Search PubMed⌕ Search

Biomedical subjects

H Laivuori

Publications and source records attributed to H Laivuori.

12 recordsLinked to original sources
PubMed2006

Relationships between maternal plasma leptin, placental leptin mRNA and protein in normal pregnancy, pre-eclampsia and intrauterine growth restriction without pre-eclampsia.

Leptin, an adipocyte hormone involved in energy homeostasis, is important in reproduction and pregnancy. Questions yet to be addressed include the source of higher leptin during pregnancy and its relationship to pregnancy outcome and fetal growth. The objective of this study was to investigate the relationship between placental leptin gene expression, placental leptin protein concentration and maternal plasma leptin concentration among control pregnant women, women with pre-eclampsia and women with growth-restricted infants. We also investigated the relationship between placental leptin expression and the placental expression of enzymes involved in cellular lipid balance: fatty acid translocase (CD36), carnitine palmitoyltransferase I (CPT-1B) and lipoprotein lipase (LPL). Placental leptin expression, placental protein and maternal plasma concentration were higher in pre-eclampsia than in controls but not in women with growth-restricted infants. Placental leptin expression and placental protein were higher in the preterm pre-eclamptic subjects, whereas maternal leptin was higher in the term pre-eclamptic subjects. The placental gene expression of CD36, CPT-1B and LPL were not different among the groups. This study suggests that despite similar failed placental bed vascular remodelling in pre-eclampsia and intrauterine growth restriction (IUGR), leptin gene expression is higher only in preterm pre-eclampsia.

Adult↗
PubMed2001

Elevation of both maternal and fetal extracellular circulating deoxyribonucleic acid concentrations in the plasma of pregnant women with preeclampsia.

OBJECTIVE: Elevated amounts of circulating fetal deoxyribonucleic acid in maternal plasma have recently been detected in pregnancies complicated by preeclampsia. We attempted to confirm this finding and simultaneously examined the quantity of maternal circulating deoxyribonucleic acid. STUDY DESIGN: Circulating deoxyribonucleic acid was measured by realtime quantitative polymerase chain reaction in plasma samples obtained from 44 women with preeclampsia and a matched cohort of 53 normotensive pregnant women. RESULTS: We confirmed that circulating fetal deoxyribonucleic acid levels were significantly elevated in pregnancies complicated by preeclampsia (3194.6 vs 332.8 copies/mL; P < .001). We also showed for the first time that circulating maternal deoxyribonucleic acid levels are also elevated (219,023.9 vs 20,235.8 copies/mL; P < .001). The increases in these deoxyribonucleic acid levels corresponded to the severity of the disorder, and values were correlated with each other in pregnancies complicated by preeclampsia (r = 0.556; P < .001) but not normotensive pregnancies (r = 0.046; P = .747). CONCLUSION: The releases of both free fetal and maternal deoxyribonucleic acid were found to be affected in preeclampsia.

Birth Weight↗
PubMed2001

Comparison between 1 year oral and transdermal oestradiol and sequential norethisterone acetate on circulating concentrations of leptin in postmenopausal women.

BACKGROUND: Oral and transdermal postmenopausal hormone replacement therapy (HRT) affects lipid and glucose metabolism differently, which is of significance in the release of leptin by adipocytes. Moreover, oestrogen and progesterone can stimulate leptin secretion in women of reproductive age. Therefore, we compared the effects of oral and transdermal oestrogen plus progestin regimen on plasma leptin in 38 healthy postmenopausal women with normal body mass index (BMI), who wished to use HRT to control incapacitating climacteric symptoms. METHODS: The women were randomized to treatment with oral HRT (2 mg oestradiol on days 1--12, 2 mg oestradiol plus 1 mg norethisterone acetate (NETA) on days 13--22, and 1 mg oestradiol on days 23--28, n = 19), or with transdermal HRT (50 microg/day of oestradiol on days 1--13, and 50 microg oestradiol plus 250 microg/day NETA on days 14--28, n = 19) for 1 year. Plasma samples were collected before and at oestradiol + NETA phase after 2, 6 and 12 months treatment and were assayed for leptin. RESULTS: The baseline leptin, ranging from 3.3 to 34.9 microg/l, was significantly associated with BMI (r = 0.78, P < 0.0001 ), but showed no difference between women in oral HRT (geometric mean 13.9 microg/l, 95% confidence interval (CI) 10.1--17.6 microg/l) or transdermal HRT group (geometric mean 12.0 microg/l, 95% CI 9.7--14.3 microg/l). Neither oral nor transdermal oestradiol + NETA caused any significant changes in plasma leptin (or BMI) after 2, 6, or 12 months of treatment. CONCLUSION: Leptin is an unsuitable factor to detect oestradiol + NETA-induced metabolic changes in postmenopausal women.

