Circulating adipokines are associated with pre-eclampsia in women with type 1 diabetes
Aims/hypothesis The incidence of pre-eclampsia, a multisystem disorder of pregnancy, is fourfold higher in type 1 diabetic than non-diabetic women; it is also increased in women with features of the metabolic syndrome and insulin resistance. In a prospective study of pregnant women with type 1 diabe...
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| Published in | Diabetologia Vol. 60; no. 12; pp. 2514 - 2524 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.12.2017
Springer Nature B.V |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0012-186X 1432-0428 1432-0428 |
| DOI | 10.1007/s00125-017-4415-z |
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| Abstract | Aims/hypothesis
The incidence of pre-eclampsia, a multisystem disorder of pregnancy, is fourfold higher in type 1 diabetic than non-diabetic women; it is also increased in women with features of the metabolic syndrome and insulin resistance. In a prospective study of pregnant women with type 1 diabetes, we measured plasma levels of adipokines known to be associated with insulin resistance: leptin, fatty acid binding protein 4 (FABP4), adiponectin (total and high molecular weight [HMW]; also known as high molecular mass), retinol binding protein 4 (RBP4) and resistin and evaluated associations with the subsequent development of pre-eclampsia.
Methods
From an established prospective cohort of pregnant type 1 diabetic women, we studied 23 who developed pre-eclampsia and 24 who remained normotensive; for reference values we included 19 healthy non-diabetic normotensive pregnant women. Plasma adipokines were measured (by ELISA) in stored samples from three study visits (Visit 1– Visit 3) at different gestational ages (mean ± SD): Visit 1, 12.4 ± 1.8 weeks; Visit 2, 21.7 ± 1.4 weeks; and Visit 3, 31.4 ± 1.5 weeks. All the women were free of microalbuminuria and hypertension at enrolment. All study visits preceded the clinical onset of pre-eclampsia.
Results
In all groups, leptin, the ratio of leptin to total or HMW adiponectin, FABP4 concentration, ratio of FABP4 to total or HMW adiponectin and resistin level increased, while total and HMW adiponectin decreased, with gestational age. At Visit 1: (1) in diabetic women with vs without subsequent pre-eclampsia, leptin, ratio of leptin to total or HMW adiponectin, and ratio of FABP4 to total or HMW adiponectin, were increased (
p
< 0.05), while total adiponectin was decreased (
p
< 0.05); and (2) in normotensive diabetic vs non-diabetic women, total adiponectin was elevated (
p
< 0.05). At Visits 2 and 3: (1) the primary findings in the two diabetic groups persisted, and FABP4 also increased in women with subsequent pre-eclampsia (
p
< 0.05); and (2) there were no differences between the two normotensive groups. By logistic regression analyses after covariate adjustment (HbA
1c
, insulin kg
−1
day
−1
and gestational age), the best predictive models for pre-eclampsia were as follows: Visit 1, doubling of leptin, OR 9.0 (
p
< 0.01); Visit 2, doubling of the leptin:total adiponectin ratio, OR 3.7 (
p
< 0.05); and Visit 3, doubling of FABP4 concentration, OR 25.1 (
p
< 0.01). The associations were independent of BMI.
