妊娠期糖耐量降低对胎儿及新生儿的影响

目的：探讨妊娠期糖耐量降低（ＧＩＧＴ）对胎儿及新生儿的影响。方法：对ＧＩＧＴ孕妇５２例（ＧＩＧＴ组），妊娠期糖尿病（ＧＤＭ）孕妇３４例（ＧＤＭ组），正常孕妇４４例（对照组）的围产儿结局进行比较。结果：ＧＩＧＴ组巨大儿发生率高于对照组（Ｐ＜０．０２５），生后２小时的血糖均值在３组中最低（Ｐ＜０．０５），低血糖、红细胞增多症等并发症高于对照组。结论：ＧＩＧＴ与ＧＤＭ均是影响胎儿及新生儿预后的重要因素。     

妊娠期糖代谢变化及其与胎盘催乳素的关系

目的探讨正常妊娠过程中孕妇糖耐量、胰岛素释放、胰岛素敏感性变化及其与胎盘催乳素的关系。方法对９４例正常孕妇进行７５ｇ葡萄糖耐量试验,检测各时相血糖和胰岛素水平,计算胰岛素曲线下面积（ＩＡＵＣ）与血糖曲线下面积（ＧＡＵＣ）,并观察胰岛素敏感指数（ＩＡＩ）的变化,同时检验空腹人体胎盘催乳素（ＨＰＬ）。结果ＩＡＵＣ、ＧＡＵＣ、ＩＡＩ及ＨＰＬ均随孕期延长而升高,各孕期比较,差异有显著性（Ｐ＜０．０５）;多重相关分析显示,ＨＰＬ与ＧＡＵＣ、ＩＡＵＣ、ＩＡＩ均呈显著正相关关系。但在消除了ＩＡＵＣ和ＩＡＩ的影响后,ＨＰＬ与ＧＡＵＣ无相关关系。结论妊娠期表现高胰岛素血症及胰岛素敏感性下降,并与ＨＰＬ有关;ＨＰＬ是影响妊娠期糖代谢变化的因素之一。     

胰岛素抵抗与妊高征

通过检测４０例妊高征患者、３０例正常孕妇口服糖耐量试验（ＯＧＴＴ）前、后血胰岛素（ＩＳ）及血糖（ＳＧ），发现重度好高征组服糖后血ＩＳ水平、ＳＧ水平、ＩＳ／ＳＧ比值及ＩＳ反应曲线下面积较正常妊娠组升高（Ｐ＜０．０５）。重度好高征患者ＯＧＴＴ胰岛素反应曲线下面积与舒张压存在正相关。上述结果表明，重度妊高征患者存在糖负荷后高胰岛素血症，提示存在胰岛素抵抗。     

妊娠期糖尿病孕妇产后糖代谢异常的研究

目的　了解妊娠期糖尿病（ＧＤＭ） 患者产后糖代谢异常情况、筛出预测产后糖代谢异常的高危因素及ＧＤＭ 患者远期糖尿病发生情况。　方法　收集１９８２ 年１１ 月～１９９８ 年４ 月在我院分娩并产后随访的９７ 例ＧＤＭ 孕妇,其中远期随访１～８ 年者３３ 例。　结果　ＧＤＭ 产后近期随访诊断为显性糖尿病者２３ 例,糖耐量减低１１ 例,列为产后糖代谢异常组。与产后糖代谢正常组（４１ 例） 进行比较发现：糖尿病家族史、孕期血糖异常出现时间、糖筛查血糖高、空腹血糖升高以及糖尿病孕期治疗情况两组间存在明显差异。远期追踪３３ 例中显性糖尿病１０ 例,糖耐量减低３ 例。　结论　ＧＤＭ产后仍有部分患者糖代谢不能恢复正常,尤其有糖尿病家族史,在妊娠２４ 周以前确诊ＧＤＭ,糖筛查血糖较高,空腹血糖升高,孕期需胰岛素治疗者更应重视产后血糖检查,以便及时发现产后糖代谢异常。产后近期糖代谢正常者,仍需进行远期随访     

