healthy subjects

Mediterranean-inspired diets have been shown to decrease cholesterol levels in patients with hypercholesterolaemia, who frequently exhibit endothelial dysfunction. The aims of the present study are to improve endothelial function by dietary intervention in healthy subjects with lipid levels representative of a Western population. Twenty-two healthy subjects (mean total cholesterol, 5.6 mmol/l) were given a Mediterranean-inspired diet rich in omega-3 fatty acids and sterol esters, but low in saturated fat, or an ordinary Swedish diet, for 4 weeks in a randomized cross-over study. The composition of the diets were: in the Swedish diet, 2090 kcal (where 1 kcal=4.184 kJ; 48% of energy from carbohydrate, 15% from protein and 36% from fat) and 19 g of fibre; in the Mediterranean-inspired diet, 1869 kcal (48% of energy from carbohydrate, 16% from protein, 34% from fat) and 40 g of fibre. After each dietary period, fasting blood lipids, insulin and glucose levels, as well as apo B (apolipoprotein B) and LDL (low-density lipoprotein) particle size, were analysed. Endothelial-dependent and -independent vasodilation was measured invasively by venous occlusion plethysmography, and arterial distensibility was assessed by echocardiography tracking. Fibrinolytic capacity across the forearm, as well as oxidative stress measured through urinary F(2)-isoprostane, were evaluated. Total, LDL- and apo B-cholesterol and triacylglycerol (triglyceride) concentrations were decreased by 17%, 22%, 16% and 17% respectively, after the Mediterranean-inspired diet compared with the Swedish diet ( P <0.05 for all). However, no differences in plasma concentrations of insulin and glucose and LDL particle size, endothelial function, arterial distensibility, fibrinolytic capacity or oxidative stress were detected. Treatment for 4 weeks with a Mediterranean-inspired diet decreased blood lipids in healthy individuals with a low-risk profile for cardiovascular disease. This beneficial effect was not mirrored in vascular function or oxidative stress evaluation.     

The DGAT2 gene is a candidate for the dissociation between fatty liver and insulin resistance in humans

The enzyme DGAT (acyl-CoA:diacylglycerol acyltransferase) catalyses the final step of triacylglycerol (triglyceride) synthesis. Mice overexpressing hepatic DGAT2 fed a high-fat diet develop fatty liver, but not insulin resistance, suggesting that DGAT2 induces a dissociation between fatty liver and insulin resistance. In the present study, we investigated whether such a phenotype also exists in humans. For this purpose, we determined the relationships between genetic variability in the DGAT2 gene with changes in liver fat and insulin sensitivity in 187 extensively phenotyped subjects during a lifestyle intervention programme with diet modification and an increase in physical activity. Changes in body fat composition [MR (magnetic resonance) tomography], liver fat and intramyocellular fat ((1)H-MR spectroscopy) and insulin sensitivity [OGTT (oral glucose tolerance test) and euglycaemic-hyperinsulinaemic clamp] were determined after 9 months of intervention. A change in insulin sensitivity correlated inversely with changes in total body fat, visceral fat, intramyocellular fat and liver fat (OGTT, all P<0.05; clamp, all P< or =0.03). Changes in total body fat, visceral fat and intramyocellular fat were not different between the genotypes of the SNPs (single nucleotide polymorphisms) rs10899116 C>T and rs1944438 C>T (all P> or =0.39) of the DGAT2 gene. However, individuals carrying two or one copies of the minor T allele of SNP rs1944438 had a smaller decrease in liver fat (-17+/-10 and -24+/-5%; values are means+/-S.E.M.) compared with subjects homozygous for the C allele (-39+/-7%; P=0.008). In contrast, changes in insulin sensitivity were not different among the genotypes (OGTT, P=0.76; clamp, P=0.53). In conclusion, our findings suggest that DGAT2 mediates the dissociation between fatty liver and insulin resistance in humans. This finding may be important in the prevention and treatment of insulin resistance and Type 2 diabetes in subjects with fatty liver.     

