Urinary C-peptide in the neonate correlates both to maternal glucose tolerance and to fetal size at birth

In 18 women with gestational diabetes the variables of an oral glucose tolerance test (fasting and 2-hour blood glucose values and area under the blood glucose curve) performed in the last trimester of pregnancy correlated significantly with the urinary C-peptide excretion during the first 12 hours of the life (r = 0.47, 0.71, and 0.60, respectively). In a combined group with 28 type II pregnant diabetic women there was also a significant correlation between the urinary C-peptide excretion of the infants and their skinfold. Assay of the urinary C-peptide excretion of the neonate, reflecting its insulin production, seems to be a sensitive parameter to study the influence of the maternal carbohydrate metabolism in the offspring.     

Sex hormone-binding globulin in gestational diabetes

BACKGROUND: Insulin is an important regulator of serum sex hormone-binding globulin (SHBG) concentration which works by inhibiting its production in hepatocytes. Low SHBG level is associated with increased insulin resistance and hyperinsulinemia. Our purpose was to compare maternal serum SHBG level between normal and gestational diabetic pregnant women and to study the relationships between SHBG, SHBG/insulin and SHBG/glucose ratio and several endocrine, metabolic and clinical parameters. METHODS: Serum SHBG concentrations were measured in 34 women with gestational diabetes and in 32 matched controls. Glucose, insulin, C-peptide, fructosamine, beta-HCG, cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, apolipoprotein A, apolipoprotein B, total and free T4, total and free estriol, T3 and IGF-1 were measured. Insulin sensitivity was estimated using the short insulin tolerance test. RESULTS: SHBG, SHBG/insulinemia ratio and SHBG/glucose ratio were significantly lower in the diabetic group (309.54 +/- 112.22 vs 460.54 +/- 144.54, p = 0.00001), (33.55 +/- 16.62 vs 72.56 +/- 66.50, p = 0.0006 using log-transformed values), (5.88 +/- 1.87 vs 3.39 +/- 1.23, p < 0.00001). SHBG was negatively correlated with insulinemia (r = -0.40, p = 0.001), C-peptide (r = -0.41, p = 0.001), glycemia (r = -0.27, p = 0.02), diastolic blood pressure (r = -0.41, p = 0.001) and beta-HCG (r = -0.41, p = 0.001) and positively correlated with LDL-c (r = 0.25, p = 0.04) and apolipoprotein B (r = 0.33, p = 0.007). CONCLUSIONS: SHBG concentrations are lower in gestational diabetic pregnant women and are related to insulin levels but not to peripheral insulin sensitivity. Since insulinemia was similar in normal and gestational diabetic pregnant women, we speculate that gestational diabetes is characterized by a higher peripheral insulin resistance, a fasting normal insulinemia and a higher hepatic insulin sensitivity, at least in other actions than on carbohydrate metabolism. The role of sex steroids, T4 and IGF-1 in regulating SHBG appears to be limited during pregnancy.     

Moderate caloric restriction in obese women with gestational diabetes

The effect of moderate caloric restriction on weight gain during pregnancy and fetal outcome in 22 obese women with gestational diabetes mellitus was assessed. A new tool was used to assess dietary compliance in an outpatient setting. The authors observed that obese gestational diabetics gained less weight during pregnancy than ten normal pregnant women or 31 lean women with gestational diabetes. Paradoxically, the placentas of obese gestational diabetics were larger (P not significant), and infants of these mothers were significantly heavier than those of normal women or lean women with gestational diabetes (P less than .03). The authors suggest that the currently recommended daily caloric allowances for normal women may be excessive for obese gestational diabetics who are not prone to ketosis but have a complex metabolic problem characterized by hyperinsulinemia and insulin resistance.     

