库普弗细胞异常在大鼠非酒精性脂肪肝病发生发展中的作用

目的探讨库普弗细胞（KCs）异常在高脂饲养大鼠非酒精性脂肪肝病（NAFLD）发病中的作用。方法24只雄性SD大鼠随机分为模型组和正常组各12只,分别予高脂饲料和普通饲料饲养12周。然后测定体重、肝重、空腹血清丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）、甘油三酯（TG）、总胆固醇（TC）水平;HE染色观察肝组织切片病理学改变,并观察KCs形态变化及分泌肿瘤坏死因子-α（TNF-α）、一氧化氮（NO）的水平。结果模型组大鼠体重、肝指数、血清ALT、AST、TG、TC水平、肝脏KCs产生的TNF-α及NO水平均高于正常组（P〈0．05）;与正常组相比,模型组肝小叶内KCs发生形态及功能改变,该变化与肝组织病理学改变呈正相关（r=0．702,0．810,0．587,0．765,P均〈0．05）。结论高脂饮食大鼠肝脏库普弗细胞呈现形态及功能异常,该异常可能与NAFLD脂肪变性及炎症坏死的发生有关。     

高脂饮食诱导的肥胖和肥胖抵抗大鼠胰岛素敏感性和血脂谱改变

目的:探讨高脂饮食诱导下大鼠各肥胖评定指标、胰岛素敏感性及血脂谱的变化,为指导人们调整不合理饮食结构提供依据.方法:20只6周龄雌性SD大鼠分为2组,正常对照组(NS)7只,高脂饮食诱导组(HS) 13只,分别给予基础饲料和高脂饲料17周.根据高脂组中大鼠体重差异分为肥胖组和肥胖抵抗组.比较各组大鼠肥胖评定指标、胰岛素敏感性及血脂谱的差异.结果:高脂饮食组大鼠与正常对照组大鼠的体重、体长及Lee指数(肥胖评定指标)比较,均无统计学差异(P＞0.05);与正常对照组相比,高脂饮食组大鼠空腹胰岛素显著升高(P＜0.05),空腹血糖及IR指数也显著升高(P＜0.01).在血脂谱方面,高脂饮食组与正常对照组的TG、HDL无统计学差异;但是,与正常对照组相比,高脂饮食组的TC显著上升(P＜0.05),LDL也显著上升(P＜0.01).肥胖组与肥胖抵抗组只有体重存在统计学差异(P＜0.05),其他指标(体长、Lee指数、空腹血糖、空腹胰岛素、IR指数及血脂)均无统计学差异(P＞0.05).但是,与正常对照组相比,肥胖抵抗组的空腹血糖、空腹胰岛素、IR指数和LDL也显著升高(P＜0.05).结论:长期高脂饮食虽然有可能不使体重产生明显增加,表现出肥胖抵抗,但仍会发生明显的胰岛素抵抗和血脂代谢的紊乱.     

高脂诱导妊娠期胰岛素抵抗大鼠模型的建立与评价

目的通过高脂喂养方法建立一种类似于人类妊娠糖尿病的妊娠期胰岛素抵抗大鼠模型。方法将12只SPF级雌性未经产SD大鼠随机分为2组,普通饮食组大鼠在妊娠前后喂养正常饮食,高脂饮食组大鼠在妊娠前后喂养高脂饮食。测量饮食干预前、孕前高脂饮食期及孕期的体重及血糖,并于妊娠第18天进行空腹葡萄糖耐量试验。结果妊娠第5、12及18天,高脂饮食组大鼠空腹血糖较普通饮食组大鼠高,差异均有统计学意义(P<0.05或P<0.01)。高脂饮食组大鼠口服葡萄糖耐量试验的所有时间点血糖均高于普通饮食组大鼠(P<0.05或P<0.01)。高脂饮食组大鼠妊娠第18天的空腹胰岛素、胰岛素抵抗指数、游离脂肪酸、低密度脂蛋白胆固醇及三酰甘油较普通饮食组大鼠高,差异均有统计学意义(P<0.05或P<0.01)。结论高脂喂养复制的妊娠期糖尿病SD大鼠模型,孕鼠从妊娠早期血糖升高且持续至妊娠晚期,同时存在明显的胰岛素抵抗,这些特征与人类妊娠期糖尿病的发病特征相似。     

