ContextPhysiologic changes of pregnancy include insulin resistance, thrombophilia, immunosuppression, and hypervolemia. These changes may herald the development of disease in later life.ObjectiveTo summarize current evidence on how pregnancy reveals risk of chronic disease.Evidence AcquisitionMEDLINE was searched for articles published between 1990 and 2005 relating pregnancy conditions to the development of chronic disease. Bibliographies and the Web sites of the International Society of Obstetric Medicine and International Society for the Study of Hypertension in Pregnancy were also reviewed.Evidence SynthesisPregnancy exaggerates atherogeniclike responses, including insulin resistance and dyslipidemia, manifesting as preeclampsia or gestational diabetes. These complications herald an increased risk of postpartum cardiovascular disease, with a 2-fold increased risk of coronary artery disease and stroke. Women with gestational diabetes mellitus can progress to type 2 diabetes mellitus. The rate of progression varies from 6% to 92% depending on diagnostic criteria, race/ethnicity, and duration of surveillance (from 6 months to 28 years). Pregnancy increases risk of venous thrombosis by 7- to 10-fold. Heritable thrombophilia is present in at least 15% of Western populations and underlies at least 50% of gestational venous thromboses. Thus, the procoagulant changes during pregnancy can unmask hereditary thrombophilia. An important adaptation leading to immunotolerance of the fetoplacental unit is a switch from helper T-cell (TH) 1 dominance to TH2 dominance. Patients with a TH1-dominant immune disease, such as rheumatoid arthritis or multiple sclerosis, improve during pregnancy. However, rheumatoid arthritis is 5 times more likely to develop after delivery than at any other time. During pregnancy, there is a 50% increase in plasma volume, which can unmask glomerulopathies, peripartum cardiomyopathy, arterial aneurysms, or arteriovenous malformations. Development of intrahepatic cholestasis of pregnancy predicts increased risk of later cholelithiasis.ConclusionsThe physiologic changes of pregnancy can reveal risk of chronic diseases. Exaggerated responses reflective of the metabolic syndrome are seen in preeclampsia and gestational diabetes and can herald future cardiovascular and metabolic disease. Pregnancy is therefore an important screening opportunity for cardiovascular and metabolic disease risk factors, with the possibility of early intervention.

https://jamanetwork.com/journals/jama/articlepdf/201942/jcr50011.pdf

Manifestations of Chronic Disease During Pregnancy

OBJECTIVE — We sought to determine whether a history of gestational diabetes mellitus (GDM) further increases the risk of cardiovascular disease (CVD) in parous women with first-degree relatives with type 2 diabetes. RESEARCH DESIGN AND METHODS — Women with ( n = 332) and without ( n = 663) a history of GDM were compared regarding 1 ) the revised National Cholesterol Education Program Adult Treatment Panel III metabolic syndrome criteria, 2 ) the prevalence of type 2 diabetes, and 3 ) self-reported CVD. RESULTS — Women with prior GDM were younger (48.6 ± 0.7 vs. 52.4 ± 0.6 years [means ± SE]; P P 2 ), women with prior GDM were more likely to have metabolic syndrome (86.6 vs. 73.5%; P P P = 0.005) that occurred at a younger age (45.5 ± 2.2 vs. 52.5 ± 1.9 years; P = 0.02) and was independent of metabolic syndrome (1.74 [1.10–2.76]; P = 0.02) and type 2 diabetes (1.56 [1.002–2.43]; P CONCLUSIONS — Among women with a family history of type 2 diabetes, those with prior GDM were even more likely to not only have CVD risk factors, including metabolic syndrome and type 2 diabetes, but also to have experienced CVD events, which occurred at a younger age. Thus, women with both a family history of type 2 diabetes and personal history of GDM may be especially suitable for early interventions aimed at preventing or reducing their risk of CVD and diabetes.

https://care.diabetesjournals.org/content/diacare/29/9/2078.full.pdf

Gestational Diabetes Mellitus Increases the Risk of Cardiovascular Disease in Women With a Family History of Type 2 Diabetes

Background
The serum level of 25-hydroxyvitamin D deficiency has long been suspected as a risk factor for glucose intolerance and perhaps 1,25-dihydroxyvitamin D has a role in the regulation of insulin secretion. This study investigates the relation between 25-hydroxyvitamin D concentrations and insulin resistance in pregnant women.

Methods
A cross-sectional study was conducted on 741 pregnant women referred to five educating hospital clinics. Universal screening was performed with a GCT-50 g, and those with plasma glucose levels ≥ 7.2 mmol/L were diagnosed as GDM if they had an impaired GTT-100 g based on Carpenter and Coustan criteria. The levels of insulin and C-peptide were measured during OGTT-100 g test. The homeostasis model assessment index (HOMA) equation was used as the insulin resistance index. The concentrations of 25-hydroxyvitamin D, and PTH were also measured.

Results
Total prevalence of vitamin D deficiency (<25 nmol/L) was found in 70.6% of pregnant women. Prevalence of severe vitamin D deficiency (<12.5) in GDM patients was higher than in normoglycaemic pregnancies. The regression model revealed a strong correlation between the HOMA index and serum levels of vitamin D.

