非肥胖的高血压病患者的非酒精性脂肪肝与代谢综合征的关系

目的探讨非肥胖的不伴有糖尿病的高血压病患者的非酒精性脂肪肝（NAFLD）与代谢综合征（MS）的关系。方法84例非肥胖的不伴有糖尿病的高血压病患者,根据B超诊断有无脂肪肝分为高血压伴NAFLD组42例,高血压不伴NAFLD组42例。对2组患者的体重指数（BMI）、血压、血糖、血脂、血胰岛素、胰岛素抵抗指数（HOMA-IR）、转氨酶及MS患病率等指标进行比较分析,并对MS与上述指标的关系进行多因素的logistic回归分析。结果高血压伴NAFLD组的BMI、甘油三酯、胰岛素、HO-MA-IR、转氨酶及MS患病率较不伴NAFLD组显著增高,而且MS与NAFLD呈独立相关。结论MS不但明显增加NAFLD发生率,而且还加重肝脏损害。     

非酒精性脂肪性肝病患者脂联水平检测及意义

目的 检测非酒精性脂肪性肝病(NAFLD)患者血清脂联素的水平并探讨其临床意义.方法 选取60例无糖尿病的NAFLD患者(NAFLD组)和40例健康对照者(对照组),测定两组的空腹血糖、血脂、胰岛素和脂联素水平,计算稳态模型评估法胰岛素抵抗指数(HOMA-IRI).结果 NAFLD组血清脂联素水平明显低于对照组[(8.04±3.20)μg/ml比(12.53±8.50)μg/ml,P＜0.001];脂联素与体重指数(BMI)、腰围、天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)、γ-谷氨酰基转移酶(GGT)、甘油三酯(TG)、HOMA-IRI呈负相关;BMI、HOMA-IRI为脂联素水平的独立影响因素.结论 NAFLD患者血清脂联素水平降低,脂联素可能参与了NAFLD患者胰岛素抵抗及动脉粥样硬化的发病过程.     

肥胖儿童非酒精性脂肪性肝病血清瘦素水平分析

目的:检测肥胖儿童和正常对照儿童血清瘦素水平,探讨瘦素与非酒精性脂肪性肝病的相关性.方法:对100例肥胖儿童及100例正常对照儿童测量身高、体重,计算体重指数(BMI);检测空腹血糖(FPG)、胰岛素(FINS)、谷丙氨酸氨基转移酶(ALT)总胆固醇(Tc)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白A(ApoA)、载脂蛋白B(ApoB);胰岛素抵抗采用稳态模式评估法的胰岛素抵抗指数(HOMA-IR)指标;血清瘦素采用酶联免疫吸附试验检测.对肥胖儿童进行肝脏B超检查,并对非酒精性脂肪性肝病病变程度分为轻、中、重度,分别积分1、2、3分.结果:肥胖组瘦素、BMI、ALT、TG、LDL-C、TC、APB、FINS、HOMA-IR较对照组高(P＜0.05),而HDL-C较对照组低P＜0.05.100例肥胖儿童组中根据B超发现非酒精脂肪性肝病(NAFLD) 55例,与其余45例单纯肥胖儿童结果比较显示:NAFLD组瘦素、BMI、TG、ALT、FINS、HOMA-IR水平较高P＜0.05,而HDL-C水平较低P＜0.05;多元Logistic回归分析显示BMI、瘦素和TG水平是脂肪肝形成的主要危险因素;多元线性回归分析显示瘦素和BMI与NAFLD评分独立相关(P值＜0.05).结论:高瘦素水平是肥胖儿童非酒精性脂肪性肝病的危险因素之一,监测血清瘦素水平有助于判断非酒精性脂肪性肝病的病变程度.     