大黄素对非酒精性脂肪肝大鼠胰岛素抵抗及瘦素作用的影响

目的 观察大黄素对非酒精性脂肪肝大鼠胰岛素抵抗、瘦素的作用,探讨其防治脂肪肝的可能机制.方法 将42只SD大鼠按体重大小编号后采用随机数字表法分为2组：正常组（A组、8只）,给予普通饲料喂养;高脂饲料喂养组（M组、34只）,给予高脂饲料喂养.于4周末验证有脂肪肝后,M组32只大鼠按体重大小编号后用随机数字表法分为M1、M2、M3、M4四个亚组,每组8只,各大鼠饲养饲料不变,其中,M2、M3、M4组分别予低剂量大黄素、高剂量大黄素、二甲双胍干预,大黄素、二甲双胍以0.5％羧甲基纤维素钠溶解,A组、M1组予0.5％羧甲基纤维素钠灌胃.8周末测定血清瘦素、稳态模式评估法胰岛素抵抗指数（HOMA-IR）、胰岛素敏感指数（ISI）,评价肝脂肪变和炎症程度.结果 与M1组比较,低、高剂量大黄素均能改善由HOMA-IR和ISI所评价的胰岛素抵抗（P ＜0.05,P＜0.01）.M1组血清瘦素较A组升高（P＜0.01）,M2、M3组血清瘦素较M1组降低（P ＜0.05,P＜0.01）;M1组血清瘦素水平与HOMA-IR呈正相关（r=0.746,P＜0.05）,与ISI呈负相关（r=-0.731,P＜0.05）.与M1组比较,低、高剂量大黄素对大鼠肝脏脂肪变有不同改善（P ＜0.05,P＜0,01）,而对肝脏炎症均有改善（P＜0.01）.结论 大黄素降低血清瘦素水平,改善胰岛素抵抗,可能是其防治大鼠非酒精性脂肪肝的重要机制之一.     

二甲双胍对大鼠2型糖尿病并发非酒精性脂肪肝治疗作用的实验研究

目的探讨二甲双胍对大鼠2型糖尿病（T2DM）并发非酒精性脂肪肝（NAFLD）的治疗作用。方法高糖高脂饮食结合小剂量链脲佐菌素（STZ）腹腔注射建立T2DM并发NAFLD大鼠模型,将成模大鼠随机分为模型组、二甲双胍治疗组,每组16只,并设立正常对照组20只。治疗组给予二甲双胍125mg／（kg·d）灌胃治疗。于实验第16（治疗后8周）、20周（治疗后12周）末分批处死大鼠,检测肝功能、空腹血糖、血清胰岛素和血脂水平,光镜下观察大鼠肝脏组织学形态,分别以免疫组织化学法和逆转录-聚合酶链反应（RT—PCR）法检测肝组织UCP-2蛋白和UCP-2mRNA的表达情况。结果模型组大鼠血清转氨酶、空腹血糖、血清胰岛素及血脂水平均较正常组明显升高,胰岛素敏感指数较正常组明显下降（P〈0．01）;肝脏于第16周末出现不同程度脂肪变性,第20周末出现严重脂肪变性;肝组织UCP-2蛋白表达高于正常组（P均〈0．01）,UCP-2mRNA表达于第16周末[（1．789±0．301）VS（0．245±0．087）,t=11．02,P〈0．011和20周末[（1．989±0．207）VS（0．262±0．058）,t=17．93,P〈0．01]均高于正常组,以20周末更为明显。在16周末（治疗后8周）和20周末（治疗后12周）,治疗组大鼠血清转氨酶、血糖及血脂水平均有改善,胰岛素敏感指数明显升高（P〈0．01或P〈0．05）,肝细胞脂肪变性明显减轻。治疗组肝组织UCP-2蛋白表达在16周末和20周末均明显低于模型组（P均〈0．01）,UCP．2mRNA表达在16周末[（0．665±0．088）VS（1．789±0．301）,t=7．81,P〈0．01]和20周末[（0．610±0．102）VS（1．989±0．207）,t=9．98,P〈0．01]均明显低于模型组,差异有统计学意义。结论二甲双胍可降低T2DM并发NAFLD大鼠肝脏脂肪含量,调控肝脏UCP-2的适度表达,对治疗2型糖尿病并发非酒精性脂肪肝具有一定的作用。     

