153 EARLY PREGNANCY ADIPONECTIN CONCENTRATIONS ARE ASSOCIATED WITHGESTATIONAL DIABETES KRISTINE LAIN1, PAUL SPEER1, STACY MCGONIGAL1,JAMES ROBERTS1, 1University of Pittsburgh, Obstetrics, Gynecology, andReproductive Sciences, Pittsburgh, Pennsylvania

OBJECTIVE: Adiponectin is the most abundant adipose-specific protein andhas anti-inflammatory, antiatherogenic, and insulin-sensitizing properties. Adi-ponectin is negatively associated with obesity and insulin resistance with plasmaconcentrations lower in individuals with polycystic ovarian syndrome, coronaryartery disease, and type 2 diabetes. We hypothesized that adiponectin concen-trations are lower in women early in pregnancy who later develop gestationaldiabetes (GDM).

STUDY DESIGN: This nested case-control study utilized first-trimester samplesfrom primiparous women enrolled in an ongoing longitudinal study. Adiponec-tin concentrations from women who developed GDM (N = 38) were comparedto those of control patients who did not (N = 30). Adiponectin concentrationswere determined by radioimmunoassay. Baseline demographic descriptors andobstetric outcomes were compared between the two groups by chi-squareanalysis and Student’s t test. Logistic regression was utilized to control forconfounding.

RESULTS: The groups were not different by baseline descriptors or obstetricoutcomes. Mean gestational age of samples was 9.4 G 2.9 and 9.5 G 2.6 weeksfor the control and GDM groups. Mean adiponectin concentrations were lower(P! .001) in the women who developed GDM compared to women who did not(4.3 G 0.3 vs 6.7 G 0.6 mg/mL). Women with adiponectin concentrations!25th% were 11.2 times more likely to develop GDM (95%CI 2.2, 56.9) andthis persisted after controlling for BMI and race (OR 8.2; 95%CI 1.6, 42.9).

CONCLUSION: This data suggests alterations in adipocyte function as early asthe first trimester in women who are later recognized to have GDM. The study islimited by the lack of first trimester glucose tolerance information and does notestablish whether these women were different before pregnancy. However, givenmost women test normal this early in pregnancy, this finding suggests thatwomen with glucose intolerance of pregnancy may have significant alterations inadipocyte homeostasis long before the diagnosis of GDM is made.

154 ESTIMATES OF INSULIN SENSITIVITY USING C-PEPTIDE FROM AN ORAL GLUCOSETOLERANCE TEST (OGTT) TATJANA RADAELLI1, PATRICK CATALANO2, 1Case WesternReserve University at MetroHealth Medical Center, OB/GYN, Cleveland, Ohio,2Case Western Reserve University, Reproductive Biology, Cleveland, Ohio

OBJECTIVE: To determine if C-peptide obtained as part of a 75 g OGTT canbe used to evaluate insulin sensitivity during pregnancy.

STUDY DESIGN: Eighty-one women enrolled in the Hyperglycemia andAdverse Pregnancy Outcome (HAPO) Study were recruited at 27.6 G 1.2 weeks(mean G SD) for a 75 g OGTT. Venous blood samples were drawn for C-peptideat 0 and 60 minutes after the glucose challenge, and glucose and insulin wereobtained at 0, 30, 60, 90 and 120 minutes. The ISOGTT as described by Matsudaand DeFronzo was used to estimate insulin sensitivity based on glucose andinsulin. The ISOGTT has the strongest correlation with insulin sensitivitymeasured by the euglycemic clamp in pregnancy (r = 0.86, P = .0001). Insulinsensitivity was also calculated for these subjects using the ISHOMA and ISQUCKI.These were calculated as follows: ISOGTT = 10,0000/O(FPG)*(FPI)*(G*I),where FGP and FPI are fasting plasma glucose and insulin respectively, whileG and I are mean glucose and mean insulin from 30 to 120 minutes;ISHOMA = (FPG*FPI)/22.5; ISQUICKI = 1/[(FPI) + log(FPG)]. Insulin sensi-tivity was then calculated using glucose and C-peptide concentrations at 0 and 60minutes.

RESULTS: The correlations of the ISQUICKI and ISHOMA with ISOGTT were(r = 0.82) and (r = 0.75), respectively. Using the fasting glucose and C-peptidedata, the correlation of ISQUICKI C-pep and ISHOMA C-pep with ISOGTT were(r = 0.64) and (r = 0.59), respectively. However, the best correlation with theISOGTT was for ISOGTT c-pep (r = 0.80, P = .0001).

CONCLUSION: Using ISOGTT c-pep (glucose and C-peptide at 0 and 60 min), weobtained an excellent correlation with the ISOGTT, comparable to the oneobtained with euglycemic-hyperinsulinemic in pregnancy. These data suggestthat ISOGTT c-pep can be used as a simple alternative to ISOGTT for assessment ofinsulin sensitivity with a 75 g OGTT during pregnancy.