Administration, Cutaneous↗
PubMed2000

Leptin during and after preeclamptic or normal pregnancy: its relation to serum insulin and insulin sensitivity.

Hyperleptinemia may be part of the insulin resistance syndrome. We studied serum leptin in preeclampsia, which is an insulin-resistant state, and sought associations between leptin and insulin or insulin sensitivity during and after pregnancy. Twenty-two proteinuric preeclamptic women and 16 normotensive controls were studied during the third trimester. Leptin was higher in preeclampsia (mean +/- SE, 34.6 +/- 3.9 v 20.0 +/- 3.3 microg/L, P = .002) and correlated directly with the level of proteinuria (r = .47, P = .03) and normal pregnancy (r = .52, P = .04), whereas insulin sensitivity as assessed by an intravenous glucose tolerance test showed no relationship to leptin. Leptin was 19.0 +/- 3.6 microg/L in 14 preeclamptic women and 10.1 +/- 2.0 microg/L (P = .11) in 11 controls 3 months after delivery. Leptin correlated directly with insulin both in preeclamptic puerperal women (r = .63, P = .02) and in controls (r = .81, P = .003). Leptin and insulin sensitivity correlated only in preeclamptic puerperal women (r = -.59, P = .02). In conclusion, (1) serum leptin is elevated in preeclampsia, (2) insulin is an important determinant of serum leptin in preeclamptic and normotensive women both during pregnancy and in the puerperium, and (3) hyperleptinemia may be part of the insulin resistance syndrome also in women with prior preeclampsia.

Adult↗
PubMed2000

677 C-->T polymorphism of the methylenetetrahydrofolate reductase gene and preeclampsia.

OBJECTIVE: To evaluate C to T substitution at nucleotide 677 of N(5), N(10)-methylenetetrahydrofolate reductase gene in women with prior preeclamptic or normotensive pregnancies. METHODS: Methylenetetrahydrofolate reductase genotypes were determined in 113 Finnish women with preeclamptic first pregnancies and 103 controls with one or more normotensive pregnancies, using polymerase chain reaction and restriction enzyme analysis. Preeclampsia was defined as severe in 100 women who fulfilled one or more of the subsequent criteria: systolic blood pressure (BP) at least 160 mmHg, diastolic BP at least 110 mmHg, or proteinuria at least 2 g per 24-hour urine collection. RESULTS: There were no significant differences in prevalences of the methylenetetrahydrofolate reductase genotypes (CC, CT, and TT) between groups (57%, 40%, and 3% in the preeclamptic group and 54%, 39%, and 7%, respectively, in controls). The frequency of the T677 allele was 0.23 in the preeclamptic group and 0.26 in the control group (difference 0.03; 95% confidence interval -0.08, 0.14; P =.51). Our sample had 60% power to detect a difference of the allele frequencies similar to that (0.12) reported previously. The result was similar when analysis was restricted to patients with severe preeclampsia (T677 allele frequency 0.22). CONCLUSION: A carrier status for the T677 allele of the methylenetetrahydrofolate reductase gene does not predispose to preeclampsia, at least in the Finnish population.

Adult↗
PubMed1999

Evidence of a state of increased insulin resistance in preeclampsia.