儿童超重及肥胖与代谢综合征的相关性

目的 探讨儿童超重与代谢综合征(MS)的相关性.方法 回顾性调查分析某院2002年1月～2011年12月期间在门诊就诊的肥胖儿及超重儿为研究对象,按照体重指数分组分为超重儿174例、肥胖儿154例.同时以同期住院治疗体重指数正常的仅仅患呼吸道疾病患儿325例为对照组.分析腰围、臀围、收缩压(SBP)、舒张压(DBP)、空腹血糖(FBG)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)、丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、空腹胰岛素(FINS)及计算胰岛素抵抗指数(HOMA-IR).结果 (1)对照组MS患病率0.00％,超重儿MS患病率6.90％,肥胖儿MS患病率25.32％,随着体重指数的升高,MS患病率呈现升高趋势,三组MS患病率比较差异有统计学意义(x2=93.35,P＜ 0.01). (2)腰围、臀围、SBP、DBP、FBG、TC、TG、HDL-C、LDL-C、ALT、AST、FINS、HOMA-IR等检测指标结果在对照组、超重儿、肥胖儿中以逐渐升高趋势分布,并且超重儿与对照组、肥胖儿与对照组组间各指标比较差异均有统计学意义(P＜0.05). (3) BMI、腰围、SBP、TC、TG、LDL-C、ALT、AST、FINS与HOMA-IR呈正相关,HDL-C与HOMA-IR呈负相关(均P＜0.01).结论 超重及肥胖儿童MS发病率明显较正常体重儿童升高,MS发病与超重及肥胖密切相关,应注重预防超重及肥胖.     

成都地区非酒精性脂肪肝与代谢综合征相关性研究

目的调查分析非酒精性脂肪肝(nonalcoholic fatty liver disease,NAFLD)和代谢综合征(metabolic syndrome,MS)的关系。方法采集2011年2～5月成都地区在四川大学华西医院进行健康检查的20～80岁受检者的疾病史、体格检查、生化检测以及上腹部超声检查的结果,并对数据进行统计分析。结果 NAFLD患病率12.33%,NAFLD、MS两病的共患病率3.47%。NAFLD、MS两病共患病率随体重指数(BMI)增加而升高。单纯NAFLD组BMI、收缩压(SBP)、舒张压(DBP)、空腹血糖(FPG)、甘油三酯(TG)、低密度脂蛋白(LDL-C)均高于正常组(P﹤0.01),高密度脂蛋白(HDL-C)低于正常组(P﹤0.01);NAFLD合并MS组丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)、谷氨酰转肽酶(GGT)均高于单纯组(P﹤0.01)。结论 NAFLD与MS紧密相关,二者发病过程中的相互加重、相互促进作用应当引起足够的重视并应进行综合防治。     

2型糖尿病合并非酒精性脂肪肝与血清脂联素的相关性研究

目的研究2型糖尿病(T2DM)合并非酒精性脂肪肝(NAFLD)与血清脂联素(APN)的相关性。方法选取2011年8月—2013年7月宁波大学医学院附属医院收治的76例初发或病史3年的T2DM患者,按照是否合并NAFLD分为T2DM+NAFLD和T2DM两组,每组各38例,另选30名正常体检者作为对照组(NC组)。测量三组的体质指数(BMI)、血脂、血糖、肝功能、胰岛素抵抗指数(HOMA-IR)和APN等指标水平并进行比较。结果 T2DM+NAFLD组的BMI、三酰甘油(TG)、胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、谷丙转氨酶(ALT)、空腹胰岛素(FINS)及HOMA-IR等指标水平明显高于T2DM组和NC组,APN水平明显低于其他两组(P0.05);Pearson相关分析显示,APN与BMI、高密度脂蛋白胆固醇(HDL-C)和HOMA-IR呈负相关,与TC、LDL-C和ALT呈正相关(P均0.05);多元线性回归分析显示HDL-C、HOMA-IR是APN的独立影响因子(P0.05)。结论 T2DM合并NAFLD患者存在严重的胰岛素抵抗和糖脂代谢紊乱,APN水平是影响NAFLD发生与发展的关键因子。     