妊娠期糖尿病病史妇女远期血清胰岛素水平观察

目的　测定妊娠期糖尿病（ Ｇ Ｄ Ｍ） 病史妇女,远期未发生糖尿病者的血糖和血清胰岛素水平,间接了解胰岛β细胞功能。方法　对远期未发生糖尿病的 Ｇ Ｄ Ｍ 病史者３０ 例（ 观察组） ,口服糖耐量试验（ Ｏ Ｇ Ｔ Ｔ） 单项异常史者２９ 例（ 异常史组） ,正常孕妇３８ 例（ 对照组） 进行追访,复查空腹血糖并行７５ｇ 糖负荷试验,同时测定胰岛素水平。结果　（１） 服糖后２ 小时观察组血糖为（６ ．１ ±１ ．７）ｍｍｏｌ／ Ｌ,异常史组血糖为（５ ．５ ±１ ．２） ｍｍｏｌ／ Ｌ,均高于对照组的（４ ．８ ±０ ．５） ｍ ｍｏｌ／ Ｌ,尤以观察组为著（ Ｐ＜０ ．００１） 。（２） 服糖后２ 小时,观察组的血清胰岛素水平为（６０ ．７ ±３８ ．６） ｍ Ｕ／ Ｌ,高于对照组的（３８ ．４ ±１６ ．２）ｍ Ｕ／ Ｌ,两组比较,差异有极显著性（ Ｐ＜ ０ ．００１） 。结论　远期未发生糖尿病者,仍存在着胰岛素抵抗,有可能是以后发生糖尿病的信号。     

正常妊娠妇女及妊娠期糖尿病患者胰岛素和C肽水平的变化

目的 探讨正常妊娠妇女、妊娠期糖尿病（ＧＤＭ）及妊娠合并糖耐量减低（ＧＩＧＴ０患者孕期胰岛素、Ｃ肽水平的变化,了解其胰岛β细胞的功能状况。方法 用放射免疫法测定ＧＤＭ患者４８例（Ⅰ组）;ＧＩＧＴ患者３９例（Ⅱ组）;正常妊娠妇女４２例（Ⅲ组）;正常非妊娠妇女２２例（Ⅳ组）的胰岛素和Ｃ肽水平。结果 Ⅲ组孕晚期的胰岛素、Ｃ肽水平明显高于Ⅳ组（Ｐ均〈０．０１）,且从孕３４周至孕晚期,有上升趋势,至产时呈高     

炔雌醇对绝经后妇女糖代谢的影响

目的：探讨合成雌激素炔雌醇对绝经后妇女糖代谢的影响。方法：将绝经后妇女１９例随机分为两组，口服炔雌醇（ＥＥ）０．０２５ｍｇ９例为Ａ组，口服ＥＥ０．０５ｍｇ１０例为Ｂ组，共服药３个月。服药前后均进行口服葡萄糖耐量试验和多样本的静脉葡萄糖耐量试验，同时测定血糖、胰岛素和计算曲线下面积（ＡＵＣ）以及胰岛素敏感指数（ＳＩ）。结果：两组均可有效降低空腹血糖、胰岛素水平，明显减少胰岛素ＡＵＣ，提高胰岛素ＳＩ。Ａ组血糖ＡＵＣ无多大变化，Ｂ组血糖ＡＵＣ明显增加。结论：炔雌醇可有效降低绝经后妇女的空腹血糖、胰岛素水平，减弱胰岛素抵抗。０．０５ｍｇＥＥ可损害糖耐量。     

妊高征患者母血及新生儿脐血胰岛素、C肽水平变化的研究

目的：研究妊娠高血压综合征（妊高征）患者母血及新生儿脐血中胰岛素、Ｃ肽水平的变化。方法：测定妊高征和正常孕妇中期、晚期母静脉血及脐血的Ｃ肽、胰岛素水平及比较两组新生儿体重、孕晚期脐动脉收缩末期与舒张末期血流比值（Ｓ／Ｄ）。结果：两组孕晚期Ｃ肽和胰岛素水平均高于孕中期,而新生儿脐血中最低。妊高征组在中、晚期Ｃ肽和胰岛素水平均高于正常妊娠组（Ｐ＜００１）。妊高征组新生儿体重低于正常妊娠组（Ｐ＜００１）。妊高征组新生儿脐血流Ｓ／Ｄ高于对照组（Ｐ＜００１）。结论：妊高征患者由于胰岛素抵抗,存在着糖代谢异常,可能与妊高征发病有关,并影响胎儿的生长发育。     

