Consequences of gestational diabetes to the brain and behavior of the offspring

Sousa, Ricardo Augusto Leoni De; Torres, Yasmin S; Figueiredo, Cláudia P.; Passos, Giselle F.; Clarke, Julia R.

doi:10.1590/0001-3765201720170264

Cited by 28 publications

(15 citation statements)

References 93 publications

(48 reference statements)

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“…GDM increases perinatal morbidity and increases the risk of developing type 2 diabetes mellitus later in life [4][5][6]. Moreover, children born to mothers with poor gestational glucose control suffer neurobehavioral and cognitive dysfunction compared to children born to non-diabetic women [7,8]. Docosahexaenoic acid (DHA, 22:6 n − 3) is a long-chain polyunsaturated fatty acid that is essential for neurogenesis and brain development during the early stages of fetal life [9,10].…”

Section: Introductionmentioning

confidence: 99%

Elevated Glucose and Insulin Levels Decrease DHA Transfer across Human Trophoblasts via SIRT1-Dependent Mechanism

et al. 2020

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Gestational diabetes mellitus (GDM) results in reduced docosahexaenoic acid (DHA) transfer to the fetus, likely due to placental dysfunction. Sirtuin-1 (SIRT1) is a nutrient sensor and regulator of lipid metabolism. This study investigated whether the high glucose and insulin condition of GDM regulates DHA transfer and expression of fatty acid transporters and if this effect is related to SIRT1 expression and function. Syncytialized primary human trophoblasts were treated with and without glucose (25 mmol/L) and insulin (10−7 mol/L) for 72 h to mimic the insulin-resistance conditions of GDM pregnancies. In control conditions, DHA transfer across trophoblasts increased in a time- and dose-dependent manner. Exposure to GDM conditions significantly decreased DHA transfer, but increased triglyceride accumulation and fatty acid transporter expression (CD36, FABP3, and FABP4). GDM conditions significantly suppressed SIRT1 mRNA and protein expression. The SIRT1 inhibitor decreased DHA transfer across control trophoblasts, and recombinant SIRT1 and SIRT1 activators restored the decreased DHA transport induced by GDM conditions. The results demonstrate a novel role of SIRT1 in the regulation of DHA transfer across trophoblasts. The suppressed SIRT1 expression and the resultant decrease in placental DHA transfer caused by high glucose and insulin levels suggest new insights of molecular mechanisms linking GDM to fetal DHA deficiency.

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Section: Introductionmentioning

confidence: 99%

Elevated Glucose and Insulin Levels Decrease DHA Transfer across Human Trophoblasts via SIRT1-Dependent Mechanism

et al. 2020

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“…Fetuses and infants of mothers with PGDM and GDM have high rates of complications, including perinatal mortality, macrosomia, and hypoglycemia, as well as hypertension and diabetes later in life, compared to controls (Berger et al, 2016;Colstrup, Mathiesen, Damm, Jensen, & Ringholm, 2013;Group et al, 2008;Macintosh et al, 2006;Monteiro, Norman, Rice, & Illanes, 2016;Pinney & Simmons, 2012;Veeraswamy, Vijayam, Gupta, & Kapur, 2012). Potential effects on the developing nervous system may differ between pre-gestational and gestational diabetes, as may the causative pathways, which are multiple and complex (Badehnoosh et al, 2018;Schaefer-Graf et al, 2018;Sousa, Torres, Figueiredo, Passos, & Clarke, 2018). Maternal diabetes may exert "toxic" teratogenic effects during embryonic development mediated by metabolic, epigenetic and inflammatory mechanisms (Badehnoosh et al, 2018;Schaefer-Graf et al, 2018;Sousa et al, 2018).…”