GDM孕中、晚期及子代胰岛素抵抗与正常妊娠的对照研究

目的探讨妊娠期糖尿病(GMD)与正常妊娠孕中、晚期及子代胰岛素抵抗、胰岛β细胞功能及胎儿脐血流的差异。方法选择上海交通大学医学院附属国际和平妇幼保健院产检、分娩的70例GDM产妇及其子代为GDM组,同期产检、分娩的70例健康母子配对样本为对照组。两组孕妇孕24~28周OGTT筛查时行胰岛素释放试验、孕33~34周、孕37~38周检测空腹血糖、胰岛素及C肽;比较两组稳态模型评估的胰岛素抵抗指数(HOMA-IR);B超测定孕晚期胎儿脐血流;分娩时检测脐血血糖、胰岛素及C肽值并获取胎儿出生体重、胎龄等资料;比较两组母子配对样本间各项指标的差异。结果 GDM组OGTT时胰岛素峰值较对照组延迟1h;GDM组孕33~34周母血空腹胰岛素、C肽高于对照组,差异有统计学意义(P<0.05);孕37~38周母血空腹胰岛素、C肽虽仍高于对照组,但差异无统计学意义(P>0.05);GDM组孕中、晚期HOMA-IR高于对照组,差异有统计学意义(P<0.05);GDM组新生儿脐血胰岛素、C肽高于对照组,差异有统计学意义(P<0.05);两组间孕晚期胎儿脐动脉S/D值、搏动指数(PI)、阻力指数(RI)比较差异无统计学意义(P>0.05)。结论 GDM患者孕中、晚期胰岛素抵抗较正常孕妇增加,并出现胰岛β细胞功能下降,其胎儿在宫内已发生糖代谢异常,但脐血流未受到显著影响。     

De novo clinical hypothyroidism in pregnancies complicated by type I diabetes, subclinical hypothyroidism, and proteinuria: a new syndrome

Fifty-one women with type I diabetes who had normal thyroxine values before becoming pregnant were evaluated. Abnormalities of thyroid tests other than thyroxine were encountered in 26 women, of whom 8 developed a low serum thyroxine level, an elevated thyroid-stimulating hormone level, and a low insulin requirement in the second trimester subsequent to an increase in 24-hour urinary protein excretion to greater than 4 gm/24 hr. Thyroid replacement led to an increase in insulin requirement to levels appropriate for gestational age. It is concluded that the woman with type I diabetes who develops proteinuria greater than 4 gm/24 hr during gestation is at risk for the development of de novo hypothyroidism during pregnancy, evidenced by a low serum thyroxine level, an elevated thyroid-stimulating hormone level, and a drop in insulin requirement.     

Accelerated starvation in late pregnancy: a comparison between obese women with and without gestational diabetes mellitus

We compared the glucose, insulin, free fatty acid, and 3-hydroxybutyrate responses to a briefly extended overnight fast during the third trimester of pregnancy between two groups: obese women with normal glucose tolerance (n = 10) and age- and weight-matched women with gestational diabetes mellitus (n = 10). After a 12-hour overnight fast, plasma glucose (95 +/- 4 vs. 78 +/- 2 mg/dl; p less than 0.01), insulin (32 +/- 5 vs. 17 +/- 2 microU/ml; p less than 0.02), and free fatty acid (860 +/- 63 vs. 639 +/- 79 mmol/L; p less than 0.05) levels were higher in the patients with gestational diabetes mellitus. 3-Hydroxybutyrate levels were similar in the two groups at that time (0.23 +/- 0.04 vs. 0.18 +/- 0.03 mmol/L; p greater than 0.3). When the fast was extended to 18 hours by having the patients skip breakfast, glucose levels fell more rapidly in the group with gestational diabetes mellitus but remained elevated compared with the nondiabetic women. Insulin levels declined at a similar rate in the two groups. Free fatty acid levels did not increase significantly in the group with gestational diabetes mellitus during the extended fast. In contrast, free fatty acid levels increased by 44% in the normal pregnant women, reaching the level observed in the group with gestational diabetes mellitus after 18 hours. 3-Hydroxybutyrate levels remained virtually identical in the two groups throughout the brief fast. Thus, compared with that of normal pregnant women, the response of obese women with gestational diabetes mellitus to brief caloric deprivation during late pregnancy was characterized by a greater fall in plasma glucose values without a greater propensity to ketosis. Our findings may have important implications for the dietary management of obese patients with gestational diabetes mellitus.     