315例非酒精性脂肪性肝病的追踪观察与临床分析

目的 研究非酒精性脂肪性肝病(NAFLD)的临床特征及其在转归过程中的变化.方法 对315例NAFLD患者(NAFLD组)与2474例无脂肪肝(FL)人员(非FL组)的临床资料进行比较,并对NAFLD患者进行平均(28.0±3.2)个月的追踪观察.结果 NAFLD组合并肥胖、高血脂、高血压、高血糖、心肌缺血和胆道疾病的发生率均高于非FL组(P<0.01).追踪终点时按照超声诊断,NAFLD进展患者的体重指数、收缩压、舒张压、空腹血糖、三酰甘油、总胆固醇、丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)和γ-谷氨酰转移酶(γ-GT)均高于改善患者(P<0.01);低密度脂蛋白、间接胆红素和尿酸高于改善患者(P<0.05);高密度脂蛋白低于改善患者(P<0.01);白蛋白、球蛋白、直接胆红素、尿素氮和肌酐与改善患者比较差异无统计学意义(P>0.05).另外,NAFLD改善患者的体重指数和三酰甘油水平终点低于起点(P<0.01).NAFLD进展患者的体重指数、收缩压、空腹血糖、ALT、AST、γ-GT水平终点高于起点(P<0.01);舒张压终点高于起点(P<0.05).结论 在NAFLD改善或加重的过程中,伴随着脂质代谢、血糖、血压和肝肾功能的变化,预防和逆转NAFLD具有重要的临床意义.     

浙西南地区肥胖儿童的非酒精性脂肪肝的发生特点 危险因素及针对性预防措施研究

目的了解该地区肥胖儿童非酒精性脂肪肝(NAFLD),探究该地区肥胖儿童患NAFLD的独立危险因素;将肥胖儿童NAFLD进行合理分级,针对不同等级严重程度,进行分级细化的个性化管理,明确科学有效的改善肥胖儿童NAFLD的治疗方案。方法选取在全市中小学校筛查以及2015年10月-2018年10月在丽水市中心医院内分泌科和肥胖专科门诊就诊的肥胖儿童,共160例。根据B超及血生化分为两组:无肝脏损害的肥胖儿童(OCWLD组) 100例; NAFLD组60例。比较OCWLD组和NAFLD组在腰围/身高比值、体质指数(BMI)、有无黑棘皮、谷草转氨酶(AST)、谷丙转氨酶(ALT)、谷安酰转移酶(GGT)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、总胆固醇(TC)、三酰甘油(TG)、空腹血糖、胰岛素抵抗指数(HOMA-IR)、B超及肝纤维化指标差别等,探讨分析肥胖儿童患NAFLD的独立危险因素。对患儿随访6个月,予以必要的升降阶梯治疗,针对每个患儿实行量身定制的个性化治疗,患儿每3个月进行一次复查,研究针对性预防措施。结果通过调查该地区NAFLD肥胖儿童,肥胖儿童发病的危险因素为体质量、肝纤维化指标、血脂,且采取针对性预防措施能积极改善患儿身体健康,差异有统计学意义(P0.05)。结论对患儿进行分级细化的针对个性化管理,明确科学有效的改善肥胖儿童NAFLD的治疗方案。     

血同型半胱氨酸对新诊断2型糖尿病患者非酒精性脂肪性肝病的影响

目的研究血清同型半胱氨酸(HCY)对新诊断2型糖尿病(T2DM)患者非酒精性脂肪性肝病(NAFLD)的影响。方法选取本院2015年6月至2017年3月收治的117例T2DM患者进行研究,将所选患者按照是否合并NAFLD分为观察组与对照组。观察组为合并NAFLD,有59例;对照组为不合并NAFLD,有58例。检测两组患者的血清HCY及肝功能、血脂、空腹血糖(FPG)、空腹胰岛素(FINS)等水平,并计算胰岛素抵抗指数(HOMA-IR)及体质量指数(BMI)。结果观察组患者的BMI、FINS、HCY、HOMA-IR、TG、ALT、LDL-C、HDL-C水平与对照组比较均有显著差异(P0.05)。HCY与BMI、FINS、HOMA-IR、TG、ALT、LDL-C呈正相关关系,与HDL-C呈负相关关系。结论 HCY浓度的升高是T2DM患者并发NAFLD的一个危险因素,且HCY与BMI、FINS、HOMA-IR、TG、ALT、LDL-C呈正相关关系,与HDL-C呈负相关关系。     