饮食控制对胰岛素抵抗大鼠骨骼肌中糖原合成酶激酶-3表达的影响

目的 观察饮食控制对高脂高糖饮食诱导的胰岛素抵抗模型大鼠骨骼肌中糖原合成酶激酶-3（GSK-3）表达的影响。方法 将30只Wistar大鼠随机分为正常组、胰岛素抵抗组和饮食治疗组，每组10只。正常组以常规饲料喂养，胰岛素抵抗组和饮食治疗组均以高糖高脂饲料喂养，4周后饮食治疗组大鼠改以常规饲料喂养，持续6周。采用Western blotting法检测各组大鼠骨骼肌中GSK-3的表达，于实验第1、5和11周分别检测其体质量、血甘油三脂和胆固醇、空腹血糖和胰岛素水平，并计算胰岛素敏感指数。结果 胰岛素抵抗组大鼠骨骼肌GSK-3的表达量较正常组增高70％（P〈0．01），饮食控制6周后饮食治疗组大鼠骨骼肌中GSK．3的表达量较胰岛素抵抗组减少23％（P〈0．01），较正常组增高31％（P〈0．05）。而饮食治疗组的胰岛素敏感指数与胰岛素抵抗组相比明显上升（P〈0．05）。结论 饮食控制可降低胰岛素抵抗大鼠骨骼肌细胞GSK-3表达水平，从而加强葡萄糖的摄取和利用，改善胰岛素抵抗。     

硫辛酸对高脂诱导肥胖大鼠糖、脂代谢的影响

目的探讨硫辛酸（LA）对高脂诱导肥胖大鼠糖、脂代谢的影响,为防治肥胖及相关慢性疾病发生提供新措施。方法健康雄性Wistar大鼠随机分为对照组和高脂组,6周末高脂组随机分为高脂组、LA干预组（LA组）,分别用生理盐水和LA进行腹腔注射。4周后测量大鼠体重、内脏脂肪含量以及血清三酰甘油（TG）、总胆固醇（TC）、高密度脂蛋白（HDL）、低密度脂蛋白（LDL）、血糖、空腹胰岛素,计算胰岛素抵抗指数（HOMA—IR）和胰岛素敏感指数（ISI）。结果与对照组比较,高脂组体重、内脏脂肪含量、血糖、胰岛素水平、血清TG和LDL水平均升高,肝、肾系数和ISI降低,差异有统计学意义（P〈0．05）。与高脂组比较,LA组体重、内脏脂肪含量和胰岛素水平降低,肝、肾系数和血清HDL水平增加,差异有统计学意义（P〈0．05）。结论LA能显著降低高脂诱导肥胖大鼠的体重和内脏脂肪含量,升高血清HDL水平,降低胰岛素水平,能明显改善高脂诱导肥胖大鼠糖、脂代谢紊乱。     

高脂高糖低蛋白构建大鼠非酒精性脂肪肝模型的实验研究

目的利用高脂高糖低蛋白饲料构建大鼠非酒精性脂肪肝模型。方法将40只SD大鼠随机分成两组,对照组20只,喂普通饲料;模型组20只,喂高脂高糖低蛋白饲料。于第5和第10周进行肝功能生化指标检查和肝脏超声检查。第10周全部处死并取肝组织作病理切片分析。结果超声声像图提示,模型组较对照组肝脏B超弥漫性光点增强,肝轮廓清。病理学检查证实模型组肝脏重度脂肪变性。两组大鼠体重变化无明显差异。模型组肝指数、天冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)活力明显高于对照组,除第5周谷丙氨酸转氨酶(ALT)外各项指标差异均有统计学意义(P0.01)。结论 10周的高脂高糖低蛋白饮食可成功构建适用于脂肪肝研究的大鼠脂肪肝模型。     