Insulin sensitivity and B-cell responsiveness to glucose during late pregnancy in lean and moderately obese women with normal glucose tolerance or mild gestational diabetes

We used the minimal model technique to obtain concurrent measurements of whole-body insulin sensitivity and pancreatic B-cell responsiveness to glucose during the third trimester of pregnancy. Insulin sensitivity in normal pregnant women (n = 8) was reduced to only one third that of a group of nonpregnant women (n = 7) of similar age and relative weight. This marked insulin resistance was compensated by reciprocal enhancement of the first and second-phase insulin responses to intravenous glucose, which were increased threefold as compared with the nonpregnant women. Women with gestational diabetes mellitus (n = 16) had mean insulin sensitivity that was similar to that of the normal pregnant group, which indicates that insulin action was appropriate for the late phase of pregnancy in the gestational diabetic group. By contrast, the mean first-phase insulin response was significantly reduced in women with gestational diabetes mellitus, as compared with that of normal pregnant women (p less than 0.001). However, approximately one fifth of the group with gestational diabetes mellitus had first-phase responses that did not fall below the 95% confidence interval for the mean in normal pregnant women. The mean second-phase response was also lower in the group with gestational diabetes, although the difference was of borderline statistical significance (p less than 0.09). Our findings reveal the quantitative nature of the reciprocal changes in insulin sensitivity and B-cell function that normally accompany late pregnancy. They further indicate that during the third trimester, mild gestational diabetes is characterized by an impairment of pancreatic B-cell function rather than an exaggeration of the normal insulin resistance of late pregnancy.     

妊娠期糖尿病孕妇血清肿瘤坏死因子α水平变化与胰岛素抵抗关系的研究

目的　探讨妊娠期糖尿病孕妇血清肿瘤坏死因子α(TNF α)水平变化与胰岛素抵抗的关系。方法　采用酶联免疫吸附试验测定 4 2例妊娠期糖尿病孕妇 (GDM组 )、4 0例正常妊娠晚期孕妇 (正常妊娠组 )空腹血清TNF α水平 ;同时测定两组孕妇空腹血糖、C肽、胰岛素、糖化血红蛋白(HbA1c)水平。并且根据公式计算两组孕妇的胰岛素敏感指数 (ISI) ,以评价胰岛素抵抗程度。结果(1)GDM组孕妇空腹血清TNF α水平为 (5 2± 1 6 )ng/L ,正常妊娠组孕妇为 (4 5± 0 5 )ng/L ,两组比较 ,差异有极显著性 (P <0 0 1) ;GDM组孕妇ISI为 - 4 3± 0 4 ,正常妊娠组为 - 3 8± 0 3,两组比较 ,差异有极显著性 (P <0 0 1)。 (2 )GDM组孕妇空腹血糖、胰岛素、C肽水平分别为 (5 5± 0 7)mmol/L、(13 4± 3 8)mU/L、(1 6± 0 4 )nmol/L ,正常妊娠组孕妇空腹血糖、胰岛素、C肽水平分别为(4 9± 0 4 )mmol/L、(9 3± 2 5 )mU/L、(1 2± 0 3)nmol,两组比较 ,差异有极显著性 (P <0 0 1) ;GDM组孕妇HbA1c为 (5 6± 0 5 ) % ,正常妊娠组孕妇为 (5 3± 0 5 ) % ,两组比较 ,差异有显著性(P <0 0 5 )。 (3)GDM组孕妇空腹血清TNF α水平与ISI呈显著负相关 (r=- 0 70 3,P <0 0 1) ,分别与空腹血糖、C肽、HbA1c呈显著正相关 (r     