Conclusions/interpretation
As early as the first trimester in type 1 diabetic women, adipokine profiles that suggest insulin resistance are associated with subsequent pre-eclampsia, possibly reflecting maternal characteristics that precede pregnancy. These associations persist in the second and third trimesters, and are independent of BMI. Insulin resistance may predispose women with type 1 diabetes to pre-eclampsia. |
|---|---|
| AbstractList | The incidence of pre-eclampsia, a multisystem disorder of pregnancy, is fourfold higher in type 1 diabetic than non-diabetic women; it is also increased in women with features of the metabolic syndrome and insulin resistance. In a prospective study of pregnant women with type 1 diabetes, we measured plasma levels of adipokines known to be associated with insulin resistance: leptin, fatty acid binding protein 4 (FABP4), adiponectin (total and high molecular weight [HMW]; also known as high molecular mass), retinol binding protein 4 (RBP4) and resistin and evaluated associations with the subsequent development of pre-eclampsia. From an established prospective cohort of pregnant type 1 diabetic women, we studied 23 who developed pre-eclampsia and 24 who remained normotensive; for reference values we included 19 healthy non-diabetic normotensive pregnant women. Plasma adipokines were measured (by ELISA) in stored samples from three study visits (Visit 1– Visit 3) at different gestational ages (mean ± SD): Visit 1, 12.4 ± 1.8 weeks; Visit 2, 21.7 ± 1.4 weeks; and Visit 3, 31.4 ± 1.5 weeks. All the women were free of microalbuminuria and hypertension at enrolment. All study visits preceded the clinical onset of pre-eclampsia. In all groups, leptin, the ratio of leptin to total or HMW adiponectin, FABP4 concentration, ratio of FABP4 to total or HMW adiponectin and resistin level increased, while total and HMW adiponectin decreased, with gestational age. At Visit 1: (1) in diabetic women with vs without subsequent pre-eclampsia, leptin, ratio of leptin to total or HMW adiponectin, and ratio of FABP4 to total or HMW adiponectin, were increased (p < 0.05), while total adiponectin was decreased (p < 0.05); and (2) in normotensive diabetic vs non-diabetic women, total adiponectin was elevated (p < 0.05). At Visits 2 and 3: (1) the primary findings in the two diabetic groups persisted, and FABP4 also increased in women with subsequent pre-eclampsia (p < 0.05); and (2) there were no differences between the two normotensive groups. By logistic regression analyses after covariate adjustment (HbA1c, insulin kg−1 day−1 and gestational age), the best predictive models for pre-eclampsia were as follows: Visit 1, doubling of leptin, OR 9.0 (p < 0.01); Visit 2, doubling of the leptin:total adiponectin ratio, OR 3.7 (p < 0.05); and Visit 3, doubling of FABP4 concentration, OR 25.1 (p < 0.01). The associations were independent of BMI. As early as the first trimester in type 1 diabetic women, adipokine profiles that suggest insulin resistance are associated with subsequent pre-eclampsia, possibly reflecting maternal characteristics that precede pregnancy. These associations persist in the second and third trimesters, and are independent of BMI. Insulin resistance may predispose women with type 1 diabetes to pre-eclampsia. Aims/hypothesis The incidence of pre-eclampsia, a multisystem disorder of pregnancy, is fourfold higher in type 1 diabetic than non-diabetic women; it is also increased in women with features of the metabolic syndrome and insulin resistance. In a prospective study of pregnant women with type 1 diabetes, we measured plasma levels of adipokines known to be associated with insulin resistance: leptin, fatty acid binding protein 4 (FABP4), adiponectin (total and high molecular weight [HMW]; also known as high molecular mass), retinol binding protein 4 (RBP4) and resistin and evaluated associations with the subsequent development of pre-eclampsia. Methods From an established prospective cohort of pregnant type 1 diabetic women, we studied 23 who developed pre-eclampsia and 24 who remained normotensive; for reference values we included 19 healthy non-diabetic normotensive pregnant women. Plasma adipokines were measured (by ELISA) in stored samples from three study visits (Visit 1– Visit 3) at different gestational ages (mean ± SD): Visit 1, 12.4 ± 1.8 weeks; Visit 2, 21.7 ± 1.4 weeks; and Visit 3, 31.4 ± 1.5 weeks. All the women were free of microalbuminuria and hypertension at enrolment. All study visits preceded the clinical onset of pre-eclampsia. Results In all groups, leptin, the ratio