运动干预对胰岛素抵抗大鼠骨骼肌蛋白激酶B活性和蛋白与基因表达的影响

目的：探讨一次性游泳运动对胰岛素抵抗大鼠骨骼肌蛋白激酶B（protein kinaes, PKB）mRMA表达、蛋白总量（t- PKB）及磷酸化PKB（p-PKB）的影响。方法：SD大鼠随机分为正常饮食组、高脂饮食组、高脂饮食+运动组。分别对高脂饮食组与高脂饮食+运动组饲以高脂饲料,4周后对高脂饮食+运动组大鼠运动干预2h。测血液葡萄糖和胰岛素浓度;Western blot法检测骨骼肌t-PKB蛋白表达、p-PKB磷酸化水平;RT-PCR法分析PKB mRNA表达。结果：高脂饮食组血糖和胰岛素浓度明显高于对照组;高脂饮食+运动组血糖和胰岛素浓度低于高脂饮食组;高脂饮食组PKB mRNA表达下降;高脂饮食+运动组 PKB磷酸化水平和蛋白总量高于高脂饮食组。结论：运动干预改善高脂饮食诱发胰岛素抵抗大鼠对胰岛素的敏感性,增加PKB磷酸化水平和蛋白与基因的表达。     

Effects of replacing saturated fat with complex carbohydrate in diets of subjects with NIDDM

This study examined the safety of an isocaloric high-complex carbohydrate low-saturated fat diet (HICARB) in obese patients with non-insulin-dependent diabetes mellitus (NIDDM). Although hypocaloric diets should be recommended to these patients, many find compliance with this diet difficult; therefore, the safety of an isocaloric increase in dietary carbohydrate needs assessment. Lipoprotein cholesterol and triglyceride (TG, mg/dl) concentrations in isocaloric high-fat and HICARB diets were compared in 7 NIDDM subjects (fat 32 +/- 3%, fasting glucose 190 +/- 38 mg/dl) and 6 nondiabetic subjects (fat 33 +/- 5%). They ate a high-fat diet (43% carbohydrate; 42% fat, polyunsaturated to saturated 0.3; fiber 9 g/1000 kcal; cholesterol 550 mg/day) for 7-10 days. Control subjects (3 NIDDM, 3 nondiabetic) continued this diet for 5 wk. The 13 subjects changed to a HICARB diet (65% carbohydrate; 21% fat, polyunsaturated to saturated 1.2; fiber 18 g/1000 kcal; cholesterol 550 mg/day) for 5 wk. NIDDM subjects on the HICARB diet had decreased low-density lipoprotein cholesterol (LDL-chol) concentrations (107 vs. 82, P less than .001), but their high-density lipoprotein cholesterol (HDL-chol) concentrations, glucose, and body weight were unchanged. Changes in total plasma TG concentrations in NIDDM subjects were heterogeneous. Concentrations were either unchanged or had decreased in 5 and increased in 2 NIDDM subjects. Nondiabetic subjects on the HICARB diet had decreased LDL-chol (111 vs. 81, P less than .01) and unchanged HDL-chol and plasma TG concentrations).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of rosiglitazone treatment on the pentose phosphate pathway and glutathione-dependent enzymes in liver and kidney of rats fed a high-fat diet