Maternal plasma leptin levels and their relationship to insulin and glucose in gestational-onset diabetes

To investigate the changes in leptin levels and the relationship between this substance and insulin and glucose in pregnant women with gestational-onset diabetes, we measured plasma leptin levels in the maternal peripheral vein of 17 healthy and 17 diabetic women at 29 and 33 weeks of gestation. We also correlated maternal plasma leptin levels in diabetic women with fasting plasma insulin levels and plasma glucose levels obtained 1 h after oral administration of 50 g of glucose. Maternal serum leptin levels in women with gestational diabetes (mean +/- SD 16.52 +/- 5.07 ng/ml, range 10.84-27.4 ng/ml) were significantly higher (p < 0.001) than those found in uncomplicated pregnancies (10.61 +/- 1.47 ng/ml, range 7.28-13.4 ng/ml). A positive correlation was found between maternal serum leptin levels and glycosylated haemoglobin values in diabetic pregnant women (r = 0.94, p < 0.001). A positive correlation was also found between maternal leptin concentrations and fasting serum insulin levels, as well as between leptin concentrations and plasma glucose levels obtained 1 h after the administration of 50 g of glucose in women with gestational diabetes (r = 0.84, p < 0.001, and r = 0.92, p < 0.001, respectively). We conclude that leptin levels are elevated in pregnant women with gestational diabetes, and its metabolism depends on insulin levels and the severity of diabetes.     

Could serum levels of irisin be used in gestational diabetes predicting?

ObjectiveGestational diabetes mellitus (GDM) is a metabolic disorder during pregnancy leading to acute and chronic complications in both mother and newborn. The pathogenesis of GDM has not been fully understood, However, since the disease shares risk factors with type 2 diabetes mellitus (T2DM), a relationship between these two disease states is plausible. The recently discovered peptide irisin has been hypothesized to be a regulator of body metabolism. However, studies ended up with controversial results. In the present study, we aimed to investigate the relationship between irisin levels and gestational diabetes mellitus and the possible benefits of the metabolic profile.Materials and methodsWe performed a cross-sectional analysis of circulating levels of irisin in 100 pregnant women similar for age and body mass index and the groups included 50 gestational diabetic patients and 50 healthy pregnant volunteers. Serum irisin levels were measured by ELISA kit.ResultsMean age and body mass index levels were similar in both groups. Median HbA1c, fasting blood glucose, Glucose 1 h, Glucose 2 h and fasting insülin levels were higher in with gestational diabetic patients compared to the control group. In gestational diabetic group, the median irisin level was lower than in the control group.ConclusionSerum irisin levels were lower in gestational diabetic patients. Further investigations are needed to explore the underlying biological effects of irisin on pregnant women.     

Glucose transporter (Glut1, Glut3) mRNA in human placenta of diabetic and non-diabetic pregnancies

Transport of glucose into the cell is catalyzed by glucose transporters (Glut). Glut1 and Glut3 are expressed at various levels in many human tissues, including the placenta. It has been reported that ambient glucose can affect both glucose transport activity and expression of the Glut genes, and protein. To date, very few studies concerning Glut in the placenta have been published, and studies in vivo in human diabetic pregnancy are lacking. We therefore investigated placental Glut1 and Glut3 mRNA by Northern blot analysis in ten diabetic (five insulin dependent diabetes mellitus (IDDM), two non-insulin dependent diabetes mellitus (NIDDM) and three gestational diabetes mellitus (GDM)) and nine non-diabetic women. The quantitative results of specific mRNA/beta-actin ratios were expressed as arbitrary units. The results were evaluated according to metabolic and clinical findings. Glut1 and Glut3 mRNA values in diabetic and non-diabetic pregnant women were similar. The metabolic environment seems to affect the Glut3 mRNA levels in IDDM pregnant women but not the control women. In addition, Glut3 mRNA decreased in late pregnancy in the diabetic but not in the control women. Moreover, Glut1 mRNA levels were correlated with maternal age in the diabetic as well as in the control women (significantly). Finally, an inverse correlation was found between Glut1 mRNA levels and placental weight (in both diabetic and non-diabetic women). These results, although preliminary, shed some light on the function of these glucose transporters in normal as well as in diabetic pregnancies and prompt us to carry out a further investigation to better elucidate fetomaternal metabolic correlation at the placental level.     