of leptin to total or HMW adiponectin, FABP4 concentration, ratio of FABP4 to total or HMW adiponectin and resistin level increased, while total and HMW adiponectin decreased, with gestational age. At Visit 1: (1) in diabetic women with vs without subsequent pre-eclampsia, leptin, ratio of leptin to total or HMW adiponectin, and ratio of FABP4 to total or HMW adiponectin, were increased ( p < 0.05), while total adiponectin was decreased ( p < 0.05); and (2) in normotensive diabetic vs non-diabetic women, total adiponectin was elevated ( p < 0.05). At Visits 2 and 3: (1) the primary findings in the two diabetic groups persisted, and FABP4 also increased in women with subsequent pre-eclampsia ( p < 0.05); and (2) there were no differences between the two normotensive groups. By logistic regression analyses after covariate adjustment (HbA 1c , insulin kg −1 day −1 and gestational age), the best predictive models for pre-eclampsia were as follows: Visit 1, doubling of leptin, OR 9.0 ( p < 0.01); Visit 2, doubling of the leptin:total adiponectin ratio, OR 3.7 ( p < 0.05); and Visit 3, doubling of FABP4 concentration, OR 25.1 ( p < 0.01). The associations were independent of BMI. Conclusions/interpretation As early as the first trimester in type 1 diabetic women, adipokine profiles that suggest insulin resistance are associated with subsequent pre-eclampsia, possibly reflecting maternal characteristics that precede pregnancy. These associations persist in the second and third trimesters, and are independent of BMI. Insulin resistance may predispose women with type 1 diabetes to pre-eclampsia. The incidence of pre-eclampsia, a multisystem disorder of pregnancy, is fourfold higher in type 1 diabetic than non-diabetic women; it is also increased in women with features of the metabolic syndrome and insulin resistance. In a prospective study of pregnant women with type 1 diabetes, we measured plasma levels of adipokines known to be associated with insulin resistance: leptin, fatty acid binding protein 4 (FABP4), adiponectin (total and high molecular weight [HMW]; also known as high molecular mass), retinol binding protein 4 (RBP4) and resistin and evaluated associations with the subsequent development of pre-eclampsia.AIMS/HYPOTHESISThe incidence of pre-eclampsia, a multisystem disorder of pregnancy, is fourfold higher in type 1 diabetic than non-diabetic women; it is also increased in women with features of the metabolic syndrome and insulin resistance. In a prospective study of pregnant women with type 1 diabetes, we measured plasma levels of adipokines known to be associated with insulin resistance: leptin, fatty acid binding protein 4 (FABP4), adiponectin (total and high molecular weight [HMW]; also known as high molecular mass), retinol binding protein 4 (RBP4) and resistin and evaluated associations with the subsequent development of pre-eclampsia.From an established prospective cohort of pregnant type 1 diabetic women, we studied 23 who developed pre-eclampsia and 24 who remained normotensive; for reference values we included 19 healthy non-diabetic normotensive pregnant women. Plasma adipokines were measured (by ELISA) in stored samples from three study visits (Visit 1- Visit 3) at different gestational ages (mean ± SD): Visit 1, 12.4 ± 1.8 weeks; Visit 2, 21.7 ± 1.4 weeks; and Visit 3, 31.4 ± 1.5 weeks. All the women were free of microalbuminuria and hypertension at enrolment. All study visits preceded the clinical onset of pre-eclampsia.METHODSFrom an established prospective cohort of pregnant type 1 diabetic women, we studied 23 who developed pre-eclampsia and 24 who remained normotensive; for reference values we included 19 healthy non-diabetic normotensive pregnant women. Plasma adipokines were measured (by ELISA) in stored samples from three study visits (Visit 1- Visit 3) at different gestational ages (mean ± SD): Visit 1, 12.4 ± 1.8 weeks; Visit 2, 21.7 ± 1.4 weeks; and Visit 3, 31.4 ± 1.5 weeks. All the women were free of microalbuminuria and hypertension at enrolment. All study visits preceded the clinical onset of pre-eclampsia.In all groups, leptin, the ratio of leptin to total or HMW adiponectin, FABP4 concentration, ratio of FABP4 to total or HMW adiponectin and resistin level increased, while total and HMW adiponectin decreased, with gestational age. At Visit 1: (1) in diabetic women with vs without subsequent pre-eclampsia, leptin, ratio of leptin to total or HMW adiponectin, and ratio of FABP4 to total or HMW adiponectin, were increased (p < 0.05), while total adiponectin was decreased (p < 0.05); and (2) in normotensive diabetic vs non-diabetic women, total adiponectin was elevated (p < 0.05). At Visits 2 and 3: (1) the primary findings in the two diabetic groups persisted, and FABP4 also increased in women with subsequent pre-eclampsia (p < 0.05); and (2) there were no differences between the two normotensive groups. By logistic regression analyses after covariate adjustment (HbA1c, insulin kg-1 day-1 and gestational age), the best predictive models for pre-eclampsia were as follows: Visit 1, doubling of leptin, OR 9.0 (p < 0.01); Visit 2, doubling of the leptin:total adiponectin ratio, OR 3.7 (p < 0.05); and Visit 3, doubling of FABP4 concentration, OR 25.1 (p < 0.01). The associations were independent of BMI.RESULTSIn all groups, leptin, the ratio of leptin to total or HMW adiponectin, FABP4 concentration, ratio of FABP4 to total or HMW adiponectin and resistin level increased, while total and HMW adiponectin decreased, with gestational age. At Visit 1: (1) in diabetic women with vs without subsequent pre-eclampsia, leptin, ratio of leptin to total or HMW adiponectin, and ratio of FABP4 to total or HMW adiponectin, were increased (p < 0.05), while total adiponectin was decreased (p < 0.05); and (2) in normotensive diabetic vs non-diabetic women, total adiponectin was elevated (p < 0.05). At Visits 2 and 3: (1) the primary findings in the two diabetic groups persisted, and FABP4 also increased in women with subsequent pre-eclampsia (p < 0.05); and (2) there were no differences between the two normotensive groups. By logistic regression analyses after covariate adjustment (HbA1c, insulin kg-1 day-1 and gestational age), the best predictive models for pre-eclampsia were as follows: Visit 1, doubling of leptin, OR 9.0 (p < 0.01); Visit 2, doubling of the leptin:total adiponectin ratio, OR 3.7 (p < 0.05); and Visit 3, doubling of FABP4 concentration, OR 25.1 (p < 0.01). The associations were independent of BMI.As early as the first trimester in type 1 diabetic women, adipokine profiles that suggest insulin resistance are associated with subsequent pre-eclampsia, possibly reflecting maternal characteristics that precede pregnancy. These associations persist in the second and third trimesters, and are independent of BMI. Insulin resistance may predispose women with type 1 diabetes to pre-eclampsia.CONCLUSIONS/INTERPRETATIONAs early as the first trimester in type 1 diabetic women, adipokine profiles that suggest insulin resistance are associated with subsequent pre-eclampsia, possibly reflecting maternal characteristics that precede pregnancy. These associations persist in the second and third trimesters, and are independent of BMI. Insulin resistance may predispose women with type 1 diabetes to pre-eclampsia. The incidence of pre-eclampsia, a multisystem disorder of pregnancy, is fourfold higher in type 1 diabetic than non-diabetic women; it is also increased in women with features of the metabolic syndrome and insulin resistance. In a prospective study of pregnant women with type 1 diabetes, we measured plasma levels of adipokines known to be associated with insulin resistance: leptin, fatty acid binding protein 4 (FABP4), adiponectin (total and high molecular weight [HMW]; also known as high molecular mass), retinol binding protein 4 (RBP4) and resistin and evaluated associations with the subsequent development of pre-eclampsia. From an established prospective cohort of pregnant type 1 diabetic women, we studied 23 who developed pre-eclampsia and 24 who remained normotensive; for reference values we included 19 healthy non-diabetic normotensive pregnant women. Plasma adipokines were measured (by ELISA) in stored samples from three study visits (Visit 1- Visit 3) at different gestational ages (mean ± SD): Visit 1, 12.4 ± 1.8 weeks; Visit 2, 21.7 ± 1.4 weeks; and Visit 3, 31.4 ± 1.5 weeks. All the women were free of microalbuminuria and hypertension at enrolment. All study visits preceded the clinical onset of pre-eclampsia. In all groups, leptin, the ratio of leptin to total or HMW adiponectin, FABP4 concentration, ratio of FABP4 to total or HMW adiponectin and resistin level increased, while total and HMW adiponectin decreased, with gestational age. At Visit 1: (1) in diabetic women with vs without subsequent pre-eclampsia, leptin, ratio of leptin to total or HMW adiponectin, and ratio of FABP4 to total or HMW adiponectin, were increased (p < 0.05), while total adiponectin was decreased (p < 0.05); and (2) in normotensive diabetic vs non-diabetic women, total adiponectin was elevated (p < 0.05). At Visits 2 and 