Disproportionate Body Composition and Neonatal Outcome in Offspring of Mothers With and Without Gestational Diabetes Mellitus

OBJECTIVE

High birth weight is a risk factor for neonatal complications. It is not known if the risk differs with body proportionality. The primary aim of this study was to determine the risk of adverse pregnancy outcome in relation to body proportionality in large-for-gestational-age (LGA) infants stratified by maternal gestational diabetes mellitus (GDM).

RESEARCH DESIGN AND METHODS

Population-based study of all LGA (birth weight [BW] >90th percentile) infants born to women with GDM (n = 1,547) in 1998–2007. The reference group comprised LGA infants (n = 83,493) born to mothers without diabetes. Data were obtained from the Swedish Birth Registry. Infants were categorized as proportionate (P-LGA) if ponderal index (PI) (BW in grams/length in cm³) was ≤90th percentile and as disproportionate (D-LGA) if PI >90th percentile. The primary outcome was a composite morbidity: Apgar score 0–3 at 5 min, birth trauma, respiratory disorders, hypoglycemia, or hyperbilirubinemia. Logistic regression analysis was used to obtain odds ratios (ORs) for adverse outcomes.

RESULTS

The risk of composite neonatal morbidity was increased in GDM pregnancies versus control subjects but comparable between P- and D-LGA in both groups. D-LGA infants born to mothers without diabetes had significantly increased risk of birth trauma (OR 1.19 [95% CI 1.09–1.30]) and hypoglycemia (1.23 [1.11–1.37]). D-LGA infants in both groups had significantly increased odds of Cesarean section.

CONCLUSIONS

The risk of composite neonatal morbidity is significantly increased in GDM offspring. In pregnancies both with and without GDM, the risk of composite neonatal morbidity is comparable between P- and D-LGA.High birth weight (BW), in both diabetic and nondiabetic pregnancies, is associated with increased risk of maternal and perinatal complications as well as long-term adverse health consequences for the offspring (1–10). Gestational diabetes and maternal obesity are well-established risk factors for high BW (11–14). In pregnancies with gestational diabetes mellitus (GDM), reported rates of high-BW infants range between 15 and 62.5% (15–18), corresponding to a several-fold increased risk compared with the general obstetric population (19). Complications associated with high BW include excessive maternal bleeding, prolonged labor, instrumental delivery, Cesarean section, perineal tears, stillbirth, neonatal birth trauma, low Apgar scores, acute respiratory disorders, hypoglycemia, and neonatal death (1–7). Irrespective of BW, GDM offspring face an excess risk of future morbidities (20–23). However, the risk may be even further increased in infants born with fetal macrosomia (24,25).The definition for high BW is not consistent. Current definitions are based on either absolute BW (>4,000 or 4,500 g) and referred to as fetal macrosomia or BW in relation to gestational age and sex (large for gestational age [LGA], BW >90th or 97.5th percentile). It is unclear which of these definitions best predicts the risk of adverse outcome. None of the current definitions take into account body proportionality, i.e., the relation between the infant''s BW and birth length (BL). The ponderal index (PI; i.e., BW in grams/BL in cm³) is a marker for body proportionality, and at a population level, the PI is a useful estimate of body proportionality when BW and BL are routinely collected. Fetal macrosomia or LGA in infants born to mothers with GDM and/or obesity is characterized by a disproportionate body composition with high BW in relation to BL (26) and increased fat mass (27–29).The primary aim of this study was to determine the risk of adverse pregnancy outcome in relation to body proportionality in LGA infants (BW >90th percentile) stratified by maternal GDM status. We hypothesized that infants with a disproportionate body composition, most likely as a consequence of fetal hyperinsulinemia, would have an increased risk of perinatal complications compared with those with a proportionate body composition.     

Predictors of Overweight During Childhood in Offspring of Parents With Type 1 Diabetes

OBJECTIVE

To study which perinatal factors affect the risk of childhood overweight in offspring with a first-degree relative (FDR) with type 1 diabetes and to determine whether maternal diabetes is an independent contributor to overweight risk.