糖代谢异常孕妇胰岛素抵抗程度与巨大儿的关系

目的探讨糖代谢异常孕妇中胰岛素抵抗（IR）和胰岛β细胞功能的关系,以及胰岛素抵抗程度与巨大儿发生的关系。方法测定35例妊娠期糖耐量异常孕妇（GIGT）和12例妊娠期糖尿病孕妇（GDM）的空腹血糖、胰岛素,采用稳态模型评估法（HOMA）计算GIGT和GDM的胰岛素抵抗指数（HOMA-IR）和胰岛β细胞功能指数（HBCI）。结果GIGT、GDM两组孕妇HBCI无统计学差异（P〉0.05）,而HOMA-IR差异有统计学意义（P〈0.05）;HOMA-IR与巨大胎儿的发生没有显著相关性。结论GDM较GIGT孕妇存在更为明显的胰岛素抵抗,没有发现胰岛素抵抗指数与巨大儿的发生相关。     

妊娠期糖耐量降低与妊娠结局关系的前瞻性研究

随机对２８９例孕妇作５０ｇ葡萄糖应激试验（５０ｇＧＣＴ），阳性者进一步作７５ｇ葡萄糖耐量试验（７５ｇＧＴＴ），并随访妊娠结局。结果：５０ｇＧＣＴ阳性率为１６．９６％，妊娠期糖耐量降低（ＧＩＧＴ）患病率为５．１９％，妊娠期糖尿病（ＧＤＭ）患病率为１．７３％；ＧＩＧＴ及ＧＤＭ孕妇中，好高征、胎膜早破、巨大儿、手术产、新生儿患病等的发生率明显增加；５０ｇＧＣＴ时孕妇血糖水平与新中儿出生体重呈正相关。提示：妊娠期可发生不同程度的糖耐量降低，并由此导致孕产妇及胎婴儿病率增加；ＧＤＭ的诊断标准应以孕产妇和胎婴儿异常为依据。     

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。     

妊娠期糖耐量异常妇女胰岛功能与胰岛素抵抗的相关研究

目的:研究妊娠期糖耐量异常与胰岛β细胞功能、胰岛素抵抗等的关系。方法:对孕24~36周上海市孕妇共4568例(孕前有糖尿病或糖尿病家族史者排除),先行50g葡萄糖筛查试验,异常者再行75g口服葡萄糖耐量试验(OGTT)-胰岛素释放试验,选取OG-TT异常者318例作为试验组,OGTT正常者中随机选取320例作为对照组,获取各阶段的血糖值及血清胰岛素值,通过计算,用胰岛素敏感指数(ISI)、稳态评估模式、胰岛素储备能力/血糖最大升高值(ΔPI/ΔPG)了解胰岛β细胞功能及外周胰岛素抵抗情况。结果:OGTT异常组的OGTT后1h血清胰岛素(PI1)、胰岛素释放曲线下面积较OGTT正常组显著增高(P<0·05),而胰岛素敏感指数、ΔPI/ΔPG及HOMA-β细胞较OGTT正常组降低(P<0.05)。糖尿病(GDM)组与妊娠期糖耐量减退(GIGT)组相比:GDM组的BMI高于GIGT组,而胰岛素敏感指数、HOMA-β细胞低于GIGT组(P<0.05)。其它指标均无明显差异。结论:妊娠期糖耐量异常形成的主要原因为胰岛素抵抗而非胰岛分泌功能降低。     

Serum levels of 1,5-anhydro-D-glucitol during the normal and diabetic pregnancy and puerperium