Postprandial walking exercise in pregnant insulin-dependent (type I) diabetic women: reduction of plasma lipid levels but absence of a significant effect on glycemic control

In this study 42 pregnant women with type I diabetes and 28 nondiabetic controls were recruited to participate in a postprandial walking exercise program. Exercise patients were instructed to walk 20 minutes (1 mile) after each meal and were divided into two groups: group 1 were normal nondiabetic controls and group 2 were women with type I diabetes. There were two nonexercise comparison groups: group 3, nondiabetic controls, and group 4, women with type I diabetes. Diabetic women were followed weekly in an intensive perinatal program. Glycemic control was assessed by serial hemoglobin A1 concentration measurements, home blood glucose monitoring, 24-hour glucose profiles, and 24-hour quantitative urinary glucose loss. Glycemic control was modestly but not significantly superior in the diabetic exercise group 2 compared with the diabetic nonexercise group 4. Exercise was associated with lower fasting cholesterol and triglyceride values in both controls and diabetic women, with significantly lower fasting plasma triglyceride levels in the diabetic exercise group (p less than 0.02). There were no adverse effects of postprandial walking exercise in mothers or infants.     

Postpartum testing for antecedent gestational diabetes

Gestational diabetes is a predictor of glucose intolerance in subsequent pregnancies and in the nongravid state. Many pregnant women are not tested for gestational diabetes, although they or their offspring may show signs suggestive of antecedent hyperglycemia. We examined the diagnostic utility of a postpartum (within 48 hours), 100 gm, oral glucose tolerance test and cord plasma glucose, cord plasma C-peptide, and 2-hour neonatal plasma glucose tests to detect antecedent gestational diabetes in women with documented gestational diabetes (n = 37) or with normal glucose tolerance test results late in the third trimester (n = 28). The 1-hour, 2-hour, and incremental 1-hour + 2-hour [( 1-hour - fasting] + [2-hour - fasting]) [2-hour - fasting]) glucose values of the postpartum glucose tolerance test showed significant differences between study participants with and without gestational diabetes (164 +/- 30 versus 115 +/- 22, 145 +/- 31 versus 101 +/- 21, and 153 +/- 51 versus 67 +/- 33 mg/dl, respectively, p less than 0.025). Maternal fasting and 3-hour postpartum glucose tolerance test glucose, cord plasma glucose, cord plasma C-peptide, and 2-hour neonatal plasma glucose values showed no significant between-group differences. Receiver operating characteristic curve analyses for these tests indicated that the incremental 1-hour + 2-hour postpartum glucose tolerance test glucose values best sustain test specificity at the low test threshold values necessary for high test sensitivity. A threshold of 110 mg/dl for this test yielded a predicted specificity of 90% and sensitivity of 80% with regard to antecedent gestational diabetes.     

Prolactin and glucose tolerance in normal and gestational diabetic pregnancy

The relationship between the deterioration of glucose tolerance and plasma prolactin (PRL) levels was investigated in 15 normal pregnant women and in 15 women with gestational diabetes mellitus. Oral glucose tolerance tests were performed in late pregnancy and postpartum, and the insulin, glucagon, and PRL responses were measured. In late pregnancy the gestational diabetics revealed significantly elevated fasting glucose levels compared with the normal pregnant women and after the glucose challenge their insulin responses were significantly diminished and the suppression of glucagon less pronounced. These differences in glucose metabolism were markedly reduced early postpartum. There was no difference in basal PRL concentrations between the two groups neither in pregnancy nor postpartum. The PRL levels were not altered during the oral glucose tolerance tests and no correlation between the deterioration of glucose tolerance and the PRL concentrations could be demonstrated in either group. These results indicate that abnormal PRL levels are not of pathophysiologic importance for the development of gestational diabetes mellitus.     