RESEARCH DESIGN AND METHODS

Data on a child''s weight and height were collected at age 2, 5, and 8 years from 1,214 children participating in the prospective BABYDIAB study. All children had an FDR with type 1 diabetes, including 783 whose mothers had type 1 diabetes. Overweight was defined as BMI percentile ≥90. Data on birth size, breast-feeding, maternal age, and smoking during pregnancy were collected by questionnaires. Risk estimates were calculated by logistic regression analyses.

RESULTS

Breastfeeding duration and birth size both contributed significantly to overweight risk at all age intervals. Full breast-feeding >4 months or any breast-feeding >6 months reduced risk of overweight (aged 8 years: odds ratio 0.3 [95% CI 0.2–0.7], P = 0.004; and 0.3 [0.1–0.6], P = 0.001). Large-for-gestational-age status increased risk of overweight (aged 8 years: 2.4 [1.4–4.3], P = 0.002). Importantly, no evidence was found for an independent contribution of maternal type 1 diabetes to childhood overweight.

CONCLUSIONS

Our findings indicate that maternal type 1 diabetes is not an independent risk factor for overweight during childhood in offspring of type 1 diabetic mothers but that factors associated with maternal type 1 diabetes, such as short breast-feeding duration and high birth size, predispose children to overweight during childhood.The increasing prevalence of overweight and obesity in children is a major health problem, as obesity-related medical conditions affect almost every organ system in the body (1). Gestational and perinatal factors have been shown to influence weight in childhood. Among these, maternal diabetes during pregnancy has been associated with an increased prevalence of childhood obesity (2–6). This has led to the hypothesis that in utero exposure to increased concentrations of glucose and insulin leads to increased risk of obesity and insulin resistance later in life (2). Previous studies (3–5) have been small or retrospective in design. Moreover, it is not clear whether maternal diabetes as such, or factors such as birth size and breast-feeding, which are affected by maternal diabetes, modify obesity risk.Here, we have examined weight and BMI during childhood in a cohort of 1,214 children whose mothers or fathers have type 1 diabetes and who were followed from age ≤3 months. The aim of the analysis was to determine which gestational and perinatal factors may increase the risk of childhood obesity and whether maternal diabetes is an independent contributor to obesity risk.     

补充维生素D对妊娠期糖尿病孕妇胰岛素抵抗及新生儿胰岛素的影响

目的：探讨补充维生素D（VD）对妊娠期糖尿病（GDM）胰岛素抵抗及新生儿胰岛素的影响。方法：将56名GDM孕妇随机分为VD组26例和对照组30例,VD组在饮食控制的同时口服维生素D,400IU,每日二次,以20名健康孕妇为正常组;比较三组空腹血糖（FBG）、空腹胰岛素（FINS）、血清25-（OH）VD3、胰岛素抵抗指数（HOMA—IRI）和新生儿的胰岛素水平。结果：VD组补充VD一个月后,25-（OH）VD,明显高于饮食控制组（P〈0．05）：三组间的FINS有统计学差异（P〈0．05）;VD组HOMA—IRI明显低于饮食控制组而高于健康孕妇组（P〈0．05）;VD组和饮食控制组的FBG无明显差异,但均显著高于对照组（P〈0．05）。对照组新生儿胰岛素与VD组和饮食控制组有明显差异（P〈0．05）,但VD组和饮食控制组无明显差异（P〉0．05）。结论：VD与GDM发生密切相关,GDM孕妇补充VD后,25-（OH）VD,水平明显升高,胰岛素抵抗明显改善,但却不能恢复至正常孕妇状态：补充VD对GDM孕妇分娩的新生儿胰岛素无明显影响。     

Body Composition Is Normal in Term Infants Born to Mothers With Well-Controlled Gestational Diabetes Mellitus

OBJECTIVE

This study aims to describe body composition in term infants of mothers with gestational diabetes mellitus (GDM) compared with infants of mothers with normal glucose tolerance (NGT).

RESEARCH DESIGN AND METHODS

This cross-sectional study included 599 term babies born at Royal Prince Alfred Hospital, Sydney, Australia. Neonatal body fat percentage (BF%) was measured within 48 h of birth using air-displacement plethysmography. Glycemic control data were based on third-trimester HbA_1c levels and self-monitoring blood glucose levels. Associations between GDM status and BF% were investigated using linear regression adjusted for relevant maternal and neonatal variables.