In 25 normally non-pregnant women, 543 normally pregnant women and 75 pregnant women with diabetes mellitus or gestational diabetes mellitus, the relationship between the serum concentration of 1,5-anhydro-D-glucitol (1-deoxy-glucose) and carbohydrate metabolism was studied. The concentration of 1,5-anhydro-D-glucitol was estimated by means of gas-liquid chromatography. In normally non-pregnant women the concentration was found to be 18.6 +/- 5.2 mg/l (mean +/- SD). During the normal pregnancy, from 9 weeks of gestation, a steadily decreasing concentration was observed as the pregnancy progressed and the lowest value (10.2 +/- 4.6 mg/l) was found in the third trimester. After 5 days of puerperium the concentrations were found to be 10.8 +/- 3.7 mg/l. On the 30th day postpartum, the level was within the range for non-pregnant subjects. The values in pregnant women with diabetes mellitus and gestational diabetes mellitus were mostly below 10 mg/l throughout the entire pregnant period. The 1,5-anhydro-D-glucitol concentration was not affected by meals or oral glucose loading. A concentration below 10 mg/l was found in 36% of the normally pregnant women, where oral glucose tolerance tests and measurement of glycohemoglobin were shown to be within the normal range. The present study suggests that a change of 1,5-anhydro-D-glucitol level during pregnancy may reflect a mild alteration of carbohydrate metabolism that goes undetected by all the other diabetic indicators.     

Differences in insulin sensitivity in pregnant women with overweight and gestational diabetes mellitus.

AIM: The purpose of the present study was to investigate changes in insulin sensitivity using homeostasis model assessment (HOMA) and the quantitative insulin sensitivity check index (QUICKI) in normal-weight and overweight women with normal glucose tolerance (NGT) and gestational diabetes mellitus (GDM) during pregnancy. METHODS: Ninety-two pregnant women in the first trimester, 202 in the second trimester and 154 in the third trimester were enrolled in this study. Fasting plasma glucose and insulin concentrations were measured in all women in the first, second and third trimesters. HOMA indices (insulin resistance, HOMA-IR and beta-cell function, HOMA-beta) and QUICKI were calculated from fasting glucose and insulin concentrations. RESULTS: HOMA-IR values in overweight women with NGT and in women with GDM were significantly (p < 0.01) higher than those in normal-weight women with NGT. HOMA-IR in women with GDM increased significantly (p < 0.05) during pregnancy, but HOMA-IR values in normal-weight and overweight women with NGT did not change significantly with advance of gestation. QUICKI values in overweight women with NGT and in women with GDM were also significantly (p < 0.01) lower than those in normal-weight women with NGT, and QUICKI in women with GDM decreased significantly (p < 0.05) during pregnancy. HOMA-beta in normal-weight women with NGT increased significantly (p < 0.01) during pregnancy. CONCLUSION: We showed that insulin sensitivities determined by using HOMA-IR and QUICKI in overweight women with NGT and women with GDM were lower than those in normal-weight women with NGT, and that insulin sensitivity in women with GDM declined with advance of gestation.     