3: (1) the primary findings in the two diabetic groups persisted, and FABP4 also increased in women with subsequent pre-eclampsia (p < 0.05); and (2) there were no differences between the two normotensive groups. By logistic regression analyses after covariate adjustment (HbA , insulin kg day and gestational age), the best predictive models for pre-eclampsia were as follows: Visit 1, doubling of leptin, OR 9.0 (p < 0.01); Visit 2, doubling of the leptin:total adiponectin ratio, OR 3.7 (p < 0.05); and Visit 3, doubling of FABP4 concentration, OR 25.1 (p < 0.01). The associations were independent of BMI. As early as the first trimester in type 1 diabetic women, adipokine profiles that suggest insulin resistance are associated with subsequent pre-eclampsia, possibly reflecting maternal characteristics that precede pregnancy. These associations persist in the second and third trimesters, and are independent of BMI. Insulin resistance may predispose women with type 1 diabetes to pre-eclampsia. |
| Author | Aston, Christopher E. Kelly, Clare B. Du, Mei Hanssen, Kristian F. Patterson, Christopher C. Hookham, Michelle B. Nankervis, Alison Jenkins, Alicia J. Garg, Satish K. Scardo, James A. Lyons, Timothy J. Yu, Jeremy Y. Lockhart, Samuel M. Henriksen, Tore Hammad, Samar M. |
| AuthorAffiliation | 11 Spartanburg Regional Hospital, Spartanburg, SC USA 7 Department of Endocrinology, Oslo University Hospital, Oslo, Norway 10 Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC, USA 3 The Department of Clinical Biochemistry, Royal Victoria Hospital, Belfast, Northern Ireland, UK 13 Centre for Public Health, Queen’s University Belfast, Belfast, Northern Ireland, UK 4 Section of Endocrinology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA 5 University of Sydney, NHMRC Clinical Trials Centre, Camperdown, Sydney, NSW, Australia 6 Royal Women’s Hospital, Melbourne, VIC, Australia 12 Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA 8 Institute of Clinical Medicine, University of Oslo, Oslo, Norway 2 Division of Endocrinology and Diabetes, CSB Suite 822, Medical University of South Carolina, Charleston, SC 29425, USA 1 Centre for Experimental Medicine, Queen’s University Belfas |
| AuthorAffiliation_xml | – name: 6 Royal Women’s Hospital, Melbourne, VIC, Australia – name: 5 University of Sydney, NHMRC Clinical Trials Centre, Camperdown, Sydney, NSW, Australia – name: 12 Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA – name: 1 Centre for Experimental Medicine, Queen’s University Belfast, Belfast, Northern Ireland, UK – name: 8 Institute of Clinical Medicine, University of Oslo, Oslo, Norway – name: 4 Section of Endocrinology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA – name: 11 Spartanburg Regional Hospital, Spartanburg, SC USA – name: 7 Department of Endocrinology, Oslo University Hospital, Oslo, Norway – name: 13 Centre for Public Health, Queen’s University Belfast, Belfast, Northern Ireland, UK – name: 9 Barbara Davis Center for Childhood Diabetes, University of Colorado, Denver, CO, USA – name: 2 Division of Endocrinology and Diabetes, CSB Suite 822, Medical University of South Carolina, Charleston, SC 29425, USA – name: 10 Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC, USA – name: 3 The Department of Clinical Biochemistry, Royal Victoria Hospital, Belfast, Northern Ireland, UK |
| Author_xml | – sequence: 1 givenname: Clare B. surname: Kelly fullname: Kelly, Clare B. organization: Centre for Experimental Medicine, Queen’s University Belfast, Division of Endocrinology and Diabetes, CSB Suite 822, Medical University of South Carolina – sequence: 2 givenname: Michelle B. surname: Hookham fullname: Hookham, Michelle B. organization: Centre for Experimental Medicine, Queen’s University Belfast, The Department of Clinical Biochemistry, Royal Victoria Hospital – sequence: 3 givenname: Jeremy Y. surname: Yu fullname: Yu, Jeremy Y. organization: Centre for Experimental Medicine, Queen’s University Belfast, Division of Endocrinology and Diabetes, CSB Suite 822, Medical University of South Carolina – sequence: 4 givenname: Samuel M. surname: Lockhart fullname: Lockhart, Samuel M. organization: Centre for Experimental Medicine, Queen’s University Belfast – sequence: 5 givenname: Mei surname: Du fullname: Du, Mei organization: Section of Endocrinology, University of Oklahoma Health Sciences Center – sequence: 6 givenname: Alicia J. surname: Jenkins fullname: Jenkins, Alicia J. organization: Division of Endocrinology and Diabetes, CSB Suite 822, Medical University of South Carolina, University of Sydney, NHMRC