Background: Animals fed high-fat diets have been shown to develop hyperglycemia, insulin resistance, hyperlipidemia, and moderate obesity, which resemble the human metabolic syndrome. Obesity, the metabolic syndrome, and some thiazolidinediones, which act as insulin sensitizers, may increase oxidative stress, and/or influence the levels of cellular reducing equivalents and homeostasis.Objective: This study investigated the effects of a high-fat diet, rosiglitazone, or a high-fat diet plus rosiglitazone on metabolic syndrome parameters and crucial liver and kidney enzyme activities in rats.Methods: Male Wistar rats were assigned to 4 groups (n = 6 per group): (1) the fat (F) group was fed a rodent diet comprising 45 kcal% fat, (2) the rosiglitazone (R) group was fed a standard rat chow comprising 4.97 kcal% fat plus rosiglitazone (3 mg/kg.d), (3) the fat + rosiglitazone (FR) group was fed a rodent diet comprising 45 kcal% fat (as lard, product D12451) plus rosiglitazone (3 mg/kg.d), and (4) the control (C) group was fed a standard rat chow comprising 4.97 kcal% fat. Animals were housed for 4 weeks, at which time the liver and kidney were isolated for spectrophotometric determination of enzyme activities. Body weight was measured before treatment (baseline) and then weekly throughout the study. Adiposity was measured at the end of the 4 weeks.Results: The activities of glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6-PGD), glutathione reductase (GR), and glutathione-S-transferase (GST) were significantly reduced in the livers of groups F, R, and FR compared with group C (all P < 0.05). Kidney G6PD, 6-PGD, and GR were found to be significantly lower in group R compared with the other groups (all P < 0.05). Kidney GST was similar in all groups. Plasma glucose, triglyceride, and insulin concentrations were significantly higher than in group F versus the other groups (all P < 0.05). Adiposity was increased in groups F and FR compared with groups C and R (all P < 0.05). Serum cholesterol concentrations were similar in all groups.Conclusions: In this study, high-fat diet in rats decreased the enzyme activities responsible for pentose phosphate pathway and glutathione-dependent metabolism in liver but not in kidney. Similarly, these enzyme activities were inhibited with rosiglitazone treatment alone in both organs.     

α硫辛酸对肥胖大鼠糖脂代谢的影响

目的观察高脂饮食诱导肥胖大鼠一般情况、糖、脂代谢的变化及α-硫辛酸(ALA)对其影响。方法 Wistar大鼠50只,随机选10只普通饲料喂养作为正常对照组,其余40只采用高脂喂养10周后评价肥胖大鼠模型,成模肥胖大鼠再随机分为两组:HFD组、HFD+ALA组,后者腹腔注射(ALA 30mg/kg,ip)2周。测定各组大鼠血清空腹血糖(FBG)、空腹胰岛素(FIns)、甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、游离脂肪酸(NEFA)。结果高脂饮食10周后成功诱导肥胖大鼠模型32只;HFD组与正常对照组相比,FIns、TG、TC、HDL-C、LDL-C明显升高(P<0.05),ALA干预后,肥胖大鼠体重降低、NEFA、胰岛素抵抗指数(IRI)明显下降,并不同程度地降低TC、TG、Fins,3组大鼠血糖比较未见明显差异。结论高脂饮食诱导的肥胖大鼠体重明显增加、血脂升高、出现胰岛素抵抗;ALA干预使大鼠食欲下降、体重减轻,并明显改善胰岛素抵抗状态。     

Protective effects of selenium-enriched peptides from Cardamine violifolia against high-fat diet induced obesity and its associated metabolic disorders in mice

Selenium-enriched peptides from Cardamine violifolia (CSP) have excellent antioxidant functions but little is known about their effects on obesity and associated metabolic disorders in mice fed with a high-fat diet (HFD). In this study, C57BL/6 mice were fed a HFD with or without CSP supplementation (CSPL: 26 μg Se per kg bw per d; CSPH: 104 μg per kg bw per d) for 10 weeks. The results showed that both CSPL and CSPH could ameliorate overweight gain, excess fat accumulation, serum lipid metabolism, and insulin resistance. The potential mechanism might be associated with the increase in thermogenesis, reduced oxidative stress, and inflammation, which regulated the gene expression in lipid and cholesterol metabolism. In addition, CSPL and CSPH also maintained the intestinal integrity and modulated the gut microbiota. Increased Blautia in CSP may be involved in the protective effect against obesity. Furthermore, a distinct increase in Lactobacillus was exclusively found in CSPH, suggesting that a more effective function of CSPH on metabolic disorders might be through the synergism of Blautia and Lactobacillus. Spearman''s correlation analysis revealed that these specific genera were significantly correlated with the metabolic improvements. Taken together, CSP supplementation prevented HFD-induced obesity and metabolic disorders, probably by ameliorating oxidative stress and inflammation, regulating metabolic genes, and modulating the gut microbiota compositions.

