Diabetic Pregnancies: The Challenge of Developing in a Pro-Inflammatory Environment

Jawerbaum, Alicia; González, Eduardo

doi:10.2174/092986706777935302

Cited by 79 publications

(36 citation statements)

References 127 publications

(188 reference statements)

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“…For example, hypertension (62) and inflammation (63), both more frequently associated with T2DM than T1DM (64, 65), are associated with distinct placental pathological abnormalities which may predominate in T2DM relative to T1DM placentas (26). In fact, one study reported that placentas of pregnancies complicated by T2DM had a significant increase in placental infarcts compared to T1DM (15), a vascular abnormality that has also been found in studies of hypertension in pregnancy (66).…”

Section: Discussionmentioning

confidence: 99%

A systematic review of placental pathology in maternal diabetes mellitus

et al. 2015

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During a pregnancy complicated by diabetes, the human placenta undergoes a number of functional and structural pathologic changes, such as increased placental weight and increased incidence of placental lesions including villous maturational defects and fibrinoid necrosis. The pathologic findings reported have differed among studies, potentially reflecting differences in type of diabetes, study methodology, or glycemic control of study participants. Alternatively, these discrepancies may represent different biologic adaptations to distinct metabolic diseases. In order to clarify these distinctions, we conducted a comprehensive review of English language citations in Pubmed and Embase using the keywords “diabetes”, “placenta”, AND “pathology”. Abstracts were reviewed for relevance then full-text articles were reviewed in order to extract a comprehensive summary of current pathological findings associated with pregestational and gestational diabetes mellitus, as well as an understanding of the impact of glycemic control on placental pathology. Placental abnormalities most consistently associated with maternal diabetes are an increased incidence of villous immaturity, increased measures of angiogenesis, and increased placental weight. The literature suggests that, despite similarities in placental abnormalities, differences in placental pathology may reflect differences in pathophysiology among different types of diabetes. Consequently, standardization of terminology used to define placental lesions is warranted. Moreover, further research is needed to investigate the impact of pathophysiology, glycemic control and clinical factors, such as infant sex, weight and race, on placental structure and function.

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Section: Discussionmentioning

confidence: 99%

A systematic review of placental pathology in maternal diabetes mellitus

et al. 2015

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“…This may constitute a relevant function in diabetic pregnancies, in which the loss of PUFAs due to peroxidation is a relevant problem that leads to the loss of many bioactive lipids, including those that activate PPARs ( Jawerbaum & Gonzalez 2006, Negre-Salvayre et al 2010.…”

Section: Discussionmentioning

confidence: 99%

Peroxisome proliferator-activated receptor ligands regulate lipid content, metabolism, and composition in fetal lungs of diabetic rats

Kurtz¹,

Capobianco²,

Careaga³

et al. 2014

Journal of Endocrinology

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Maternal diabetes impairs fetal lung development. Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors relevant in lipid homeostasis and lung development. This study aims to evaluate the effect of in vivo activation of PPARs on lipid homeostasis in fetal lungs of diabetic rats. To this end, we studied lipid concentrations, expression of lipid metabolizing enzymes and fatty acid composition in fetal lungs of control and diabetic rats i) after injections of the fetuses with Leukotriene B 4 (LTB 4 , PPARa ligand) or 15deoxyD 12,14 prostaglandin J 2 (15dPGJ 2 , PPARg ligand) and ii) fed during pregnancy with 6% olive oil-or 6% safflower oil-supplemented diets, enriched with PPAR ligands were studied. Maternal diabetes increased triglyceride concentrations and decreased expression of lipid-oxidizing enzymes in fetal lungs of diabetic rats, an expression further decreased by LTB 4 and partially restored by 15dPGJ 2 in lungs of male fetuses in the diabetic group. In lungs of female fetuses in the diabetic group, maternal diets enriched with olive oil increased triglyceride concentrations and fatty acid synthase expression, while those enriched with safflower oil increased triglyceride concentrations and fatty acid transporter expression. Both olive oil-and safflower oil-supplemented diets decreased cholesterol and cholesteryl ester concentrations and increased the expression of the reverse cholesterol transporter ATP-binding cassette A1 in fetal lungs of female fetuses of diabetic rats. In fetal lungs of control and diabetic rats, the proportion of polyunsaturated fatty acids increased with the maternal diets enriched with olive and safflower oils. Our results revealed important changes in lipid metabolism in fetal lungs of diabetic rats, and in the ability of PPAR ligands to modulate the composition of lipid species relevant in the lung during the perinatal period.

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“…Inflammation is considered one potential risk factor for diabetic pregnancy. In pregnancy, the placenta may be a source of upregulation of these inflammatory cytokines and subsequently their upregulation may result in the development of diabetic pregnancy [10]. …”

Section: Introductionmentioning

confidence: 99%

Trigonelline Inhibits Inflammation and Protects β Cells to Prevent Fetal Growth Restriction during Pregnancy in a Mouse Model of Diabetes

Zhou

Du²,

Zuo³

et al. 2017

Pharmacology

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Background: As an active component from traditional Chinese medicine, trigonelline has a protective effect on diabetes. This study evaluated the protective effects of trigonelline on diabetic mice during pregnancy. Methods: Diabetes was induced in female mice by intraperitoneal injection for continuous 5-day of 40 mg/kg/day streptozotocin. Female mice were divided into 4 groups after they were allowed to mate with normal male mice: nondiabetic, nondiabetic treated with trigonelline (70 mg/kg) for 18 days, diabetic, and diabetic treated with trigonelline (70 mg/kg). Results: Diabetic pregnant mice had significantly higher levels of blood glucose, serum total cholesterol, triglyceride, insulin, and leptin but lower serum omentin-1 level and insulin sensitivity index than the nondiabetic ones. Trigonelline improved the hyperglycemia, dyslipidemia, insulin resistance, and adipocytokine of diabetic pregnant mice. Diabetic pregnant mice had significantly reduced fetus numbers, fetal weight, and fetal/placental ratio, which were reversed by trigonelline. Trigonelline prevented the increase in proinflammatory cytokines and reduced interleukin-10 level in placenta of diabetic pregnant mice. Trigonelline increased β-cell replication and the decreased β-cell mass, and decreased the β-cell apoptosis of diabetic pregnant mice. Conclusion: These findings suggest that trigonelline protects diabetic pregnancy partly by suppressing inflammation, regulating the secretion of adipocytokines, increasing β-cell mass, replication, and decreasing β-cell apoptosis.

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Diabetic Pregnancies: The Challenge of Developing in a Pro-Inflammatory Environment

Cited by 79 publications

References 127 publications

A systematic review of placental pathology in maternal diabetes mellitus

A systematic review of placental pathology in maternal diabetes mellitus

Peroxisome proliferator-activated receptor ligands regulate lipid content, metabolism, and composition in fetal lungs of diabetic rats

Trigonelline Inhibits Inflammation and Protects β Cells to Prevent Fetal Growth Restriction during Pregnancy in a Mouse Model of Diabetes

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