RESULTS

Of 599 babies, 67 (11%) were born to mothers with GDM. Mean ± SD neonatal BF% was 7.9 ± 4.5% in infants with GDM and 9.3 ± 4.3% in infants with NGT, and this difference was not statistically significant after adjustment. Good glycemic control was achieved in 90% of mothers with GDM.

CONCLUSIONS

In this study, neonatal BF% did not differ by maternal GDM status, and this may be attributed to good maternal glycemic control.Fetal growth and development is affected through the altered intrauterine environment of gestational diabetes mellitus (GDM) (1,2). An accurate method to characterize overgrowth is by estimation of body composition, which includes fat mass (FM) and fat-free mass (FFM) (3,4). Previous studies have shown that increases in FM are present in infants of GDM pregnancies, regardless of their weight for gestational age (1,5). The gold-standard method of measuring body composition changes is air-displacement plethysmography (ADP) (4,6,7). The aim of this study was to describe body composition and anthropometric measurements at birth in term infants of women with GDM compared with infants of mothers with normal glucose tolerance (NGT) levels.     

Epigenome-Wide Association Study Reveals Methylation Loci Associated With Offspring Gestational Diabetes Mellitus Exposure and Maternal Methylome

OBJECTIVEGestational diabetes mellitus (GDM) is associated with an increased risk of obesity and insulin resistance in offspring later in life, which might be explained by epigenetic changes in response to maternal hyperglycemic exposure.RESEARCH DESIGN AND METHODSWe explored the association between GDM exposure and maternal blood and newborn cord blood methylation in 536 mother-offspring pairs from the prospective FinnGeDi cohort using Illumina MethylationEPIC 850K BeadChip arrays. We assessed two hypotheses. First, we tested for shared maternal and offspring epigenetic effects resulting from GDM exposure. Second, we tested whether GDM exposure and maternal methylation had an epigenetic effect on the offspring.RESULTSWe did not find any epigenetic marks (differentially methylated CpG probes) with shared and consistent effects between mothers and offspring. After including maternal methylation in the model, we identified a single significant (false discovery rate 1.38 × 10⁻²) CpG at the cg22790973 probe (TFCP2) associated with GDM. We identified seven additional FDR-significant interactions of maternal methylation and GDM status, with the strongest association at the same cg22790973 probe (TFCP2), as well as cg03456133, cg24440941 (H3C6), cg20002843 (LOC127841), cg19107264, and cg11493553 located within the UBE3C gene and cg17065901 in FAM13A, both susceptibility genes for type 2 diabetes and BMI, and cg23355087 within the DLGAP2 gene, known to be involved in insulin resistance during pregnancy.CONCLUSIONSOur study reveals the potential complexity of the epigenetic transmission between mothers with GDM and their offspring, likely determined by not only GDM exposure but also other factors indicated by maternal epigenetic status, such as maternal metabolic history.     

Lower Adiponectin Levels at First Trimester of Pregnancy Are Associated With Increased Insulin Resistance and Higher Risk of Developing Gestational Diabetes Mellitus

OBJECTIVE

To evaluate the associations between adiponectin levels and 1) the risk of developing gestational diabetes mellitus (GDM), and 2) insulin resistance/sensitivity, β-cell function, and compensation indices in a prospective cohort representative of the general population of pregnant women.

RESEARCH DESIGN AND METHODS

We performed anthropometric measurements and collected blood samples at 1st (6–13 weeks) and 2nd (24–28 weeks) trimesters. Diagnosis of GDM was made at 2nd trimester based on a 75-g oral glucose tolerance test (International Association of the Diabetes and Pregnancy Study Groups criteria). Insulin was measured (ELISA; Luminex) to estimate homeostasis model assessment of insulin resistance (HOMA-IR), β-cell function (HOMA-B), insulin sensitivity (Matsuda index), insulin secretion (AUC_{insulin/glucose}), and β-cell compensation (insulin secretion sensitivity index-2). Adiponectin was measured by radioimmunoassay.