番茄红素对非酒精性脂肪肝大鼠糖脂代谢及炎症水平的影响

目的探讨番茄红素对非酒精性脂肪肝大鼠糖脂代谢及炎症水平的影响。方法 60只成年雄性SD大鼠,按体重随机分为空白对照组、非酒精性脂肪肝模型组、番茄红素20、60 mg/kg干预组,每组15只。空白对照组喂普通饲料,其余3组以高脂高果糖饲料喂养4周建立非酒精性脂肪性肝病模型。造模成功后,干预组分别给予不同剂量的番茄红素灌胃,8周后处死,称取大鼠体重与肝重,计算肝脏指数;苏木精-伊红染色观察肝脏组织形态学变化;收集血清,检测空腹血糖(fasting blood glucose,FBG)、空腹胰岛素(fasting insulin,INS)、计算胰岛素抵抗指数(insulin resistance index,HOMA-IR);测定肝功能指标丙氨酸氨基转移酶(alanine aminotransferase,ALT)、天门冬氨酸氨基转移酶(aspartate aminotransferase,AST);检测血清甘油三酯(triglycerides,TG)、总胆固醇(total cholesterol,TC)、高密度脂蛋白胆固醇(high density lipoprotein-cholesterol,HDL-C)、低密度脂蛋白胆固醇(low density lipoprotein-cholesterol,LDL-C)及炎症因子白细胞介素-6(interleukin-6,IL-6)、IL-18、IL-1β水平。结果与空白对照组相比,模型组大鼠肝重和肝脏指数分别升高了27%和24%;肝组织出现脂肪变性;血清ALT、TG、TC、LDL-C、IL-6、IL-1β水平显著上升,HDL-C水平显著下降(P<0.05)。与模型组相比,20、60 mg/kg番茄红素干预组大鼠肝重、肝脏指数、血清ALT、TG、FBG、IL-6、IL-1β水平均明显降低(P<0.05),INS、HOMA-IR指数均呈下降趋势;肝脏组织病变呈不同程度减轻,且以60 mg/kg番茄红素组改善效果更为显著。结论番茄红素可通过改善大鼠糖脂代谢、降低炎症因子水平来改善非酒精性脂肪肝。     

非酒精性脂肪性肝病的危险因素分析

目的探讨非酒精性脂肪肝（NAFLD）发病与患者空腹血糖（FBG）、胰岛素抵抗指数（IR）、体重指数（BMI）及血脂紊乱的关系。方法67例诊断为AFLD患者为研究组，在年龄、性别相匹配情况下，与正常对照者67例进行1：1配对，检测空腹血糖，空腹胰岛素水平及血脂，采用稳态模式评估法计算胰岛素抵抗指数、测量身高、体重，计算BMI及腰臀比。结果研究组与对照组之间空腹胰岛素、胰岛素抵抗指数、BMI及血脂紊乱比较有显著差异（P〈0．05或0．01）；多元逐步回归显示，胰岛素抵抗、腰臀比是影响肝脏脂肪含量主要的危险因素。结论胰岛素抵抗、腰臀比是影响NAFLD的主要危险因素。     

Amelioration of Hepatic Steatosis in Mice through Bacteroides uniformis CBA7346-Mediated Regulation of High-Fat Diet-Induced Insulin Resistance and Lipogenesis

Dietary habits and gut microbiota play an essential role in non-alcoholic fatty liver disease (NAFLD) and related factors such as insulin resistance and de novo lipogenesis. In this study, we investigated the protective effects of Bacteroides uniformis CBA7346, isolated from the gut of healthy Koreans, on mice with high-fat diet (HFD)-induced NAFLD. Administration of B. uniformis CBA7346 reduced body and liver weight gain, serum alanine aminotransferase and aspartate aminotransferase levels, liver steatosis, and liver triglyceride levels in mice on an HFD; the strain also decreased homeostatic model assessment for insulin resistance values, as well as serum cholesterol, triglyceride, lipopolysaccharide, leptin, and adiponectin levels in mice on an HFD. Moreover, B. uniformis CBA7346 controlled fatty liver disease by attenuating steatosis and inflammation and regulating de novo lipogenesis-related proteins in mice on an HFD. Taken together, these findings suggest that B. uniformis CBA7346 ameliorates HFD-induced NAFLD by reducing insulin resistance and regulating de novo lipogenesis in obese mice.     