学龄期儿童肥胖相关性脂肪肝及血脂代谢异常对照研究

目的 探讨兰州市学龄期儿童肥胖非酒精性脂肪肝(nonalcoholic fatty liver disease, NAFLD)、血脂代谢异常及其相关因素。方法 2011年6-10月选取3所小学1至6年级7~14岁小学生作为研究对象。选取年龄、性别匹配体质指数(body mass index, BMI)正常儿童作为对照。行腹部B超、采空腹静脉血5 mL进行实验室检查, 包括天冬氨酸氨基转移酶(aspartate aminotransferase, AST)、丙氨酸氨基转移酶(alanine aminotransferase, ALT)、谷氨酰转肽酶(gamma glutamyl transpeptidase, GGT)、总胆固醇(total cholesterol, CHOL)、甘油三酯(triglyceride, TG)、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)。结果 筛查出肥胖儿童80例, 与51例正常对照儿童比较, 肥胖组儿童的AST、ALT、GGT、CHOL、TG、LDL-C增高, HDL-C减低, 差异有统计学意义(P<0.05)。AST、ALT、GGT、TG、LDL-C与NAFLD发病呈正相关且为危险因素;HDL-C呈负相关为保护因素。肥胖儿童NAFLD检出率为27.5%(22/80);对照组未检出NAFLD, 肥胖儿童的NAFLD发生率明显高于正常儿童(P<0.05)。肥胖伴有NAFLD组较肥胖不伴NAFLD组AST、ALT、GGT、TG升高, HDL-C降低;差异具有统计学意义(P<0.05)。结论 肥胖导致学龄期儿童的肝功能损害、血脂代谢异常甚至可造成非酒精性脂肪肝的发生;非酒精性脂肪肝更进一步加重了肝功能损害及血脂代谢紊乱。     

代谢综合征患者血浆内脂素水平的变化

目的探讨代谢综合征(MS)患者血浆内脂素(visfatin)水平及与胰岛素抵抗(IR)的关系。方法筛选MS患者45例、年龄、性别相匹配的健康成年人40例为对照组。ELISA法测定各组空腹血浆visfatin水平,同时检测空腹血糖(FPG)、胰岛素(FINS)、血脂、血压,测量身高、体重、腰围、臀围计算体重指数(BNI)、腰臀比(WHR),采用HOMA-IR模型公式计算胰岛素抵抗指数。结果MS组visfatin水平明显高于对照组,差异有统计学意义。在MS组,visfatin与BMI、WC、FPG、2hPG、FINS、TG、HOMA-IR呈正相关,r值分别为0.378,0.231,0.419,0.363,0.448,0.423,P均<0.05;与HDL-C无明显相关关系。多元逐步回归分析表明,BMI和visfatin是HOMA-IR的独立影响因素。结论MS患者血浆visfatin水平增高,visfatin与机体糖、脂代谢紊乱密切联系。     

Plasma adiponectin levels in high risk African-Americans with normal glucose tolerance, impaired glucose tolerance, and type 2 diabetes