糖耐量异常的晚期妊娠妇女胰岛素分泌与胰岛素抵抗的研究

OBJECTIVE: To investigate whether insulin secretion and resistance are different in glucose tolerant and intolerant women with normal pre-pregnant body mass index (BMI) during late pregnancy and to find out if there is association between gestational diabetes and insulin resistance syndrome. METHODS: On the basis of a 4-hour oral glucose tolerance test (OGTT), 32 gestational diabetes mellitus (GDM) patients, 21 gestational impaired glucose tolerant (GIGT) patients, and 50 normal glucose tolerant (NGT) cases were selected from uncomplicated pregnant women. Those had normal pre-pregnant BMI who had a 1-hour 50-g glucose-screening test (> or = 7.2 mmol/L), performed between 24-28 weeks of gestation. During the OGTT, several indexes of insulin resistance, insulin secretion, lipid metabolism were measured in addition to the standard glucose measurements. RESULTS: Glucose area under curve (GAUC), insulin area under curve (IAUC), insulin sensitivity index (ISI) transformed to natural logarithm and triglycerides (TG) are all significantly higher (P < 0.05) in GDM women. The means of these indexes in GDM group are 26.3 mmol/L.h-1, 276.5 mU/L.h-1, 4.2 and 3.2 mmol/L, respeetively. On the other hand, however, the differences of these indexes (except TG) between GIGT and NGT women are not statistically significant. The ratio of IAUC/GAUC has an increasing trend from GDM group, GIGT group to NGT group (10.5, 11.4 and 11.7, respectively), but the difference is not statistically significant. Multiple correlation coefficient study demonstrated that ISI is significantly positively correlated with GAUC, IAUC and TG (P < 0.01). CONCLUSIONS: Compared with NGT women, GDM women has impaired insulin secretion, abnormally increased insulin resistance, and relatively dyslipidemia. GDM seems to be a component of the syndrome of insulin resistance that provides an excellent model for study and prevention in a relatively young aged group.     

Resistin: a hormone which induces insulin resistance is increased in normal pregnancy

AIMS: Resistin, a newly discovered adipokine, is thought to play a key role in the regulation of insulin resistance. The objectives of this study were to develop a nomogram of maternal plasma concentrations of resistin from 11 weeks of gestation to term and to determine whether resistin concentrations differ between normal and overweight pregnant women. METHODS: In this cross-sectional study, plasma concentrations of resistin were determined in normal pregnant women of normal body mass index (BMI 18.5-24.9; n=261), overweight pregnant women (BMI > or =25; n=140), and non-pregnant women of normal BMI (n=40). Blood samples were collected once from each woman between the first trimester and term. Percentiles for resistin concentration were determined for five pre-specified windows of gestational age. Plasma resistin concentration was determined by immunoassay. Non-parametric statistics were used for analysis. RESULTS: The median maternal plasma concentration of resistin between 11 to 14 weeks of gestation in women of normal weight was significantly higher than non-pregnant women; the plasma concentration of resistin increased with gestational age. CONCLUSIONS: Normal pregnant women have a higher median plasma concentration of resistin than non-pregnant women and the concentration of this adipokine increases with advancing gestation. Alterations in the maternal plasma concentration of resistin during pregnancy could contribute to metabolic changes of pregnancy.     

妊娠期糖尿病患者与正常孕妇妊娠中晚期胰岛素抵抗及胰岛B细胞功能观察

目的前瞻性纵向观察中期妊娠诊断为妊娠期糖尿病(GDM)患者及血糖正常孕妇在妊娠中晚期胰岛素抵抗及胰岛B细胞功能变化,并比较两者之间的差别。方法 2009年2月至2010年3月在中山大学孙逸仙纪念医院产前检查的82例孕妇于妊娠20～24周行葡萄糖耐量试验(OGTT)及胰岛素释放试验,诊断为GDM43例为GDM组,血糖正常的39例为对照组。于32～36周复查OGTT及胰岛素释放试验,纵向观察两组孕妇胰岛素抵抗及胰岛B细胞功能的变化。结果两组的胰岛B细胞分泌指数(HOMA-β)晚期妊娠均高于中期妊娠,时间主效应有统计学意义(F=7.863,P=0.007);GDM组的早期胰岛素分泌指数(△I30/△G30)中期妊娠及晚期妊娠均低于对照组,组间主效应差异有统计学意义(F=6.052,P=0.018),但GDM组从中期妊娠到晚期妊娠有所升高,而对照组逐渐下降。GDM组的血糖曲线下面积(AUCG)在中期妊娠及晚期妊娠均大于对照组(分别为P<0.0001,P=0.001),同时对照组的AUCG晚期妊娠显著高于中期妊娠(P=0.001);稳态模式胰岛素抵抗指数(HOMA-IR)及混合胰岛素敏感度的时间及组间主效应差异均无统计学意义。结论中晚期妊娠正常孕妇及GDM患者胰岛素抵抗均增加,后者胰岛素抵抗程度高于前者,胰岛B细胞代偿功能两者均增强;GDM组的早期胰岛素分泌功能较正常妊娠组下降。胰岛素抵抗和胰岛素分泌代偿不足是GDM发生、发展的重要机制。     

Insulin secretion and insulin sensitivity in normal pregnancy and gestational diabetes mellitus.