Similarities in certain biochemical variables between preeclampsia and the insulin resistance syndrome imply a possible link between insulin resistance and preeclampsia. We measured insulin sensitivity by the minimal model technique between 29 and 39 weeks of gestation in 22 preeclamptic and 16 control women, whose glucose tolerance was first confirmed as normal by an oral glucose tolerance test. In addition, we measured the fasting levels of serum C-peptide, uric acid, lipids, and lipoproteins. Preeclamptic women showed a higher insulin response (P = .001) during the oral glucose tolerance test than the controls. Insulin sensitivity in preeclamptic women (1.11+/-0.15 x 10(-4) x min(-1) x microU/mL) was 37% lower (P = .009) than in control women (1.77+/-0.19 x 10(-4) x min(-1) x microU/mL). The free fatty acid (FFA) concentration in preeclamptic women (0.17+/-0.01 g/L, P = .0004) was 70% higher than in control women (0.10+/-0.01 g/L). Also, baseline serum levels of C-peptide, uric acid, and triglyceride were higher in preeclamptic women. Insulin sensitivity increased fourfold to fivefold within the first 3 postpartum months, but insulin sensitivity in preeclamptic women was still 26% lower (P = .04) than in control women. Preeclampsia is a state of increased insulin resistance, and it persists for at least 3 months after pregnancy. This may be a pathogenetic factor in preeclampsia and may contribute to the excess cardiovascular morbidity among women with prior preeclampsia.

Adult↗
PubMed1999

Plasma homocysteine levels elevated and inversely related to insulin sensitivity in preeclampsia.

OBJECTIVE: To study the plasma levels of homocysteine in preeclampsia and relate them to insulin sensitivity. METHODS: In association with a 3-hour intravenous glucose-tolerance test (glucose 0.3 g/kg at 0 and 0.03 IU insulin 20 minutes later), we measured plasma levels of homocysteine, vitamin B12, and folic acid in 22 women with preeclampsia and 16 controls between 29 and 39 weeks' gestation. In 14 women with preeclampsia and 11 controls, plasma samples also were collected 3 months after delivery. RESULTS: Levels of homocysteine in women with preeclampsia (6.7 +/- 0.4 micromol/L, mean +/- standard error) were higher (P < .001) than those in controls (3.8 +/- 0.2 micromol/L) and related significantly to the level of proteinuria (r = .49, P = .02). Vitamin B12 concentrations were lower in women with preeclampsia (166.0 +/- 10.4 compared with 212.4 +/- 16.4 pmol/L, P = .02), whereas levels of folic acid showed no difference between the groups. After delivery, levels of homocysteine increased to 9.1 +/- 0.6 and 8.2 +/- 0.6 micromol/L in women with preeclampsia and controls, vitamin B12 increased to 298.8 +/- 28.6 compared with 334.9 +/- 24.0 pmol/l, and folic acid decreased to 10.6 +/- 2.0 compared with 7.9 +/- 0.8 nmol/L, with no difference emerging between the groups. In women with preeclampsia but not in controls, plasma homocysteine was negatively related to insulin sensitivity (r = -.51, P = .02). The mean 2.9-fold increase in glucose or 52.5-fold increase in insulin during the insulin-sensitivity test failed to affect homocysteine levels. CONCLUSION: Women with preeclampsia have high plasma homocysteine levels that are inversely related to insulin sensitivity.

Adult↗
PubMed1999

Serum activin A and inhibin A elevated in pre-eclampsia: no relation to insulin sensitivity.

OBJECTIVE: To assess the possible role of serum levels of activin A, inhibin A and pro-alpha inhibin (pro-alphaC) in insulin sensitivity in pre-eclampsia. DESIGN: A prospective study. SETTING: Helsinki University Central Hospital. PARTICIPANTS: Twenty-two nulliparous women with proteinuric pre-eclampsia and 16 healthy nulliparous controls in the third trimester of pregnancy. METHODS: Serum samples were collected before and after intravenous injection of glucose (0.3 g/kg) and insulin (0.03 IU/kg) (the minimal model for testing insulin sensitivity), and were assayed for activin A, inhibin A and pro-alphaC. MAIN OUTCOME MEASURES: Comparison of the levels of activin A, inhibin A and pro-alphaC between pre-eclamptic and healthy pregnant women, and the association of these proteins with insulin sensitivity. RESULTS: In pre-eclampsia elevated levels of activin A (139%, P = 0.0001), inhibin A (39%, P = 0.003), and pro-alphaC (92%, P = 0.0008) were observed. The amount of proteinuria (0.3-10.5 g/day) correlated positively with serum concentrations of activin A (P = 0.01) and inhibin A (P = 0.02). These glycoproteins were not associated with insulin sensitivity either in women with pre-eclampsia or controls. A 2.9-fold rise in blood glucose and a 52.5-fold rise in insulin during testing using the minimal model were not accompanied by any significant changes in activin A, inhibin A, and pro-alphaC. CONCLUSION: Activin A, inhibin A, and pro-alphaC are elevated in pre-eclampsia but do not appear to relate to the insulin sensitivity in pre-eclamptic or normal pregnancies.