RESULTS

Among the 445 participants included in this study, 38 women developed GDM. Women who developed GDM had lower 1st-trimester adiponectin levels (9.67 ± 3.84 vs. 11.92 ± 4.59 µg/mL in women with normal glucose tolerance). Lower adiponectin levels were associated with higher risk of developing GDM (OR, 1.12 per 1 µg/mL decrease of adiponectin levels; P = 0.02, adjusted for BMI and HbA_1c at 1st trimester). Adiponectin levels at 1st and 2nd trimesters were associated with HOMA-IR (both: r = −0.22, P < 0.0001) and Matsuda index (r = 0.28, P < 0.0001, and r = 0.29, P < 0.0001). After adjustment for confounding factors, we found no significant association with HOMA-B and AUC_{insulin/glucose}.

CONCLUSIONS

Pregnant women with lower adiponectin levels at 1st trimester have higher levels of insulin resistance and are more likely to develop GDM independently of adiposity or glycemic measurements.Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition determined during pregnancy (1). In normal pregnancy, there is a progressive physiologic increase of insulin resistance, compensated by an increase of insulin secretion by pancreatic β-cells (2). Among GDM women, there is an imbalance between insulin resistance and insulin secretion capacity, resulting in increased circulating glucose levels (3). Over the past decades, GDM has drawn scientific attention because of its growing incidence and deleterious consequences for mothers and offspring (4,5). Nevertheless, the exact mechanisms implicated in its pathophysiology remain poorly understood.Adiponectin is an adipokine suspected to have insulin-sensitizing properties (6). Furthermore, lower adiponectin levels have been repeatedly and consistently associated with increased risk of type 2 diabetes incidence (7–9), but reports on GDM are inconsistent. Few studies investigated the association between adiponectin levels measured early in pregnancy and GDM incidence: some showed that low adiponectin levels are associated with increased risk of GDM (10–13), while others showed no association (14,15). Contradictory findings between studies can be partly explained by limited power and different study designs. Also, these studies inconsistently accounted for potential confounding factors like adiposity and baseline impaired glucose regulation in pregnant women. Therefore, larger prospective studies are needed, designed to take into account potential confounding factors to adequately assess whether there is an independent association between adiponectin levels and the risk of developing GDM.Thus, in the current study, we evaluated whether 1st-trimester adiponectin levels are associated with higher risk of developing GDM during pregnancy. Also, we assessed whether there is an association between adiponectin at both 1st and 2nd trimesters (or the change [Δ] over 1st to 2nd trimester) and insulin resistance/sensitivity or pancreatic β-cell function/compensation indices at 2nd trimester of pregnancy.     

Osteocalcin Is Related to Enhanced Insulin Secretion in Gestational Diabetes Mellitus

OBJECTIVE

There is growing evidence that osteocalcin, an osteoblast-derived protein locally acting on bone formation, can increase insulin secretion as well as insulin sensitivity and thus prevent the development of obesity and diabetes in experimental animals. In humans, osteocalcin has been reported to be decreased in patients with type 2 diabetes. Because gestational diabetes mellitus (GDM) can serve as a model of pre–type 2 diabetes, the aim of this study was to investigate osteocalcin in GDM.

RESEARCH DESIGN AND METHODS

Osteocalcin measurement and an oral glucose tolerance test were performed in 78 pregnant women (26 women had GDM and 52 women had normal glucose tolerance [NGT] during pregnancy; women were matched for age and BMI) and in 34 women postpartum.

RESULTS

During pregnancy osteocalcin was significantly higher in the women with GDM than in the women with NGT (15.6 ± 6.4 vs. 12.6 ± 4.0 ng/ml; P < 0.015), whereas no difference was observed between the two groups at 12 weeks postpartum (36.2 ± 10.2 vs. 36.2 ± 13.0 ng/ml), when osteocalcin was found to be increased compared with the level in the pregnant state in all women (+145 ± 102% in GDM vs. +187 ± 119% in NGT; P < 0.0001). Moreover, osteocalcin showed a significant correlation with basal and total insulin secretion in the whole study group (R = 0.3, P < 0.01).