Characteristics of nonalcoholic fatty liver disease induced in wistar rats following four different diets

BACKGROUND/OBJECTIVESThe prevalence of nonalcoholic fatty liver disease (NAFLD) has increased worldwide in parallel with overnutrition characterized by high-fat and high-carbohydrate intake. Our objective was to establish, in 16 weeks, a model of NAFLD in Wistar pathogen-free rats following four dietary types.MATERIALS/METHODSForty (6 weeks old) healthy Wistar male rats, weighing an average of 150 g were randomly divided into four groups of ten and assigned a diet with the same quantity (15 g/rat/day), but with different composition. The moderate-fat (MF) group was fed a moderate-fat diet (31.5% fat and 50% carbohydrates), the high-fat (HF) group was fed a fat-rich diet (51% fat), the high-sucrose (HS) group and the high-fructose (HFr) group were fed a carbohydrate-rich diet (61%). The carbohydrate contents of the HS group was composed of 60.3% sucrose while that of the HFr group was composed of 59.3% fructose.RESULTSAt week 16, the HF group had the highest percentage of cells enriched in fat (40%) and the highest weight and liver weight (P < 0.05). The HFr group showed significantly higher levels of serum triglycerides, alanine aminotransferase and adiponectin at week 16 as compared to week 1 (P < 0.05).CONCLUSIONSThe 15 g/rat/day diet composed of 51% fat or 61% carbohydrates enriched mainly in fructose may induce characteristics of NAFLD in rats.     

非酒精性脂肪性肝病大鼠肝组织NO和iNOS的变化

目的观察非酒精性脂肪性肝病大鼠肝组织NO和iNOS的变化,研究NO和iNOS在非酒精性脂肪性肝病中的作用机制。方法雄性SD大鼠20只,按体重随机分层分2组:正常对照组饲喂基础饲料,模型组以高脂饲料,喂养16W后处死大鼠,测体重、肝脏湿重,检测血清ALT、AST、ALP、胆碱酯酶(CHE)、总胆汁酸,病理组织学观察,采用硝酸还原法检测肝组织NO水平和以H3-精氨酸转化实验测定肝组织iNOS活性。结果16W末,模型组肝脏出现明显肝细胞脂肪变性和肝小叶炎症,肝指数、ALT、AST、ALP、胆碱酯酶(CHE)、总胆汁酸均高于对照组(P<0.05),模型组肝组织NO水平较正常组显著增高,模型组大鼠肝组织中iNOS活性也较正常组有明显提高,(P均<0.05)。结论高脂喂养脂肪肝大鼠肝脏中iNOS活性增强,以及诱导生成的NO水平也增高,iNOS,NO在脂肪肝肝损害中发挥重要作用。     

Resveratrol supplementation improves inflammatory biomarkers in patients with nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in the world. Resveratrol is a polyphenolic compound with antioxidant capacity that shows beneficial effects on down-regulation of inflammatory mediators and metabolic disorders. We hypothesized that supplementation with resveratrol can further improve the efficacy of lifestyle modifications in the management of NAFLD. In this randomized, double-blinded, controlled clinical trial, 50 NAFLD patients were supplemented with either a 500-mg resveratrol capsule or a placebo capsule for 12 weeks. Both groups were advised to follow an energy-balanced diet and received physical activity recommendations. Serum liver enzymes, inflammatory markers, hepatic steatosis and fibrosis, dietary intake, anthropometric measurements, and physical activity were assessed at both baseline and the end of the study. In both groups, anthropometric measurements (weight, body mass index, waist circumference), liver enzymes, and steatosis grade improved (P < 005). Resveratrol supplementation was associated with a significant reduction in liver enzyme alanine aminotransferase, inflammatory cytokines, nuclear factor κB activity, serum cytokeratin-18, and hepatic steatosis grade, as compared with placebo supplementation (P < .05). For the treatment of NAFLD, our results showed that 12 weeks of supplementation of 500 mg resveratrol, along with lifestyle modification, is superior to lifestyle modification alone. This is at least partially due to the attenuation of inflammatory markers and hepatocellular apoptosis. More studies are needed to confirm and increase the clinical application of the present results.     

Is there any association between high-density lipoprotein, insulin resistance and non-alcoholic fatty liver disease in obese children?

