BACKGROUDGestational diabetes mellitus (GDM), which is defined as glucose intolerance ofvarious degrees that is first detected during the course of pregnancy, includes diabetesmellitus and impaired glucose tolerance, except for those diagnosed as diabetesmellitus before pregnancy. The morbidity of GDM is 1%-14%,and increased as timegoes by. GDM may result in pregnent women\’s metabolism disorders, which means theincreasing risk of macrosomia, hydramnios, spontaneous abortion, fetal anomaly,fetal distress, fetal death, dead birth, hypoglycemia of newborn, hypocalcemia,hyperbilirubinemia and ketoacidosis etc. All of the complications do great harm to thepregnant women and the fetus,so GDM has always been the emphasis of clinicalprevention and care in obstetrics. Aimed to provide references for clinicalintervention, and avoid the above-mentioned complications, previously researches ofGDM were mainly centered in obstetrics field, including screening, diagnosis,preservation, management and prognosis of the pregnant women and fetus.With increasing understanding of GDM, people found it was similar to Type 2diabetes mellitus(T2DM) in clinical manifestation, and pathogenesis——Insulin resistance(IR) and defect of insulin secretion on the basis of genetic gene defect. Butthere are also differences between the two. In general, GDM is reversible and mayrecover after pregnancy but one third of GDM patients will become T2DM during 5to 10 years after parturition, and GDM is considered as early stage of T2DM. So theresearch of GDM is very important for studying morbidity, diagnosis and treatment ofT2DM and has been emphasized by those in the endocrine field in recent years.The relationship of inflammation and IR has become a hot topic in pathogenesisof diabetes mellitus,. And as a mirror, whether it is the pathogenesis of GDM?Atpresent, the above-mentioned research is mainly focus on relationship betweeninflammatory cytokines and IR or morbidity of GDM, while research at home onlylimits on the study of epidemiology, and seldom centered in exploring the pathway ofinflammation. Moreover, with the disclosed of the results of some basic researchesand large-scale diabetic preventive experiments, for example, Yuan\’s study showedhigh doses of salicylates reversed hyperglycemia, hyperinsulinemia, and dyslipidemiain obese rodents, and found high doses of salicylates could cut down the bloodglucose though inhibitor kappa B kinaseβ,because high doses of salicylates resersedIR in fa/fa rats and ob/ob mice. 134 cases became T2DM patients in WOSCOPS,mobility of diabetes mellitus in pravastatin group reduced than in control group by30%, and pravastatin cut down the serum levels interleukin-6(IL-6)、tumor necrosisfactor-a(TNF-a)、interleukin-8(IL-8) and C-reactive protein(CRP), which functionwas independent on fuction of fat reduction, supporting to the fuction of diabetesmellitus preservationin correlated with anti-inflammatory effect. In TRIPODtroglitazone(TZD) cut down the blood glucose through excitomotor of peroxisomeProliferator-activated receptor(PPARγ), which altered gene expression for Synthesis offatty, Adipocyte differentiation, Fatty acid uptaking, ect. In addition, TZD could reduceinflammation through inhibitting the production of cytokines and phagocyte activation, displaying the reduction of inflammation factors levels such as CRP andlencocyte count in T2DM, manifested that the prevention for T2DM partly relatedwith inflammatory mechanism,further supported the Etiology theory of inflammationin DM.Inflammatory cytokines usually activate c-Jun-NH2-terminal kinas(JNK) andnuclear factor kappa B (NF-κB) pathways to lead to IR. JNK directly caused serinephosphorylation of insulin receptor substrate-1 (IRS-1) at serine-302 (pS302) andserine-307 (pS307) to block insulin receptor signal transduction. Usually NF-κBcombined with its inhibitor IκB, indwells in the cytoplasm of most cells as an inactiveform. After activated by proinflammatory cytokines such as TNF-a、IL-1、IL-6, IκBand so on. kinase-β(KKβ) is highly selective toward its physiological substrates, theIκB protein inhibitors of NF-κB. Phosphorylation by IKKβtargets IκBαforproteasomal degradation, which liberates NF-κB for translocation into the nucleus,where it promotes the expression of numerous target genes whose products induceinsulin resistance. Aspirin or salicylate, as classic non-steroidal anti-inflammatorydrug(SAID), inhabited NF-κB and IKKβ-activators of it\’s upstream throughnon-Cycloxygenase and break above-mentioned vacious cycle to improve IR.Proposal of Inflammation Theory may provide a new direction for the pathogenesis ofdiabetic and the discovery of new drugs to prevent and treat diabetic. GDM,considered as the early stage in DM, provides an opportunity to study the relativeearly stage of diabetes and to develop interventions to prevent the disease.This study is to explore how inflammation reacts to the morbility anddevelopment of GDM and provide reference for searching the effective means ofclinic diagnosis, prevention and treatment through measuring the fasting serum IL-6and hs-CRP levels, and investigated the correlativity between each of them and IR,meanwhile, detect the expression of NF-κB in peripheral blood leucocyte of defferent tolerance groups.This study includes the following two parts:PART 1 The study on the relationship betwwen serum levels of lL-6 andhs-CRP and insulin resistance in gestational diabetes mellitusOBJECTIVETo investigate serum concentration of IL-6、high sensitive C-reactiveprotain(hs-CRP) and their correlation with insulin resistance in pregnant women withgestational diabetes mellitus (GDM), then to initially approach the relation betweenmorbility of GDM and Inflammatory reaction.METHODS1. Subjects were screened from pregnant women in 24～36 gestational weekswithout diabetes mellitus and abnormal glucose tolerances before gestation inout-patient clinic of maternity department in our hospital from February 2006 toDecember 2007, and divided into two groups: 40 cases of normal pregnantwomen(NGT group) and 23 cases of women with GDM(GDM group). Besides 25cases of healthy women during the child-bearing period were chose as controlgroup(control group). After 24 gestational weeks all the pregnant women wereperformed an initial screening by measuring the plasma glucose concentration 1hafter a 50-g oral glucose challenge test(GCT), then negative cases were brought intoNGT group. When the results of the screening test were abnormol[1-h glucose≥7.8mmol(140 mg/dl)],the women had to received a diagnostic 100g oral glucosetolerance test (OGTT) after 3 days. According to C

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