Selenium-enriched peptides from Cardamine violifolia (CSP) have excellent antioxidant functions but little is known about their effects on obesity and associated metabolic disorders in mice fed with a high-fat diet (HFD).     

A Mouse Model of Metabolic Syndrome: Insulin Resistance,Fatty Liver and Non-Alcoholic Fatty Pancreas Disease (NAFPD) in C57BL/6 Mice Fed a High Fat Diet

Diet-induced obesity in C57BL/6 mice triggers common features of human metabolic syndrome (MetS). The purpose is to assess the suitability of a diet-induced obesity model for investigating non-alcoholic fatty pancreatic disease (NAFPD), fatty liver and insulin resistance. Adult C57BL/6 mice were fed either high-fat chow (HFC, 60% fat) or standard chow (SC, 10% fat) during a 16-week period. We evaluated in both groups: hepatopancreatic injuries, pancreatic islets size, alpha and beta-cell immunodensities, intraperitoneal insulin tolerance test (IPITT) and oral glucose tolerance test (OGTT). The HFC mice displayed greater mass gain (p<0.0001) and total visceral fat pads (p<0.001). OGTT showed impairment of glucose clearance in HFC mice (p<0.0001). IPITT revealed insulin resistance in HFC mice (p<0.0001). The HFC mice showed larger pancreatic islet size and significantly greater alpha and beta-cell immunodensities than SC mice. Pancreas and liver from HFC were heavier and contained higher fat concentration. In conclusion, C57BL/6 mice fed a high-fat diet develop features of NAFPD. Insulin resistance and ectopic accumulation of hepatic fat are well known to occur in MetS. Additionally, the importance of fat accumulation in the pancreas has been recently highlighted. Therefore, this model could help to elucidate target organ alterations associated with metabolic syndrome.     

2型糖尿病大鼠模型抵抗素基因表达与胰岛素敏感指数的相关性

背景:抵抗素作为一种蛋白质激素,具有直接对抗胰岛素的作用,其可能是肥胖者易发2型糖尿病的关键分子.目的:构建2型糖尿病大鼠模型并观察大鼠抵抗素的基因表达与胰岛素敏感指数的关系,观察罗格列酮对抵抗素基因表达的影响.设计:随机对照,动物实验.单位:郑州大学第一附属医院老年病科.材料:选用健康雌性Wistar大鼠30只,鼠龄2个月,购自华中科技大学同济医学院动物中心.实验用普通饲料由华中科技大学同济医学院动物中心提供,总热量为14..8 J/g(质量分数:蛋白质0.2,碳水化合物0.61,脂肪0.17);高脂饲料由普通饲料加蔗糖、炼猪油、鸡蛋、奶粉混合而成,总热量为20.083 J/g(蛋白质0.09,碳水化合物0.51,脂肪0.38).大鼠抵抗素及β-actin引物由北京赛百盛公司合成.方法:实验于2006-10/2007-10在郑州大学第一附属医院完成.实验过程中对动物的处置符合动物伦理学要求.适应性喂养大鼠2周后,随机分为普通饲料组8只和高脂饲料组22只.高脂饲料组大鼠尾静脉注射链脲佐菌素25 mg/kg,注射后第2人开始给予高脂饮食;普通饲料组给予柠檬酸钠一柠檬酸缓冲液1 mL/kg尾静脉注射,继续普通饲料喂养.高脂饲料喂养12周后有15只大鼠符合2型糖尿病模型标准,被随机分为罗格列酮组8只和模型组7只,前组用罗格列酮2 mg/(kg·d)灌胃,后组用蒸馏水8 mL/(kg·d)灌胃;普通饲料组灌胃等量蒸馏水,干预4周.主要观察指标:应用葡萄糖氧化酶法测定血糖;采用磁性分离酶联免疫法测定胰岛素;采用酶法测定血清三酰甘油和总胆固醇.计算胰岛素敏感指数(1/空腹血糖×空腹胰岛素).用反转录-聚合酶链反应检测大网膜脂肪组织抵抗素mRNA的表达.应用Spearman相关分析和多元逐步回归分析显示抵抗素基因与胰岛素敏感指数的关系.结果:造模成功15只和对照组大鼠8只进入结果分析.①大网膜脂肪组织抵抗素基因表达(A值):模型组为0.27±0.031,明显高于普通饲料和罗格列酮组(0.15±0.018和0.20±0.024,P<0.01).②Spearman相关分析和多元逐步回归分析结果:抵抗素基因与空腹血糖、空腹胰岛素和胰岛素敏感指数分别呈正相关(r=0.271、0.283和0.323,P<0.01);多元逐步回归分析显示,胰岛素敏感指数对抵抗素基因的作用最显著(R2=0.081).结论:2型糖尿病大鼠抵抗素基因表达升高,且与胰岛素敏感指数相关;罗格列酮可逆转此状况.     