OBJECTIVE: We studied plasma adiponectin, insulin sensitivity, and insulin secretion before and after oral glucose challenge in normal glucose tolerant, impaired glucose tolerant, and type 2 diabetic first degree relatives of African-American patients with type 2 diabetes. RESEARCH METHODS AND PROCEDURES: We studied 19 subjects with normal glucose tolerance (NGT), 8 with impaired glucose tolerance (IGT), and 14 with type 2 diabetes. Serum glucose, insulin, C-peptide, and plasma adiponectin levels were measured before and 2 hours after oral glucose tolerance test. Homeostasis model assessment-insulin resistance index (HOMA-IR) and HOMA-beta cell function were calculated in each subject using HOMA. We empirically defined insulin sensitivity as HOMA-IR<2.68 and insulin resistance as HOMA-IR>2.68. RESULTS: Subjects with IGT and type 2 diabetes were more insulin resistant (as assessed by HOMA-IR) when compared with NGT subjects. Mean plasma fasting adiponectin levels were significantly lower in the type 2 diabetes group when compared with NGT and IGT groups. Plasma adiponectin levels were 2-fold greater (11.09+/-4.98 vs. 6.42+/-3.3811 microg/mL) in insulin-sensitive (HOMA-IR, 1.74+/-0.65) than in insulin-resistant (HOMA-IR, 5.12+/-2.14) NGT subjects. Mean plasma adiponectin levels were significantly lower in the glucose tolerant, insulin-resistant subjects than in the insulin sensitive NGT subjects and were comparable with those of the patients with newly diagnosed type 2 diabetes. We found significant inverse relationships of adiponectin with HOMA-IR (r=-0.502, p=0.046) and with HOMA-beta cell function (r=-0.498, p=0.042) but not with the percentage body fat (r=-0.368, p=0.063), serum glucose, BMI, age, and glycosylated hemoglobin A1C (%A1C). DISCUSSION: In summary, we found that plasma adiponectin levels were significantly lower in insulin-resistant, non-diabetic first degree relatives of African-American patients with type 2 diabetes and in those with newly diagnosed type 2 diabetes. We conclude that a decreased plasma adiponectin and insulin resistance coexist in a genetically prone subset of first degree African-American relatives before development of IGT and type 2 diabetes.     

Presence of the Metabolic Syndrome in Obese Adolescents Predicts Impaired Glucose Tolerance and Nonalcoholic Fatty Liver Disease

PURPOSE: To evaluate whether the presence of metabolic syndrome (MS) in obese adolescents is associated with other comorbidities of obesity METHODS: A total of 85 obese teens (70% female and 30% male) with fasting insulin >25 microU/ml and family history of type 2 diabetes mellitus and/or acanthosis nigricans were studied. Mean age was 15.8 +/- 1.7 years and body mass index (BMI) was 39.3 +/- 6.6 kg/m(2). Of the subjects, 54% were Hispanic and 35% black, 5% white, 5% American Indian, and 1% Asian. Laboratory analysis included fasting lipids, glucose, gamma-glutamyl transpeptidase (GGT), and oral glucose tolerance testing. Additional liver transaminase levels were determined and liver ultrasound (US) was performed to evaluate the presence and severity of fatty liver. RESULTS: All subjects met MS criteria for children for waist circumference, 49% for blood pressure, 54% for high-density lipoprotein, 54% for triglycerides, and 20% for impaired fasting glucose (IFG) or impaired glucose tolerance [IGT]). In all, 47 subjects had three or more MS criteria. BMI was no different between groups with and without MS. Subjects with three or more MS criteria were more likely to have IGT (p = .004), elevated alanine aminotransferase (p = .039), elevated GGT (p = .036), fatty liver on US (p < .001), and more severe fatty liver (p = .001). CONCLUSIONS: Abnormal glucose regulation and evidence of nonalcoholic fatty liver disease (NAFLD) were more common in subjects meeting three criteria for MS than in those meeting fewer criteria. The identification of MS provides value to the primary care provider. Those patients meeting criteria for MS should be evaluated for glucose intolerance and NAFLD.     

Effect of glucose tolerance status on PAI-1 plasma levels in overweight and obese subjects