CONCLUSIONS

In GDM osteocalcin was higher and thus less restrained than in women with NGT during pregnancy and furthermore correlated with insulin secretion parameters. Therefore, it could be hypothesized that osteocalcin can enhance insulin secretion in insulin-resistant states; alternatively an effect of hyperinsulinemia on osteocalcin secretion cannot be excluded.Evidence is growing regarding the reciprocal interaction between bone and energy metabolism (1). The findings that adipose tissue via leptin can regulate bone metabolism (2) and that insulin, as an anabolic hormone, influences bone metabolism via IGF-1 (3,4) raised the idea that bone in turn could also affect energy metabolism. Osteocalcin, an osteoblast-derived protein acting locally on bone formation, is suspected to be involved in the regulation of glucose and fat metabolism. Because animal models showed that mice lacking osteocalcin display insulin resistance and obesity, bone became a focus of interest concerning endocrine action as did adipose tissue when adipocytokines were detected. It has been demonstrated that osteocalcin can stimulate insulin secretion, acting directly on proliferation and secretion of the pancreatic β-cells. Osteocalcin might act via an endocrine pathway, and, indeed, osteocalcin has been reported to exert several hormone-specific features. Furthermore, it has been shown that osteocalcin can increase insulin sensitivity, probably by inducing the expression of adiponectin in adipocytes. Besides, mice lacking the Esp gene that encodes for a receptor-like protein called OST-PTP, which is thought to influence the bioactivity of osteocalcin, show increased energy expenditure and decreased levels of triglycerides and are protected from diet-induced obesity and diabetes (5).In humans, osteocalcin has been reported to be decreased in patients with type 2 diabetes (6), negatively correlated with fasting plasma glucose, A1C, insulin resistance (assessed by homeostasis model assessment of insulin resistance), high-sensitivity C-reactive protein (hs-CRP), and BMI and increased with improved glycemic control (7,8). Moderate weight loss and regular exercise have also been found to increase osteocalcin concentrations, partly by direct effects of exercise on bone remodeling and partly by a reduction in visceral fat (9). Furthermore, weight loss after bariatric surgery has been reported to be associated with a significant increase in osteocalcin (10). These findings again emphasize the connection between osteocalcin and substrate metabolism.Because gestational diabetes mellitus (GDM), defined as glucose intolerance first detected during pregnancy (11), serves as a model to study the early changes in the development of insulin resistance and type 2 diabetes, interest in the action and regulation of osteocalcin in this entity, which affects about 10% of pregnant women in the middle European population, has increased. Besides pronounced insulin resistance compared with that in women with normal glucose tolerance (NGT) during pregnancy (12), pancreatic β-cell dysfunction has been described as the main metabolic characteristic in women with GDM (13). Despite increased insulin release, women with GDM fail to cope with the increased insulin demand during the physiological insulin resistance of late pregnancy, resulting in hyperglycemia. The majority of women with GDM regain NGT after delivery but have a life-long increased risk of developing type 2 diabetes, especially within the first 10 years after delivery (14). Therefore, the aim of this study was to investigate, for the first time, osteocalcin and its associations with glucose metabolism in GDM both during pregnancy and after delivery.     

妊娠期糖尿病母婴预后的临床分析

目的：探讨妊娠期糖尿病(GDM)对母婴预后的影响。方法：回顾性分析1998年12月～2000年12月期间，28例GDM，100例无内科合并症健康孕妇的妊娠结局。结果：GDM组病理妊娠发病率50％，剖宫产率60．71％，围产儿发病率64．28％，与对照组相比均有显著差异。结论：GDM组母婴发病率及手术产率均高于对照组，应提高对GDM的认识，减少母婴并发症的发生。     

胰岛素治疗对妊娠期合并糖尿病患者妊娠结局的影响

目的探讨胰岛素治疗对妊娠期合并糖尿病患者妊娠结局的影响。方法:选取2013年10月~2015年5月我院确诊治疗的妊娠期合并糖尿病患者80例,依据随机分配原则分为胰岛双胍组和二甲双胍组,每组40例,二甲双胍组患者给予二甲双胍口服治疗,胰岛双胍组在此基础上给予胰岛素皮下注射治疗,采用新生儿窒息评分(Apgar)评估新生儿窒息情况,统计分析所有患者治疗前后空腹和餐后2h血糖及妊娠结局情况。结果:治疗前,胰岛双胍组和二甲双胍组患者空腹和餐后2h血糖基本相同,无显著差异性(P0.05),但前者治疗后空腹和餐后2h血糖明显低于后者,差异有统计学意义(P0.05);胰岛双胍组患者剖宫产率、巨大儿发生率明显低于二甲双胍组,前者Apgar得分明显高于后者,差异有统计学意义(P0.05)。结论胰岛素治疗可有效控制妊娠期合并糖尿病患者的血糖水平,有利于改善患者妊娠结局,值得临床作进一步推广。     