The purpose of this study was to evaluate insulin sensitivity, beta-cell function and islet-cell-directed autoimmunity in pregnant women with normal glucose tolerance and gestational diabetes mellitus (GDM). A total of 21 women with normal glucose tolerance and 21 women with GDM were evaluated at 24-36 weeks' gestation. Insulin resistance and beta-cell function were evaluated using the continuous infusion of glucose with model assessment (CIGMA) method, which aims to give a near-physiological stimulus and to evaluate the endogenous insulin and glucose response. Islet-cell autoantibody was positive in one woman with GDM, and glutamic acid decarboxylase autoantibodies were negative in both groups. The calculated CIGMA insulin resistance (CIGMA IR) was 2.04 +/- 1.74 and 1.08 +/- 1.22 in patients with GDM and in control subjects, respectively (p < 0.05). CIGMA percentage beta-cell values were 64.04 +/- 44.55% and 87.07 +/- 52.77% in patients with GDM and control subjects, respectively (p > 0.05). Decreased insulin sensitivity in late pregnancy was more evident in lean GDM subjects with mild hyperglycemia who did not require insulin therapy, and beta-cell function was partially preserved in this group of patients.     

Use of oral glucose tolerance test in early pregnancy to predict late-onset gestational diabetes mellitus in high-risk women

AIM: To evaluate if any single plasma glucose level from the four values of the normal 100-g oral glucose tolerance test (OGTT) in early pregnancy (< or =20 weeks of gestation) could predict gestational diabetes mellitus (GDM) diagnosed from a second OGTT in late pregnancy (28-32 weeks). METHODS: Glucose levels of pregnant women at high-risk for GDM, who had had a normal early OGTT, and who underwent the second test in late pregnancy, were studied. Each of the four plasma glucose values of the early OGTT was determined for sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV). The receiver operating characteristic curves of these four OGTT values were then constructed to find the optimal value to predict late-onset GDM. RESULTS: Of 193 pregnant women who had had a normal early OGTT, 154 also had a normal OGTT in late pregnancy while 39 had an abnormal test and were diagnosed with GDM. Among the four glucose values of the early OGTT, the 1-h value yielded the best diagnostic performance to predict late-onset GDM. The sensitivity, specificity, PPV, NPV, and area under the curve achieved from its optimal cutoff level of > or =155 mg/dL (8.6 mmol/L) were 89.7%, 64.3%, 38.9%, 96.1%, and 0.77, respectively. CONCLUSIONS: A 1-h glucose value > or =155 mg/dL at the early OGTT yielded the best diagnostic performance. However, the low specificity and PPV rendered it suboptimal to predict late-onset GDM. Nevertheless, a considerable number of high-risk women could avoid the second OGTT in late pregnancy due to its high sensitivity and NPV.     

Fuel metabolism during pregnancy.

This article reviews carbohydrate and fat metabolism in both healthy pregnant women and women with gestational diabetes. Emphasis is placed on more recent investigations that have utilized stable, nonradioactive isotopes with insulin clamps to study gestational fuel metabolism. In early pregnancy, glucose-stimulated insulin secretion is increased, insulin sensitivity is unchanged or enhanced, and glucose tolerance is normal or slightly improved. Late gestation is characterized by accelerated fetal growth, rising concentrations of several diabetogenic hormones, and increased insulin resistance. The increased resistance reduces maternal glucose utilization, sparing carbohydrates for the rapidly growing fetus. The inhibitory effect of insulin on the rate of lipolysis is also significantly reduced during the third trimester of pregnancy. An earlier than normal switch from carbohydrate to fat utilization serves to promote the use of lipids as a maternal energy source. Women with gestational diabetes have been reported to have either comparable or increased insulin resistance during late gestation with several studies also demonstrating reduced insulin secretory capacity.