S52 SMFM Abstracts

155 ANTEPARTUM HYPERGLYCEMIA FAILS TO PREDICT GDM OR MACROSOMIAJENNIFER AHN1, JUDITH HIBBARD1, MATTHEW CORCORAN2, 1University ofChicago, Obstetrics & Gynecology, Chicago, Illinois, 2University of Chicago,Medicine, Endocrinology Section, Chicago, Illinois

OBJECTIVE: To show that periods of unrecognized hyperglycemia will predictpatients who will develop Gestational Diabetes (GDM) in high risk patients.

STUDY DESIGN: All new OB patients who presented to our high risk referralcenter were evaluated for risks toward developing GDM. Those patients whodemonstrated one or more of the following risk factors were offered entry intothe study: history of GDM, history of macrosomia, family history of diabetes,prepregnancy body mass index (BMI) >30 kg/m2, or Hispanic race. Thosepatients who had pregestational diabetes or who were diagnosed with diabetesby a first trimester glucose tolerance test were excluded from the study. TheMedtronic Continuous Glucose Monitor (CGMS) was worn for 3-4 days priorto 18 weeks gestation. The subjects were followed for the duration of thepregnancy and evaluated for development of GDM and/or birth of a macrosomicinfant. Hyperglycemia was defined as glucose >120 mg/dL.

RESULTS: Twenty-three patients agreed to participate in the study: 4 patientschanged their mind, 3 patients had sensor failure, and 1 patient was lost tofollow-up. There were 15 patients who completed the study. Approximately 80%of patients experienced epsiodes of hyperglycemia while wearing the monitor.Four patients (27%) spent greater than 25% of the time on the monitor abovethe goal blood sugars, with peak blood sugars exceeding 200 mg/dL in 2 subjects.Despite these periods of unrecognized hyperglycemia, none of the patientsdeveloped GDM, nor did any deliver an infant with macrosomia (mean birthweight 3037 G 595 g).

CONCLUSION: Unrecognized periods of hyperglycemia in a high riskpopulation did not predict development of GDM. Furthermore, hyperglycemiaevidenced in the early half of pregnancy did not predict development ofmacrosomia.

156 RESISTIN: A HORMONE WHICH INDUCES INSULIN RESISTANCE IS INCREASED INNORMAL PREGNANCY JYH KAE NIEN1, RICARDO GOMEZ2, JIMMY ESPINOZA1,LUIS GONCALVES3, JOON-SEOK HONG1, SAMUEL EDWIN1, SONIA HASSAN3,MOSHE MAZOR4, ROBERTO ROMERO1, 1Perinatology Research Branch, NICHD,NIH, DHHS, Bethesda, Maryland, 2CEDIP, Sotero del Rio Hospital, PuenteAlto, Chile, Chile, 3Wayne State University School of Medicine, Department ofObstetrics and Gynecology, Detroit, Michigan, 4Soroka University MedicalCenter, Beer Sheva, Israel, Israel

OBJECTIVE: Normal pregnancy is a state of relative insulin resistance, yet theprecise mechanism responsible for this important metabolic adaptation remainsto be defined. Resistin, a recently discovered hormone (2001), is produced byadipose tissue and confers ‘‘resistance to insulin’’ and hence its name. Theobjective of this study was to determine if the plasma resistin concentration isincreased during pregnancy and to generate a reference range for this hormone.

STUDY DESIGN: A cross-sectional study was conducted in which resistin wasassayed in 261 women with normal gestation and 40 nonpregnant women.Pregnant women were considered normal if they had a negative oral glucosetolerance test, delivered an appropriate for gestational age infant at term, andwere free of obstetrical and medical complications. All women had body massindices !25. Plasma resistin concentrations were determined using specificimmunoassays (ELISA) with a sensitivity of 0.095 ng/mL.

RESULTS: The median plasma concentration of resistin was significantlyhigher in pregnant women in the first trimester than in non-pregnant women[12.8 ng/mL (4.6-81.3) vs 10.4 ng/mL (6.5-11.75)]; P ! .05). The plasmaconcentration of resistin increased with gestational age (rho = 0.22; P ! .01).The Table provides the descriptive statistics of resistin in non-pregnant andnormal pregnant women (ng/mL).

nPercentile10 Median

Percentile90

Non-pregnant 40 6.5 10.2 16.111-14 wk 63 7.3 12.8 25.915-18 wk 68 9.2 14.3 24.327-30 wk 65 8.1 12.8 30.337-42 wk 65 10.9 15.7 28.5

CONCLUSION: Pregnancy is associated with an increase in the plasmaconcentration of resistin. This hormone may play a role in an importantendocrine/metabolic adaptation of pregnancy: relative insulin resistance.