TNF-related apoptosis-inducing ligand significantly attenuates metabolic abnormalities in high-fat-fed mice reducing adiposity and systemic inflammation

TRAIL [TNF (tumour necrosis factor)-related apoptosis-inducing ligand] has recently been shown to ameliorate the natural history of DM (diabetes mellitus). It has not been determined yet whether systemic TRAIL delivery would prevent the metabolic abnormalities due to an HFD [HF (high-fat) diet]. For this purpose, 27 male C57bl6 mice aged 8 weeks were randomly fed on a standard diet, HFD or HFD+TRAIL for 12 weeks. TRAIL was delivered weekly by intraperitoneal injection. Body composition was evaluated; indirect calorimetry studies, GTT (glucose tolerance test) and ITT (insulin tolerance test) were performed. Pro-inflammatory cytokines, together with adipose tissue gene expression and apoptosis, were measured. TRAIL treatment reduced significantly the increased adiposity associated with an HFD. Moreover, it reduced significantly hyperglycaemia and hyperinsulinaemia during a GTT and it improved significantly the peripheral response to insulin. TRAIL reversed the changes in substrate utilization induced by the HFD and ameliorated skeletal muscle non-esterified fatty acids oxidation rate. This was associated with a significant reduction of pro-inflammatory cytokines together with a modulation of adipose tissue gene expression and apoptosis. These findings shed light on the possible anti-adipogenic and anti-inflammatory effects of TRAIL and open new therapeutic possibilities against obesity, systemic inflammation and T2DM (Type 2 DM).     

益智对小鼠实验性高脂血症的降脂作用

目的探讨益智 ( Alpinia oxyphylla Miq) 对小鼠实验性高脂血症的降血脂作用 . 方法实验分别用花生油和猪油造成高脂模型对照组 ( PE- HFD, LA- HFD) , 各组分别添加 2% 益智 ( AOM) 和 4% AOM. 饲养观察 28 d后 , 用显色 - 比色法测定血清总胆固醇 ( TC) 和血清高密度脂蛋白胆固醇 ( HDL- C) , 并计算出 HDL- C/TC值和动脉硬化指数 ( AI) . 结果实验中的自制高脂饲料可以成功地诱导小鼠产生高胆固醇血症及动脉硬化 ( P<0.01) . 添加 2% AOM组及添加 4% AOM组的 TC和 AI均极显著低于 HFD组 ( P< 0.01) , HDL- C/TC均极显著高于 HFD组 ( P< 0.01) ; 添加 2% AOM组的 HDL- C显著高于 HFD组 ( P< 0.05) ; 添加 4% AOM组的 HDL- C极显著高于 HFD组 ( P< 0.01) . 且添加 4% AOM的对上述 4种指标的影响效果都优于 2% AOM组的 ( P< 0.01) . 结论益智具有良好的预防和降低血脂作用 .     