Determinants of Maternal Triglycerides in Women With Gestational Diabetes Mellitus in the Metformin in Gestational Diabetes (MiG) Study

OBJECTIVE

Factors associated with increasing maternal triglyceride concentrations in late pregnancy include gestational age, obesity, preeclampsia, and altered glucose metabolism. In a subgroup of women in the Metformin in Gestational Diabetes (MiG) trial, maternal plasma triglycerides increased more between enrollment (30 weeks) and 36 weeks in those treated with metformin compared with insulin. The aim of this study was to explain this finding by examining factors potentially related to triglycerides in these women.

RESEARCH DESIGN AND METHODS

Of the 733 women randomized to metformin or insulin in the MiG trial, 432 (219 metformin and 213 insulin) had fasting plasma triglycerides measured at enrollment and at 36 weeks. Factors associated with maternal triglycerides were assessed using general linear modeling.

RESULTS

Mean plasma triglyceride concentrations were 2.43 (95% CI 2.35–2.51) mmol/L at enrollment. Triglycerides were higher at 36 weeks in women randomized to metformin (2.94 [2.80–3.08] mmol/L; +23.13% [18.72–27.53%]) than insulin (2.65 [2.54–2.77] mmol/L, P = 0.002; +14.36% [10.91–17.82%], P = 0.002). At 36 weeks, triglycerides were associated with HbA_1c (P = 0.03), ethnicity (P = 0.001), and treatment allocation (P = 0.005). In insulin-treated women, 36-week triglycerides were associated with 36-week HbA_1c (P = 0.02), and in metformin-treated women, they were related to ethnicity.

CONCLUSIONS

At 36 weeks, maternal triglycerides were related to glucose control in women treated with insulin and ethnicity in women treated with metformin. Whether there are ethnicity-related dietary changes or differences in metformin response that alter the relationship between glucose control and triglycerides requires further study.Maternal metabolism in late pregnancy is catabolic, with increasing insulin resistance, decreased adipose tissue lipoprotein lipase (LPL) activity, and increased lipolysis (1). These processes combine to ensure the availability of maternal fuels such as glucose, fatty acids, and ketone bodies for fetal use (1). It is recognized that gestational age, maternal obesity (2), and preeclampsia (3) are associated with increases in lipids during pregnancy. Gestational diabetes mellitus (GDM) is also associated with abnormalities in maternal lipid metabolism (4–6), which may contribute to the elevated fat mass seen at birth in infants of women with GDM (7–10).Maternal glucose control and the pharmacological therapies used for treatment of GDM have the potential to influence these changes in maternal lipids (11). Insulin suppresses adipose tissue lipolysis and might be expected to reduce circulating triglycerides (12). Metformin reduces insulin resistance, but it has also been suggested to influence lipid metabolism (13), independent of glycemic control. In type 2 diabetes, metformin treatment is associated with a reduction in plasma triglyceride, total cholesterol, LDL cholesterol (13), and VLDL cholesterol concentrations (14). Metformin treatment in type 2 diabetes is also associated with increases in LPL mass level and LDL cholesterol particle size (15) and with a reduction in the release of free fatty acids from adipose tissue (16).We have recently examined maternal lipids in the Metformin in Gestational Diabetes (MiG) trial and found that maternal fasting plasma triglycerides and measures of glucose control at 36 weeks were the strongest predictors of customized birth weight >90th percentile (17). Interestingly, triglycerides increased more from randomization to 36 weeks'' gestation in women allocated to metformin than in those allocated to treatment with insulin, but there was no difference in customized birth weights or other neonatal anthropometry measures between the groups; there were also no differences in cord blood triglycerides (17). The aim of this study was to examine the known and putative determinants of maternal triglyceride concentrations and determine whether the difference seen in maternal plasma triglycerides at 36 weeks was due to treatment or other factors that may have differed between treatment groups.     

