諾和力病例既往史/家族史既往史：否認(rèn)高血壓病史家族史：否認(rèn)糖尿病家族史體格檢查身高：168cm體重：83.5kgBMI：29.58kg/cm2血壓：120/85其他體查：無多毛、痤瘡和紫紋；無甲狀腺腫大及結(jié)節(jié)。實(shí)驗(yàn)室檢查血糖及β細(xì)胞功能：0Hr2Hr血糖（mmol/L）9.1423.6C肽（ng/ml）3.587.57實(shí)驗(yàn)室檢查HbA1c：11.2%血脂：總膽固醇4.91mmol/L甘油三酯4.42mmol/L肝功：ALT135u/L，AST87u/L實(shí)驗(yàn)室檢查肝炎抗原陰性（甲肝、乙肝、丙肝、戊肝）腎功能正常輔助檢查上腹B超提示：脂肪肝。心電圖：正常。甲狀腺B超：正常。診斷1、2型糖尿病2、脂肪肝3、肝功能損害日期BPWBMIFPG2hPGHbA1cALTAST6月19日120/8583.529.69.1423.611.213587諾和靈N18u，門冬胰島素22u、16u、16u6月26日125/857.110.010362加用利拉魯肽0.6mg（1.2mg），門冬胰島素30：24u、6u、18u9月9日115/807928.04.86.77.045

48

利拉魯肽1.2mgqd，二甲雙胍片0.5tid治療前后血糖、體重、血壓、ALT變化利拉魯肽1.2mg，門冬胰島素30：18u早、8u晚病例特點(diǎn)2型糖尿病合并肥胖、脂肪肝胰島素抵抗明顯肝功能損害利拉魯肽對HbA1C的影響DiabetesObesMetab.2011Mar;13(3):207-20.利拉魯肽1.8mg可使患者體重降低達(dá)3.4Kg體重的變化(kg)0.0-0.5-1.0-1.5-2.0-1.8-2.051%43%-2.5-2.8-2.5-3.0-3.2-3.52.52.01.51.00.5-0.2艾塞那肽-2.9安慰劑格列美脲羅格列酮甘精胰島素格列美脲+1.1+1.6+0.6+1.0

+2.1利拉魯肽1.8mg*與對照相比具有顯著差異*****-3.4-1.0西格列汀SU聯(lián)合治療

(LEAD-1)

Met聯(lián)合治療

(LEAD-2)

Met+TZD聯(lián)合治療

(LEAD-4)

Met+SU聯(lián)合治療(LEAD-5)

單藥治療(LEAD-3)Met±SU

聯(lián)合治療(LEAD-6)

Met聯(lián)合治療

(Liravs.sita)

Marreetal.DiabeticMedicine2009;26;268–78(LEAD-1);Naucketal.DiabetesCare2009;32;84–90(LEAD-2);Garberetal.Lancet2009;373:473–81(LEAD-3);Zinmanetal.

DiabetesCare2009;32:1224–30

(LEAD-4);Russell-Jonesetal.Diabetologia2009;52:2046-2055(LEAD-5);Buseetal.Lancet2009;374(9683):39–47(LEAD-6);Pratleyetal.Lancet2010;375:1447-56(liravs.sita)利拉魯肽減輕的體重大部分是脂肪組織利拉魯肽1.2mg/天利拉魯肽1.8mg/天格列美脲4mg/天組織體積的變化(kg)420–2–4–6脂肪組織**NSNS**瘦組織LEAD-3組織體積的變化(kg)420–2–4–6脂肪組織瘦組織***********LEAD-2利拉魯肽1.2mg/天+二甲雙胍利拉魯肽1.8mg/天+二甲雙胍安慰劑+二甲雙胍格列美脲8mg/day+二甲雙胍DEXA,雙能X線吸收測量儀；數(shù)據(jù)用平均數(shù)±倍標(biāo)準(zhǔn)誤表示;**p<0.01;***p<0.001vs.格列美脲+二甲雙胍inLEAD-2andvs.格列美脲inLEAD-3

Jendleetal.DiabetObesMetabol2009;11:1163–72(LEAD-2andLEAD-3substudies).利拉魯肽主要減少內(nèi)臟脂肪體脂的變化DEXA掃描內(nèi)臟脂肪vs.皮下脂肪CT掃描內(nèi)臟脂肪皮下脂肪Jendleetal.DiabetesObesMetab2009;11:1163-72TheeffectivenessofliraglutideinnonalcoholicFattyliverdiseasepatientswithtype2diabetesmellituscomparedtositagliptinandpioglitazone.OhkiT,IsogawaA,IwamotoM,OhsugiM,YoshidaH,TodaN,TagawaK,OmataM,KoikeK.SourceDepartmentofGastroenterology,MitsuiMemorialHospital,Kanda-izumicho1,Chiyoda-ku,Tokyo101-8643,Japan.AbstractBackground.Liraglutideleadingtoimprovenotonlyglycaemiccontrolbutalsoliverinflammationinnon-alcoholicfattyliverdisease(NAFLD)patients.Aims.TheaimofthisstudyistoelucidatetheeffectivenessofliraglutideinNAFLDpatientswithtype2diabetesmellitus(T2DM)comparedtositagliptinandpioglitazone.Methods.Weretrospectivelyenrolled82JapaneseNAFLDpatientswithT2DManddividedintothreegroups(liraglutide:N=26,sitagliptin;N=36,pioglitazone;N=20).Wecomparedthebaselinecharacteristics,changesoflaboratorydataandbodyweight.Results.Attheendoffollow-up,ALT,fastbloodglucose,andHbA1clevelsignificantlyimprovedamongthethreegroups.ASTtoplateletratiosignificantlydecreasedinliraglutidegroupandpioglitazonegroup.Thebodyweightsignificantlydecreasedinliraglutidegroup(81.8?kgto78.0?kg,P<0.01).Ontheotherhands,thebodyweightsignificantlyincreasedinpioglitazonegroupanddidnotchangeinsitagliptingroup.Multivariateregressionanalysisindicatedthatadministrationofliraglutideasanindependentfactorofbodyweightreductionformorethan5%(OR9.04;95%CI1.12-73.1,P=0.04).Conclusions.AdministrationofliraglutideimprovedT2DMbutalsoimprovementofliverinflammation,alterationofliverfibrosis,andreductionofbodyweight.TheeffectivenessofliraglutideinnonalcoholicFattyliverdiseasepatientswithtype2di