OBJECTIVE: The aim of our study was to examine whether plasminogen activator inhibitor-1 (PAI-1) plasma levels varied as a function of differences in glucose tolerance status independently of body fatness, body-fat distribution, and insulin sensitivity. RESEARCH METHODS AND PROCEDURES: Plasma PAI-1 antigen levels, along with insulin resistance [measured by homeostatic model assessment (HOMA(IR))], central fat accumulation, body composition, blood pressure, and fasting concentrations of glucose, insulin, and lipids, were measured in 229 overweight and obese [body mass index (BMI) > or =25 kg/m(2)) subjects with normal glucose tolerance (NGT) and in 44 age- and BMI-matched subjects with impaired glucose tolerance (IGT). RESULTS: Plasma PAI-1 antigen levels were significantly higher in IGT than in NGT subjects. Log PAI-1 was positively correlated with BMI, HOMA(IR), and log insulin, and inversely associated with high-density lipoprotein-cholesterol both in IGT and in NGT individuals. On the other hand, log PAI-1 was positively correlated with waist circumference, fat mass (FM), fat-free mass, systolic and diastolic blood pressure, and log triglycerides only in the NGT group. After multivariate analyses, the strongest determinants of PAI-1 levels were BMI, FM, waist circumference, and high-density lipoprotein cholesterol in the NGT group and only HOMA(IR) in the IGT cohort. DISCUSSION: This study demonstrates that PAI-1 concentrations are higher in IGT than in NGT subjects. Furthermore, we suggest that the influences of total adiposity, central fat, and insulin resistance, main determinants of PAI-1 concentrations, are different according to the degree of glucose tolerance.     

青春期多囊卵巢综合征患者糖代谢评估

目的　研究青春期多囊卵巢综合征 (PCOS)患者糖耐量异常的发生率 ,探讨糖代谢异常与胰岛素抵抗、体重的关系以及早期评估方法。　方法　 4 3例青春期PCOS患者 ,口服 75 g葡萄糖 ,行糖耐量及胰岛素释放实验。用稳态模型胰岛素抵抗指数 (HOMAIR)评价胰岛素抵抗。　结果　 (1)糖耐量低减发生率为 11 6 % (5 /43) ;(2 )糖耐量低减患者的体重指数、空腹血糖、空腹胰岛素及服糖后 6 0、 12 0min的血糖值、胰岛素值、HOMAIR均高于糖耐量正常患者 ,差异有显著性 (P <0 0 5 )。 (3)体重指数与服糖后 12 0min血糖值成正相关 (r =0 35 5 ,P <0 0 5 )。HOMAIR与服糖后 12 0min血糖值成正相关 (r=0 5 78,P <0 0 5 )。　结论　青春期PCOS患者存在糖代谢异常 ,肥胖和胰岛素抵抗是影响其糖耐量的重要因素 ,口服糖耐量试验是用于监测青春期PCOS患者糖代谢的较好指标。     

Body fat distribution and insulin resistance: beyond obesity in nonalcoholic fatty liver disease among overweight men

OBJECTIVE: The aim of this study was to characterize the relationship between nonalcoholic fatty liver disease (NAFLD) and body fat distribution and insulin resistance in a sample of non-diabetic overweight men. SUBJECTS AND METHODS: We conducted a cross-sectional survey of 117 overweight men with NAFLD, as well as 117 controls, who were matched with regard to age and body mass index. None of the study subjects exhibited signs of alcohol abuse, hepatitis B or C, diabetes or fasting hyperglycemia, or hypertension. The diagnosis of NAFLD was based on dual findings of elevated alanine aminotransferase levels and sonographically-determined fatty liver. Body fat distribution was assessed via bioelectrical impedance. Insulin resistance was evaluated via homeostasis model assessment (HOMA-IR). RESULTS: The risk of developing NAFLD was found to be profoundly associated with elevated measurements of waist circumference, fat mass, percentage of body fat and abdominal fat, iron, triglycerides, apolipoprotein B, and results of HOMA-IR. Multivariate analysis revealed that NAFLD was significantly associated with elevated measurements of waist circumference, iron, apolipoprotein B, and HOMA-IR. CONCLUSIONS: Our study provides evidence for a profound and dose-dependent association of NAFLD with central adiposity, insulin resistance in overweight men lacking complications of metabolic syndrome. Overweight subjects with insulin resistance or central adiposity were at more risk of NAFLD than were those subjects with less insulin resistance or central adiposity, even those with a similar degree of obesity.     