Activins↗
PubMed1998

Evidence of high circulating testosterone in women with prior preeclampsia.

Women with prior preeclampsia are characterized by hyperinsulinemia and a 2- to 3-fold excess risk of hypertension and ischemic heart disease in later life. We therefore studied whether these women present changes in pituitary, ovarian, and endothelial factors that could also affect the risk of vascular disorders. Twenty-two women with prior preeclampsia and 22 control women matched by age and body mass index were studied an average of 17 yr after delivery. Women with prior preeclampsia had elevated serum free testosterone levels (20.6 +/- 2.2 vs. 15.0 +/- 1.3 pmol/L, mean +/- SE, P = 0.03), an elevated free androgen index (3.2 +/- 0.5 vs. 1.9 +/- 0.2, P = 0.04), and an elevated free testosterone estradiol ratio (0.089 +/- 0.017 vs. 0.046 +/- 0.006, P = 0.02). The levels of insulin-like growth factor binding protein-1 decreased as expected during a 3-h oral glucose tolerance test without differences between the groups. Levels of FSH, LH, androstenedione, dehydroepiandrosterone sulfate, and endothelin-1, as well as urinary output of prostacyclin and thromboxane A2 metabolites, showed no difference between study groups. A history of preeclampsia an average of 17 yr earlier thus appears to be associated with elevated levels of testosterone, which may contribute to the increased risk of vascular morbidity in such women.

Adult↗
PubMed1996

Hyperinsulinemia 17 years after preeclamptic first pregnancy.

Insulin resistance syndrome predisposes to occlusive vascular disorders in nonpregnant subjects. Because preeclampsia, representing a pregnancy-specific occlusive vascular disorder, is known to be accompanied by metabolic changes similar to those in insulin resistance syndrome, we compared carbohydrate and lipid metabolism in 22 women who had a preeclamptic first pregnancy and in 22 control women who had normotensive first pregnancy, both, on the average, 17.0 +/- 0.7 yr earlier. The study groups were comparable in regard to body mass index at the follow-up study. Women with prior preeclampsia were normoglycemic (baseline, 3 h oral glucose tolerance), but showed a significant hyperinsulinemia, as seen from elevated immunoreactive insulin (IRI) levels at the baseline (mean +/- SE, 7.3 +/- 0.6 vs. 5.5 +/- 0.5 mU/L; P < 0.03), after 1 h (45.7 +/- 5.5 vs. 35.6 +/- 3.5 mU/L; P = 0.13), after 2 h (32.4 +/- 4.1 vs. 23.8 +/- 2.3 mU/L; P = 0.08), and after 3 h (10.1 +/- 1.4 vs. 6.4 +/- 0.6 mU/L; P = 0.02). The area under the IRI curve was larger in the women with prior preeclampsia (86.8 +/- 9.1 vs. 65.4 +/- 5.2 mU/h.L; P = 0.05). The serum levels of total cholesterol, high density lipoprotein (HDL) cholesterol (with its subfractions HDL2 and HDL3), low density lipoprotein cholesterol, triglyceride, or uric acid did not differ significantly between the study groups. In women with prior preeclamsia, the area under the IRI curve was negatively related to HDL2 cholesterol, but positively related to triglyceride and systolic blood pressure. We conclude that a history of preeclampsia is associated with mild hyperinsulinemia in nonpregnant women.

Adult↗
PubMed1993

Dietary supplementation with primrose oil or fish oil does not change urinary excretion of prostacyclin and thromboxane metabolites in pre-eclamptic women.

To study whether balance between antiaggregatory, vasodilatory prostacyclin (PGI2) and proaggregatory, vasoconstrictory thromboxane A2 (TXA2) could be affected by dietary manipulation, 18 pre-eclamptic women were treated in randomized order between 31 and 36 weeks of gestation either with primrose oil (n = 7), with fish oil (n = 5), or with placebo (n = 6). Urinary excretions of the degradation products of PGI2 (6-keto-PGF1 alpha, 2,3-dinor-6-keto-PGF1 alpha) and TXA2 (TXB2, 2,3-dinor-TXB2) were measured in 24 h urines before and serially during the supplementation. Fatty acid supplementation did not affect urinary prostanoid excretions or clinical signs of pre-eclampsia.

Epoprostenol↗