Amniotic fluid C-peptide and phosphatidyl glycerol in diabetic pregnancy

The concentrations of C-peptide and phosphatidylglycerol in the amniotic fluid were determined in 36 pregnant diabetic women. Twenty-one patients who were being treated with insulin for gestational diabetes as well as 15 patients who were insulin dependent were studied. All patients were subjected to a program of strict metabolic control, and amniocentesis was performed at gestational week 36-37. Phosphatidyl glycerol was present in the amniotic fluid in 15 cases and absent in 21. The mean concentration of C-peptide did not differ whether phosphatidyl glycerol was present or absent. (C-peptide: 0.56 +/- 0.06 and 0.43 +/- 0.05 nmol/l respectively). Although the mean value for amniotic fluid C-peptide in both groups was close to that in diabetic pregnancies with an uneventful neonatal outcome, it was significantly higher than that in non-diabetic pregnancies, indicating minor fetal hyperinsulinemia. The level of C-peptide in the amniotic fluid showed a correlation to the subsequent birthweight of the infant (r = 0.50; p less than 0.01). It is concluded that with rigorous metabolic control of the pregnant diabetic patient, the presence or absence of phosphatidyl glycerol, as an index of fetal lung maturity, is apparently not related to the level of C-peptide in the amniotic fluid.     

Insulin glargine versus neutral protamine Hagedorn insulin for treatment of diabetes in pregnancy

We compared maternal and neonatal outcomes in diabetic pregnancies treated with either insulin glargine or neutral protamine Hagedorn (NPH) insulin. We performed a retrospective chart review of diabetic pregnant patients using the Diabetes Care Center of Wake Forest University during the years 2000 to 2005. Outcomes of interest included maternal hemoglobin A1C, average fasting and 2-hour postprandial blood sugars, mode of delivery, birth weight, 5-minute Apgar score < 7, umbilical artery pH < 7.20, incidence of neonatal hypoglycemia, and pregnancy complications. A total of 52 diabetic pregnant patients were included in this study. Twenty-seven women used insulin glargine. A total of 13 women used insulin glargine during the first trimester. Glycemic control was similar in women who used NPH insulin and insulin glargine, as determined by hemoglobin A1C levels and mean blood sugar values. There were no differences in mode of delivery, average birth weight, or neonatal outcomes. Maternal and fetal/neonatal outcomes appear similar in pregnant diabetic women who use either NPH insulin or insulin glargine in combination with a short-acting insulin analogue to achieve adequate glycemic control during pregnancy. Insulin glargine appears to be an effective insulin analogue for use in women whose pregnancies are complicated by diabetes.     

The pathophysiological influence of leptin and the tumor necrosis factor system on maternal insulin resistance: negative correlation with anthropometric parameters of neonates in gestational diabetes.

The contribution of the tumor necrosis factor (TNF) system and leptin was studied in insulin resistance and neonatal development during the course of normal pregnancy and gestational diabetes mellitus (GDM). Thirty patients with GDM and their neonates (n = 30), 35 healthy pregnant women (15 in the first, nine in the second and 11 in the third trimester) and their neonates (n = 20), and 25 healthy matched non-pregnant women participated in the study. Significantly elevated levels of maternal TNF-alpha, sTNF receptor (R)-1 and R-2, leptin (detected by enzyme-linked immunosorbent assay) and fasting C-peptide (measured by radioimmunossay and raised body mass index (BMI) were found in GDM patients and in the third trimester of normal pregnancies. TNF-alpha, sTNFR-2, C-peptide, leptin concentrations and BMI positively correlated with each other in GDM. An inverse relationship between the body length, head circumference and body weight of the newborns, and maternal TNF-alpha, leptin and C-peptide concentrations was shown in GDM. In healthy pregnancies the maternal serum leptin level was in a negative linear correlation with the head circumference of the newborns. In conclusion, increased TNF-alpha and leptin levels may contribute to insulin resistance in GDM and in the third trimester of normal pregnancy and may negatively influence the anthropometric parameters of the newborns.     