Protective effect of Caralluma fimbriata against high-fat diet induced testicular oxidative stress in rats

High-fat diet (HFD) promotes the oxidative stress formation, which in turn has hazardous effects on reproductive system and fertility. The objective of this study was to evaluate the protective effect of Caralluma fimbriata on high-fat diet-induced oxidative stress in the testis of rat. Male Wistar rats were randomly divided into five groups: Control (C), Control treated with CFE (C+ CFE), High fat diet fed (HFD), High fat diet fed treated with CFE (HFD + CFE) and High fat diet fed treated with Metformin (HFD + Met). CFE was orally administered (200 mg/kg body weight) for 90 days to groups-C + CFE and HFD + CFE rats. The effects of HF-diet on the reproductive organs were determined by measuring relative and absolute testes and epididymal fat pads weights. Regarding testes antioxidant status, high-fat fed rats showed higher levels of lipid peroxidation, protein oxidation, polyol pathway enzymes and lower GSH levels and lower activities of antioxidants, while CFE treatment prevented all these observed abnormalities. The present study clearly indicates that CFE offers a significant protection against HF-diet induced testicular oxidative stress in rats.     

Beneficial effects of rosuvastatin on insulin resistance, adiposity, inflammatory markers and non-alcoholic fatty liver disease in mice fed on a high-fat diet

The aim of the present study was to evaluate the effects of ST (rosuvastatin) and GZ (rosiglitazone) on IR (insulin resistance) and on liver as well as adipose tissue in mice fed on an HF (high-fat) diet. Our data show that treatment with ST resulted in a marked improvement in insulin sensitivity characterized by enhanced glucose clearance during the insulin tolerance test and a 70% decrease in the HOMA-IR (homoeostasis model assessment of insulin resistance) index level (P=0.0008). The ST-treated mice exhibited lower gains in BM (body mass; -8%; P<0.01) and visceral fat pad thickness (-60%; P<0.01) compared with the untreated HF group. In comparison with HF-diet-fed mice, HF+ST-treated mice showed a significant reduction in hepatomegaly and liver steatosis (-6%, P<0.05; and -21%, P<0.01 respectively). In HF+ST-treated mice, the hepatic TAG (triacylglycerol) levels were reduced by 58% compared with the HF group (P<0.01). In addition, the expression of SREBP-1c (sterol-regulatory-element-binding protein-1c) was decreased by 50% in the livers of HF+ST-treated mice (P<0.01) relative to the HF-diet-fed mice. The levels of resistin were lower in the HF+ST-treated group compared with the HF group (44% less, P< 0.01). In conclusion, we demonstrated that ST treatment improved insulin sensitivity and decreased liver steatosis in mice fed on an HF diet. Furthermore, ST reduced BM gains, improved the circulating levels of plasma cholesterol and TAG, and reduced hepatic TAG, which was concomitant with lower resistin levels.     

Effect of a high‐calcium energy‐reduced diet on abdominal obesity and cardiometabolic risk factors in obese Brazilian subjects

Background: Clinical trials designed to examine the effects of calcium supplementation on abdominal obesity have had ambiguous results. Aims: This study aimed to evaluate, during energy restriction, the effects of a high‐calcium diet (HCD) on measures of abdominal obesity and cardiometabolic risk factors in Brazilian obese subjects of multiethnic origin. Methods: We conducted a randomised clinical trial. Fifty obese subjects of both sexes, aged 22–55 years, with stable body weight and a low calcium intake were randomised into the following outpatient dietary regimens: (i) a low‐calcium diet (LCD; < 500 mg/day) or (ii) a HCD [1200–1300 mg/day, supplemented with non‐fat powdered milk (60 g/day)]. Both groups followed an energy‐restricted diet (?800 kcal/day) throughout the study (16 weeks). Results: Thirty‐nine participants completed the study. After 16 weeks of energy restriction, a significant reduction was observed in all anthropometric parameters, metabolic variables (except for high‐density lipoprotein cholesterol) and blood pressure levels in both the groups. Insulin was significantly reduced only in the HCD group. Subjects on the HCD compared with those on the LCD exhibited a greater reduction in waist circumference (p = 0.002), waist‐to‐hip ratio (p = 0.0001), diastolic blood pressure (p = 0.04) and mean blood pressure (p = 0.03). Conclusions: Our study suggests that increased calcium intake may enhance the beneficial effects of energy restriction on abdominal obesity and blood pressure.