The Relative Contribution of Prepregnancy Overweight and Obesity,Gestational Weight Gain,and IADPSG-Defined Gestational Diabetes Mellitus to Fetal Overgrowth

OBJECTIVE

The International Association of Diabetes in Pregnancy Study Groups (IADPSG) criteria for diagnosis of gestational diabetes mellitus (GDM) identifies women and infants at risk for adverse outcomes, which are also strongly associated with maternal overweight, obesity, and excess gestational weight gain.

RESEARCH DESIGN AND METHODS

We conducted a retrospective study of 9,835 women who delivered at ≥20 weeks’ gestation; had a prenatal, 2-h, 75-g oral glucose tolerance test; and were not treated with diet, exercise, or antidiabetic medications during pregnancy. Women were classified as having GDM based on IADPSG criteria and were categorized into six mutually exclusive prepregnancy BMI/GDM groups: normal weight ± GDM, overweight ± GDM, and obese ± GDM.

RESULTS

Overall, 5,851 (59.5%) women were overweight or obese and 1,892 (19.2%) had GDM. Of those with GDM, 1,443 (76.3%) were overweight or obese. The prevalence of large-for-gestational-age (LGA) infants was significantly higher for overweight and obese women without GDM compared with their normal-weight counterparts. Among women without GDM, 21.6% of LGA infants were attributable to maternal overweight and obesity, and the combination of being overweight or obese and having GDM accounted for 23.3% of LGA infants. Increasing gestational weight gain was associated with a higher prevalence of LGA in all groups.

CONCLUSIONS

Prepregnancy overweight and obesity account for a high proportion of LGA, even in the absence of GDM. Interventions that focus on maternal overweight/obesity and gestational weight gain, regardless of GDM status, have the potential to reach far more women at risk for having an LGA infant.Both International Association of Diabetes in Pregnancy Study Groups (IADPSG)–defined gestational diabetes mellitus (GDM) (1,2) and maternal overweight and obesity (2–4) are associated with increased risk for adverse maternal and perinatal outcomes, such as fetal overgrowth, shoulder dystocia and birth injury, pre-eclampsia, and preterm delivery. Although most studies addressing the effects of maternal BMI on adverse outcomes include women with GDM (2–6), a few have reported these associations in overweight or obese women with normal glucose tolerance (7–9). Scant data exist that demonstrate associations between GDM and adverse outcomes in the absence of overweight or obesity (9).Although it is currently estimated that 10–25% of pregnant women develop GDM by IADPSG criteria (1,2,10), 50–60% of women are overweight or obese at the start of their pregnancies (6,7,11,12). Prepregnancy overweight and obesity are also associated with GDM development, as 65–75% of women with GDM are also overweight or obese (11,13). As such, the relative impact of prepregnancy BMI and maternal glycemia during pregnancy on adverse maternal and perinatal outcomes is difficult to tease apart. Moreover, excess gestational weight gain complicates a large number of pregnancies and is highly correlated with maternal overweight and obesity, as well as the development of GDM (14–16). Despite the fact that studies have reported increases in the risk of adverse outcomes with increasing gestational weight gain (13,15–18), many studies examining the effects of maternal obesity and/or glucose levels have not accounted for this important factor.The purpose of this study was to examine the effects of prepregnancy overweight and obesity among women with and without IADPSG-defined GDM on clinically important adverse outcomes, focusing primarily on fetal overgrowth, one of the most prevalent adverse conditions associated with maternal and neonatal morbidity. In addition to magnitude of association, we determine the proportion of large-for-gestational-age (LGA) infants attributable to each risk factor and combinations thereof. We also examine the relative contribution of increasing gestational weight gain to the development of LGA.     