Normoglycemic diabetic ketoacidosis in pregnancy.

The clinical presentation of diabetic ketoacidosis in pregnancy is usually the same as in nonpregnant women, although the blood glucose may not be as high as in the nongravid state. We report a case of a pregnant woman who developed diabetic ketoacidosis with a normal blood glucose and review the pertinent medical literature. A 29-year-old woman with type I diabetes developed diabetic ketoacidosis during induction of labor. She had a glucose level of 87 mg per 100 ml with ketonuria, a metabolic acidosis, and an anion gap of 20 mmol l(-1). Normoglycemic diabetic ketoacidosis during pregnancy is truly unusual but can occur with relatively low, or even normal, blood sugars and necessitates prompt recognition and treatment. In this case, the combination of an initial episode of hypoglycemia and subsequent blood glucose levels below 95 mg per 100 ml led to a prolonged delay in the initiation of a planned insulin infusion for insulin coverage during the induction of labor. A significant ketoacidosis consequently developed, despite the absence of even a single elevated blood glucose measurement. This case illustrated the importance of not withholding insulin in a patient with type I diabetes for more than a few hours even if the blood glucose is normal.     

妊娠期糖尿病孕妇外周血、脐血及胎盘中的chemerin表达

目的:探讨正常孕妇和妊娠期糖尿病(GDM)患者外周血、脐血以及胎盘中趋化素(chemerin)的表达差异及其临床意义。方法:选取2010年10月至2011年10月上海交通大学医学院附属第一人民医院20例正常孕妇及20例GDM孕妇。应用ELISA法检测外周血及脐血中chemerin水平,Western blot法测定其在胎盘中的表达,并分析其与临床相关特征的关系。结果:chemerin在正常孕妇和GDM孕妇外周血中的表达无显著差异,而在脐血和胎盘中的表达差异显著(P<0.05),与空腹血糖、餐后2h血糖、空腹胰岛素、胰岛素抵抗指数(HOMA-IR)、C反应蛋白(CRP)、胰岛素用量呈正相关(P<0.05)。结论:chemerin是影响GDM的一个独立因素,在GDM孕妇的脐血和胎盘中表达较高,并随着胰岛素用量的增加而表达增多,其可能通过糖代谢途径及炎症反应在GDM的发生发展中起着重要作用。     

Hormone replacement therapy and cancer

The contribution of the tumor necrosis factor (TNF) system and leptin was studied in insulin resistance and neonatal development during the course of normal pregnancy and gestational diabetes mellitus (GDM). Thirty patients with GDM and their neonates (n = 30), 35 healthy pregnant women (15 in the first, nine in the second and 11 in the third trimester) and their neonates (n = 20), and 25 healthy matched non-pregnant women participated in the study. Significantly elevated levels of maternal TNF-α, sTNF receptor (R)-1 and R-2, leptin (detected by enzyme-linked immunosorbent assay) and fasting C-peptide (measured by radioimmunossay and raised body mass index (BMI) were found in GDM patients and in the third trimester of normal pregnancies. TNF-α, sTNFR-2, C-peptide, leptin concentrations and BMI positively correlated with each other in GDM. An inverse relationship between the body length, head circumference and body weight of the newborns, and maternal TNF-α, leptin and C-peptide concentrations was shown in GDM. In healthy pregnancies the maternal serum leptin level was in a negative linear correlation with the head circumference of the newborns. In conclusion, increased TNF-α and leptin levels may contribute to insulin resistance in GDM and in the third trimester of normal pregnancy and may negatively influence the anthropometric parameters of the newborns.