Non-alcoholic fatty liver disease (NAFLD) is estimated to occur in about 50% of obese children. The purpose of this study is to examine the association of anthropometric, biochemical and liver indexes in obese children with and without NAFLD and its relation with insulin resistance (IR). Forty-three obese children participated in the study. NAFLD was diagnosed by ultrasonography. Liver indices (SGOT, SGPT), lipid profile, glucose and insulin levels were performed in all patients. IR was measured by means of the homeostasis model assessment and oral glucose insulin sensitivity. Among the 43 obese patients, 18/43 (41.8%) had NAFLD based on ultrasonography. Fifty percent of them had mild steatosis and 50% had moderate/severe steatosis. In logistic regression analysis of factors associated with NAFLD, homeostasis model assessment IR (ExpB, 1.607; 95% confidence interval, 1.058-2.440; P <0.02) and high-density lipoprotein (0.952; 95% confidence interval, 0.814-1.075; P <0.03) were the most significant. IR, as has already been proved, is associated with NAFLD. Furthermore, high-density lipoprotein levels seem to play an additional role in predicting NAFLD in obese children.     

茵陈蒿汤对代谢综合征-脂肪肝大鼠增强胰岛素敏感性及抗脂肪肝作用

目的观察茵陈蒿汤(capillaris decoction)对高脂-高糖诱导代谢综合征(metabolic syndrome,MetS)-脂肪肝(fattyliver,FL)大鼠的防治作用及机制。方法 SD大鼠,雌雄各半,除空白对照组食用标准饲料和饮用蒸馏水外,其余动物随机喂饲富含高脂肪(25%)饲料和高蔗糖(10%)饮水,造模8周;然后将大鼠随机分为模型对照、silibinin150mg.kg-1以及茵陈蒿汤5.0g.kg-1及2.5g.kg-1两个剂量组;分别灌胃给药或蒸馏水,qd×4w,测定大鼠空腹血清胰岛素(Fins)、血糖(FBG)、三酰甘油(TG)、胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、游离脂肪酸(FFA)、脂联素,天门冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)、胆碱酯酶(ChE)、超氧化物歧化酶(SOD)、丙二醛(MDA)、一氧化氮合酶(NOS)和一氧化氮(NO),并计算胰岛素敏感指数(ISI)、胰岛素抵抗指数(IRI)及肝指数;光学显微镜下观察肝脏组织的病理学改变。结果 MetS-FL大鼠TC、FFA、TG、LDL-C、MDA、FBG和Fins含量升高,HDL-C、NO和脂联素含量下降,AST、ALT、ChE活性升高,NOS和SOD活性降低,ISI减弱,肝指数升高并呈脂肪肝组织病理改变,与正常对照组比较,差异有显著性(P<0.05或P<0.01)。茵陈蒿汤5.0g.kg-1及2.5g.kg-1以及silibinin150mg.kg-1处理MetS-FL大鼠后,不同程度地降低MetS-FL大鼠TC、FFA、TG、LDL-C、MDA、FBG、Fins含量和AST、ALT、ChE活性,升高HDL-C、NO和脂联素含量,增强ISI,肝指数下降并改善脂肪肝组织病理改变,差异有显著性(P<0.05或P<0.01)。结论茵陈蒿汤对抗MetS-FL大鼠IR、增强胰岛素敏感性、纠正高胰岛素血症,改善血糖-脂代谢紊乱,抑制氧化应激反应和肝细胞损伤,降低氨基转移酶和ChE活性,以及不同程度地改善脂肪肝组织的病理改变,是茵陈蒿汤拮抗代谢综合征-脂肪肝的部分作用机制。茵陈蒿汤抗脂肪肝效应显示量效关系。     

Nutritional Management of Insulin Resistance in Nonalcoholic Fatty Liver Disease (NAFLD)

Nonalcoholic fatty liver disease (NAFLD) is an emerging global health concern. It is the most common form of chronic liver disease in Western countries, affecting both adults and children. NAFLD encompasses a broad spectrum of fatty liver disease, ranging from simple steatosis (NAFL) to nonalcoholic steatohepatitis (NASH), and is strongly associated with obesity, insulin resistance, and dyslipidemia. First-line therapy for NAFLD includes weight loss achieved through diet and physical activity. However, there is a lack of evidenced-based dietary recommendations. The American Diabetes Association’s (ADA) recommendations that aim to reduce the risk of diabetes and cardiovascular disease may also be applicable to the NAFLD population. The objectives of this review are to: (1) provide an overview of NAFLD in the context of insulin resistance, and (2) provide a rationale for applying relevant aspects of the ADA recommendations to the nutritional management of NAFLD.