2型糖尿病和葡萄糖耐量异常患者游离脂肪酸升高及其意义

目的　观察 2型糖尿病 (DM)和葡萄糖耐量异常 (IGT)患者血清游离脂肪酸 (FFA)的水平 ,探讨FFA与胰岛素(INS)、胰岛素抵抗 (IR)和甘油三酯 (TG)的关系。方法　采用酶法测定 2 0例 2型DM和 2 0例IGT患者口服葡萄糖耐量试验 (OGTT) 0和 2h血清FFA水平 ,同步测定血浆葡萄糖 (PG)、血清INS以及空腹TG和胆固醇 (TC) ,并与 2 0例正常人对照。结果　 2型DM和IGT患者OGTT 0和 2hINS均显著高于正常对照组 ,且 2型DM患者INS高于IGT患者 ,P <0 .0 5 ;空腹FFA和胰岛素抵抗指数 (HOMA -IR) 2型DM患者高于IGT患者 ,IGT患者高于正常对照组 ,P <0 .0 1;TG和OGTT 2hFFA 2型DM患者高于IGT患者和正常对照组 ,P <0 .0 5 ,而IGT患者和正常对照组之间比较差异无显著性 ;多元逐步回归显示空腹FFA是HOMA -IR的独立影响因素。结论　不仅 2型DM患者而且IGT患者存在FFA异常升高 ,FFA升高与IR有关 ;2型DM和IGT患者存在IR和脂代谢紊乱 ,FFA反映脂代谢紊乱可能较TG更灵敏的指标     

达英-35对非肥胖型PCOS患者内分泌代谢的影响

目的:探讨达英-35对非肥胖型多囊卵巢综合征(PCOS)患者胰岛素敏感性的影响。方法:2006～2007年在本院妇科内分泌门诊就诊的非肥胖型PCOS患者(BMI<25),予达英-35连续治疗6个周期。于治疗前记录体重指数(BMI)、腰臀比(WHR)、多毛评分(F-G评分)和痤疮评分,于早卵泡期测定血清总睾酮(T)、黄体生成素(LH)、卵泡刺激素(FSH)、LH/FSH比值、空腹胰岛素FINS、HOMA-IR。分别于治疗3个月后、6个月后观察这些指标的变化。结果:共41例非肥胖PCOS患者完成了本研究,平均年龄(22.7±3.6)(18～31)岁,平均BMI(21.14±0.65)(18.59～24.20)。治疗期间患者BMI和WHR无显著性变化,F-G评分、痤疮评分、血清T、LH水平和LF/FSH比值均显著降低(P<0.001)。治疗6个月后FINS和HOMA-IR没有明显改变(P>0.05)。结论:非肥胖型PCOS患者短期应用达英-35可明显改善高雄激素血症,而不影响胰岛素敏感性。     

Associations between combinations of body mass index plus non-alcoholic fatty liver disease and diabetes mellitus among Korean adults

The purpose of this study was to investigate associations between combinations of body mass index (BMI) categories plus non-alcoholic fatty liver disease (NAFLD) and diabetes mellitus (DM) among Korean adults. We prepared the data of 5665 subjects aged 20 years and over who had visited a health promotion center. We excluded 582 subjects as they had a viral or alcoholic liver disease. According to BMI-NAFLD status, the subjects were categorized as non-obese (BMI<25 kg/m2) without NAFLD (n=2568), obese (BMI≥25 kg/m2) without NAFLD (n=572), non-obese with NAFLD (n=748), or obese with NAFLD (n=1195). The prevalence of NAFLD was highest in the obese subjects with DM (87.9%). In non-obese and non-DM subjects, the prevalence of NAFLD was lowest (18.4%). After adjustment of age, gender, waist circumference, smoking status, alcohol drinking, regular exercise, the odd ratios for DM or DM plus impaired fasting glucose (IFG) of subjects with mild NAFLD regardless of obesity were almost 2-fold compared to non-obese subjects without NAFLD. Moreover, those of subjects with moderate or severe NAFLD regardless of obesity were about 4- fold. Clinicians and investigators need to pay attention to non-obese patients with fatty liver.