Section: Diabetes In Pregnancymentioning

confidence: 99%

“…Potential effects on the developing nervous system may differ between pre-gestational and gestational diabetes, as may the causative pathways, which are multiple and complex (Badehnoosh et al, 2018;Schaefer-Graf et al, 2018;Sousa, Torres, Figueiredo, Passos, & Clarke, 2018). Maternal diabetes may exert "toxic" teratogenic effects during embryonic development mediated by metabolic, epigenetic and inflammatory mechanisms (Badehnoosh et al, 2018;Schaefer-Graf et al, 2018;Sousa et al, 2018). The resulting developmental anomalies include neural tube defects and anencephaly (Ornoy, Reece, Pavlinkova, Kappen, & Miller, 2015).…”

Section: Diabetes In Pregnancymentioning

confidence: 99%

Exposures influencing the developing central autonomic nervous system

Schlatterer

Plessis

2020

Birth Defects Research

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Autonomic nervous system function is critical for transition from in-utero to ex-utero life and is associated with neurodevelopmental and neuropsychiatric outcomes later in life. Adverse prenatal and neonatal conditions and exposures can impair or alter ANS development and, as a result, may also impact longterm neurodevelopmental outcomes. The objective of this article is to provide a broad overview of the impact of factors that are known to influence autonomic development during the fetal and early neonatal period, including maternal mood and stress during and after pregnancy, fetal growth restriction, congenital heart disease, toxic exposures, and preterm birth. We touch briefly on the typical development of the ANS, then delve into both in-utero and exutero maternal and fetal factors that may impact developmental trajectory of the ANS and, thus, have implications in transition and in long-term developmental outcomes. While many types of exposures and conditions have been shown to impact development of the autonomic nervous system, there is still much to be learned about the mechanisms underlying these influences. In the future, more advanced neuromonitoring tools will be required to better understand autonomic development and its influence on long-term neurodevelopmental and neuropsychological function, especially during the fetal period.

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“…Gestational diabetes mellitus (GDM) is defined as a form of insulin resistance that usually occurs from the middle to the end of pregnancy in previously normoglycemic females (Sousa, Torres, Figueiredo, Passos, & Clarke, ). GDM‐induced adverse intrauterine environment has been reported to cause many complex diseases and dysfunctions in foetus not only during prenatal and lactational period but also later in life (Ahmed, ).…”

Section: Introductionmentioning

confidence: 99%

Effect of gestational diabetes mellitus on testis and pancreatic tissues of male offspring

et al. 2018

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The purpose of this study was to determine the effect of gestational diabetes mellitus (GDM) on some reproductive characteristics, testicular and pancreatic oxidative status and pancreatic endocrine receptor densities of male offspring at post-pubertal stage. A total of 36 1-day-old Wistar Albino male offspring including 12 pups of nontreated mothers (control group), 14 pups of 40 mg/kg STZ-injected mothers (STZ-40 group) and 10 pups of 60 mg/kg STZ-injected mothers (STZ-60 group) were used. The offspring were euthanised on post-natal day 60, their blood, reproductive organs and pancreatic tissues were obtained and examined. When compared with the control group, there was a significant decrease in body and absolute reproductive organ weights, serum testosterone level, testicular and pancreatic catalase activities, pancreatic glutathione level, epididymal sperm concentration of both STZ-40 and STZ-60 groups as well as in testicular glutathione level of only STZ-60 group. Significant increases were determined in testicular and pancreatic malondialdehyde level and glutathione peroxidase activity in both groups and in fasting serum glucose of only STZ-60 group in comparison with the control group. Although some histopathological damages were observed in testes of both STZ-40 and STZ-60 groups, there were no detectable differences between the groups in density of insulin, glucagon and somatostatin receptors in pancreas. In conclusion, GDM has negative effects on reproductive efficiency and testicular-pancreatic tissue oxidant/antioxidant balance of male offspring at post-pubertal stage.

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Consequences of gestational diabetes to the brain and behavior of the offspring

Cited by 28 publications

References 93 publications

Elevated Glucose and Insulin Levels Decrease DHA Transfer across Human Trophoblasts via SIRT1-Dependent Mechanism

Elevated Glucose and Insulin Levels Decrease DHA Transfer across Human Trophoblasts via SIRT1-Dependent Mechanism

Exposures influencing the developing central autonomic nervous system

Effect of gestational diabetes mellitus on testis and pancreatic tissues of male offspring

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