2型糖尿病患者血清脂联素水平与胰岛素抵抗的关系

【目的】探讨2型糖尿病（T2DM）患者血清脂联素（APN）水平与肥胖、胰岛素及胰岛素抵抗的关系。【方法】采用病例对照研究,T2DM伴有肥胖组（DO）42例,T2DM不伴肥胖组（NDO）42例,正常对照组（NC）28名。检测三组对象血脂、血糖、空腹胰岛素（Fins）、APN水平。用HOMA模型公式计算胰岛素抵抗指数（HOMAIR）。【结果JDO组和NDO组的血清APN水平均明显低于NC组[DO组（8．02±3．57）mg／L,NDO组（8．35±2．68）mg／L比NC组（14．04±4．75）mg／L,均P〈O．01],DO组与NDO组APN水平差异无显著性。APN与体质指数（BMI）、腰围（w）、腰臀比（WHR）、空腹血糖（FBG）、甘油三脂（TG）、Fins、HO—MAIR呈显著负相关（P〈0．01）,APN与高密度脂蛋白（HDL-C）呈显著正相关（P〈0．01）。多元逐步回归分析显示HOMAIR和WHR是血清APN浓度的主要影响因素。【结论】脂联素参与了胰岛素抵抗的发生,与2型糖尿病的发生相关。     

妊娠期糖尿病的筛查与处理

目的探讨妊娠期糖尿病(GDM)的诊断及处理方法。方法对2311例孕妇行葡萄糖筛查,诊断GDM57例作为观察组,选取同期符合GDM诊断标准未经正规治疗的49例作为对照组,比较两组的母儿结局。结果观察组羊水过多、巨大儿、高胆红素血症、新生儿呼吸窘迫综合征、围生儿死亡率等均明显低于对照组,差异有显著性(P<0.05)。结论及早诊断、积极治疗,可改善母儿预后。     

妊娠糖尿病患者胎盘LPL基因Hind片段多态性与新生儿发生胰岛素抵抗风险的相关性研究

目的　研究妊娠糖尿病（gestational diabetes mellitus, GDM）患者胎盘脂蛋白酯酶（lipoprotein lipase, LPL）基因Hind片段多态性与新生儿发生胰岛素抵抗（insulin resistance, IR）的关系。方法　收集2018年4月～2020年4月84例GDM患者作为观察组,另纳入同期84例健康孕妇作为对照组。比较两组孕妇LPL多态性分布,比较两组新生儿血糖（FPG,HbA1c及2h PG）和血脂（TC,TG,HDL-C及LDL-C）指标水平,计算胰岛素抵抗指数（homeostasis model assessment of insulin resistance, HOMA-IR）值。分析胎盘LPL多态性与子代胰岛素抵抗的关系。结果　观察组H+H+基因型48例,H+H-基因型24例,H-H-基因型12例。对照组H+H+基因型32例,H+H-基因型38例,H-H-基因型14例,两组孕妇胎盘LPL基因型分布比较,差异有统计学意义（χ2=6.52,P<0.05）。GDM不同基因型患者所生新生儿TC,TG,HDL-C,LDL-C及HOMA-IR水平差异均有统计学意义（F=5.29~16.33,均P<0.05）。多元逐步回归分析结果显示胎盘LPL多态性是新生儿HOMA-IR的重要影响因素（t=2.86,P<0.05）。结论　胎盘LPL多态性与GDM发病有关,H+H+基因型产妇子代发生胰岛素抵抗的风险更高。     

胰岛素泵治疗妊娠期糖尿病的临床疗效观察

【目的】探讨胰岛素泵（CSⅡ）对妊娠期糖尿病（GDM）血糖控制、母婴并发症及住院费用的影响。【方法】72例需胰岛素治疗的GDM随机分为每天胰岛素多次注射组（MDI组）和CSⅡ组,分析比较两组治疗前后的血糖变化、母婴并发症,并进行费用比较。【结果】与MDI组相比,CSⅡ组能快速控制空腹、餐后血糖,血糖达标所需时间及胰岛素用量少（P〈0．05）,母婴并发症少,所需住院时间短,CSⅡ组日平均费用高于MDI组,但两组住院总费用相比较无差异。【结论】胰岛素泵能更好的控制血糖,减少胰岛素用量,显著降低母婴并发症,缩短住院时间,且不增加患者经济负担,故值得推广应用。