Clinical Trials Centre – sequence: 7 givenname: Alison surname: Nankervis fullname: Nankervis, Alison organization: Royal Women’s Hospital – sequence: 8 givenname: Kristian F. surname: Hanssen fullname: Hanssen, Kristian F. organization: Department of Endocrinology, Oslo University Hospital, Institute of Clinical Medicine, University of Oslo – sequence: 9 givenname: Tore surname: Henriksen fullname: Henriksen, Tore organization: Institute of Clinical Medicine, University of Oslo – sequence: 10 givenname: Satish K. surname: Garg fullname: Garg, Satish K. organization: Barbara Davis Center for Childhood Diabetes, University of Colorado – sequence: 11 givenname: Samar M. surname: Hammad fullname: Hammad, Samar M. organization: Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina – sequence: 12 givenname: James A. surname: Scardo fullname: Scardo, James A. organization: Spartanburg Regional Hospital – sequence: 13 givenname: Christopher E. surname: Aston fullname: Aston, Christopher E. organization: Department of Pediatrics, University of Oklahoma Health Sciences Center – sequence: 14 givenname: Christopher C. surname: Patterson fullname: Patterson, Christopher C. organization: Centre for Public Health, Queen’s University Belfast – sequence: 15 givenname: Timothy J. surname: Lyons fullname: Lyons, Timothy J. email: lyonstj@musc.edu organization: Centre for Experimental Medicine, Queen’s University Belfast, Division of Endocrinology and Diabetes, CSB Suite 822, Medical University of South Carolina |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28875223$$D View this record in MEDLINE/PubMed |
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| Copyright | Springer-Verlag GmbH Germany 2017 Diabetologia is a copyright of Springer, 2017. |
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| Issue | 12 |
| Keywords | Pregnancy Fatty acid binding protein Leptin Adipokine Diabetes Pre-eclampsia Adiponectin |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Contribution statement CBK, MBH, JYY, SML, MD, AJJ, AN, KFH, TH, SKG, SMH, JAS, CEA, CCP and TJL all made significant contributions to the study concept, design and acquisition of data. CBK, CEA, CCP and TJL undertook the statistical analysis of the data, and all authors engaged in its interpretation. CBK and TJL drafted the manuscript and all authors participated critically in its revision. All authors approved the final version to be published, and agree to be accountable for all aspects of the work. |
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| PublicationDate | 2017-12-01 |
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| PublicationPlace | Berlin/Heidelberg |
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| PublicationSubtitle | Clinical, Translational and Experimental Diabetes and Metabolism |
| PublicationTitle | Diabetologia |
| PublicationTitleAbbrev | Diabetologia |
| PublicationTitleAlternate | Diabetologia |
| PublicationYear | 2017 |
| Publisher | Springer Berlin Heidelberg Springer Nature B.V |
| Publisher_xml | – name: Springer Berlin Heidelberg – name: Springer Nature B.V |
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The incidence of pre-eclampsia, a multisystem disorder of pregnancy, is fourfold higher in type 1 diabetic than non-diabetic women; it is also... The incidence of pre-eclampsia, a multisystem disorder of pregnancy, is fourfold higher in type 1 diabetic than non-diabetic women; it is also increased in... |
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| SubjectTerms | Adipokines - blood Adipokines - metabolism Adiponectin Adiponectin - blood Adiponectin - metabolism Adult Diabetes Diabetes mellitus Diabetes Mellitus, Type 1 - blood Diabetes Mellitus, Type 1 - metabolism Enzyme-linked immunosorbent assay Fatty acid-binding protein Fatty Acid-Binding Proteins - blood Fatty Acid-Binding Proteins - metabolism Female Gestational age Health risk assessment Human Physiology Humans Insulin Insulin resistance Internal Medicine Leptin Leptin - blood Leptin - metabolism Medicine Medicine & Public Health Metabolic Diseases Metabolic syndrome Molecular weight Plasma levels Pre-eclampsia Pre-Eclampsia - blood Pre-Eclampsia - metabolism Preeclampsia Pregnancy Prospective Studies Resistin - blood Resistin - metabolism Retinol-Binding Proteins, Plasma - metabolism Vitamin A Womens health Young Adult |
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| Title | Circulating adipokines are associated with pre-eclampsia in women with type 1 diabetes |
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