Conclusions
These results show that a positive correlation of 25(OH) vitamin D concentrations with insulin sensitivity and vitamin D deficiency could be a confirmative sign of insulin resistance. Copyright © 2007 John Wiley & Sons, Ltd.

Correlation between vitamin D3 deficiency and insulin resistance in pregnancy

Gender-specific care of the patient with diabetes: review and recommendations.

Aims/hypothesis. Insulin resistance as well as marked changes in body weight and energy metabolism are associated with pregnancy. Its impact on plasma leptin is not known and was determined in this longitudinal study in both diabetic and normal pregnancy. Methods. At 28 gestational weeks plasma concentrations of leptin and B-cell hormones were measured at fasting and after an oral glucose load (OGTT:75 g) in women with gestational diabetes and pregnant women with normal glucose tolerance and compared with women who were not pregnant (C). Results. Plasma leptin (ng/ml) was higher (p < 0.001) in women with gestational diabetes (24.9 ± 1.6) than in women with normal glucose tolerance (18.2 ± 1.5) and increased in both groups when compared with the non-pregnant women (8.2 ± 1.3; p < 0.0005). No change in plasma leptin concentrations was induced by OGTT in any group. Basal insulin release was higher (p < 0.05) in women with gestational diabetes compared with the pregnant women with normal glucose tolerance. Marked insulin resistance was confirmed by a 20 % lower (p < 0.05) insulin sensitivity in subgroup analysis and a decrease of almost 40 % in fasting glucose/insulin ratio (p < 0.005) in women with gestational diabetes. Leptin correlated in women with gestational diabetes with basal plasma concentrations of glucose (p < 0.02), insulin (p < 0.004) and proinsulin (p < 0.01) as well as with BMI (p < 0.001) and overall pregnancy induced maternal weight gain (p < 0.009). With normalisation of blood glucose 8 weeks after delivery in women with gestational diabetes their plasma leptin decreased (p < 0.0005) to 17.3 ± 1.9 ng/ml but did not completely normalize (p < 0.05 vs non-pregnant women). Conclusion/interpretation. Our data show that women with gestational diabetes without any change in plasma leptin upon oral glucose loading have increased plasma leptin concentrations during and after pregnancy, a clear association of plasma leptin with the respective concentration of glucose and insulin resistance as well as with changes in body weight, and a failure to normalize spontaneously BMI to the same extent as pregnant women with normal glucose tolerance when compared with matched control subjects. [Diabetologia (2001) 44: 164–172]

/pdf/increased-plasma-leptin-in-gestational-diabetes-3gzqc1q5qu.pdf

Increased plasma leptin in gestational diabetes

OBJECTIVE The significance of gestational diabetes mellitus (GDM) results from its short-term detrimental effects on the fetus and its long-term prediction of NIDDM in the mother. We compared several variables associated with insulin resistance between GDM and non-GDM pregnant women to show the similarities between GDM and NIDDM (and thus insulin resistance). RESEARCH DESIGN AND METHODS On the basis of a 3-h oral glucose tolerance test (OGTT), 52 GDM patients and 127 non-GDM patients were recruited from pregnant, non-diabetic women who had a nonfasting 1-h-50-g glucose screening test ≥ 7.2 mmol/l (130 mg/dl) performed between 16 and 33 weeks of gestation (a total of 518 of 3,041 women drawn from six community health care prenatal clinics were screened positive). During the OGTT, several potential markers of insulin resistance were measured at fasting and 2-h time points, in addition to the standard glucose measurements. The relationship of these variables with the diagnosis of GDM was studied. RESULTS GDM patients, compared with non-GDM patients, had 1) higher prepregnancy weight ( P = 0.011), prepregnancy BMI ( P = 0.006), C-peptide at fasting ( P = 0.002) and at 2 h ( P P = 0.001) and at 2 h ( P P = 0.005) and at 2 h ( P = 0.003), free fatty acids at fasting ( P = 0.017), β-hydroxybutyrate at fasting ( P = 0.007); and 2) lower HDL cholesterol at fasting ( P = 0.029). These variables were all predictive of GDM ( P P = 0.019) and 2-h ( P P = 0.031), and fasting β-hydroxybutyrate ( P = 0.036) were statistically significant as jointly predictive of GDM. Comparisons between GDM patients and non-GDM patients matched by BMI confirmed that the metabolic abnormalities persisted when difference in BMI was taken into account. Concomitant blood pressure measurements in women with GDM did not differ significantly from those without GDM. CONCLUSIONS Our results show that many of the known metabolic components of the syndrome of insulin resistance (syndrome X) are predictive of GDM. These results are in keeping with the argument that GDM is one phase of the syndrome of insulin resistance. We suggest that GDM be looked upon as a component of the syndrome of insulin resistance that provides an excellent model for the study and prevention of NIDDM in a relatively young age-group.

Gestational Diabetes: Should It Be Added to the Syndrome of Insulin Resistance?

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Gestational Diabetes: Should It Be Added to the Syndrome of Insulin Resistance?