Long-term effects of diabetes during pregnancy on the offspring

Wróblewska-Seniuk, Katarzyna; Wender-Ożegowska, Ewa; Szczapa, Jerzy

doi:10.1111/j.1399-5448.2009.00507.x

Cited by 50 publications

(49 citation statements)

References 38 publications

(64 reference statements)

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“…The consequences of an adverse intrauterine and neonatal environment for adult health have been broadly studied from various viewpoints (25)(26)(27). In this study, we show that impaired nutrient supply during perinatal growth induces adaptive changes in different tissues, leading to metabolic disorders when the organism is challenged to increased caloric intake.…”

Section: Discussionmentioning

confidence: 80%

Predominant Role of GIP in the Development of a Metabolic Syndrome-like Phenotype in Female Wistar Rats Submitted to Forced Catch-up Growth

et al. 2014

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Catch-up growth has been associated with the appearance of metabolic dysfunctions such as obesity and type 2 diabetes in adulthood. Because the entero-insular axis is critical to glucose homeostasis control, we explored the relevance of the incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) in the development of these pathologies. Offspring of rat dams fed ad libitum (control [C]) or 65% food-restricted during pregnancy and suckling time (undernourished [U]) were weaned onto a high-fat (HF) diet (CHF and UHF, respectively) to drive catch-up growth. Both male and female UHF rats showed an obese phenotype characterized by hyperphagy, visceral fat accumulation, and adipocyte hypertrophy. High-fat diet induced deterioration of glucose tolerance in a sex-dependent manner. Female UHF rats experienced much more severe glucose intolerance than males, which was not compensated by insulin hypersecretion, suggesting insulin resistance, as shown by homeostatic model assessment of insulin resistance values. Moreover, female, but not male, UHF rats displayed enhanced GIP but not GLP-1 secretion during oral glucose tolerance test. Administration of the GIP receptor antagonist (Pro3)GIP to UHF female rats over 21 days markedly reduced visceral fat mass and adipocyte hypertrophy without variations in food intake or body weight. These changes were accompanied by improvement of glucose tolerance and insulin sensitivity. In conclusion, the exacerbated production and secretion of GIP after the catch-up growth seems to represent the stimulus for insulin hypersecretion and insulin resistance, ultimately resulting in derangement of glucose homeostasis. Overall, these data evidence the role of GIP as a critical link between catch-up growth and the development of metabolic disturbances. (Endocrinology 155: 3769 -3780, 2014)

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Section: Discussionmentioning

confidence: 80%

Predominant Role of GIP in the Development of a Metabolic Syndrome-like Phenotype in Female Wistar Rats Submitted to Forced Catch-up Growth

et al. 2014

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“…Macrososmic infants are also at increase risk for obesity in adulthood (30% overweight in adolescence), glucose intolerance and type 2 diabetes (Bellamy et al 2009;Wroblewska-Seniuk et al 2009). It should be noted that the GDM mothers are also at risk of developing another GDM during subsequent pregnancies with a probability of 30 to 84% (Kim et al 2007;Reece et al 2009).…”

Section: Introductionmentioning

confidence: 99%

“…Gestational diabetes mellitus (GDM) is a state of glucose intolerance which disappears shortly after delivery (Torloni et al 2009), but might cause some complications to mother and, the newborn babies are born with an increased incidence of neonatal obesity, i.e., macrosomia (Wroblewska-Seniuk et al 2009). Macrosomic babies have increased rates of birth trauma, shoulder dystocia, respiratory distress syndrome and cesarean delivery (Galtier et al 2008;Yogev and Catalano 2009).…”

Section: Introductionmentioning

confidence: 99%

Placental infiltration of inflammatory markers in gestational diabetic women

Mrizak¹,

Grissa²,

Henault³

et al. 2014

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Abstract. Gestational diabetes mellitus (GDM) is pathology of glucose intolerance during pregnancy. It is influenced by maternal hyperglycemia and insulinemia through placental circulation. The study was undertaken to investigate the implication of pro-inflammatory factors in the placenta of GDM women. Thirty GDM women have delivered macrosomic babies, and 30 healthy age-matched pregnant women have delivered non macrosomic babies, were recruited in the study. The mRNAs encoding for IL-6, TLR4, TGF-β, CD68, CD14, EMR-1, CCL2, TCR-α, T-bet, GATA-3, leptin and adiponectin were quantified in placental samples by using RT-qPCR. The mRNA expression of the pro-inflammatory factors, i.e., IL-6, TLR4 and TGF-β, was increased in GDM placenta. The mRNA expression of markers of infiltration of macrophage, i.e., CD68, CD14 and EMR-1, was higher in the GDM placenta than the control placenta. The expression of mRNA of TCR-α, an indicator of T-cell infiltration, was significantly higher in the GDM placenta. Interestingly, the expression of mRNA of GATA-3, an indicator of Th2 phenotype differentiation, was unregulated in the GDM placenta. Leptin and adiponectin mRNAs were also significantly increased in the placenta of the GDM group. Our results revealed that there is an increase of inflammation in the GDM placenta which might be involved, in part, in the pathogenesis of macrosomia.

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“…For example, children born to mothers with gestational diabetes are at higher risk of obesity and other metabolic disturbances. 5 In addition, children of diabetic mothers have an increased predisposition to obesity and type 2 diabetes. 6 Fetal exposure to a hyperglycemic environment alters embryonic transcriptional program affecting normal development.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Prevents Impairment in Activation of Retinoic Acid Receptors and MAP Kinases in the Embryos of a Rodent Model of Diabetic Embryopathy

et al. 2012

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Diabetes induces impairments in gene expression during embryonic development that leads to premature and improper tissue specialization. Retinoic acid receptors (RARs and retinoid X receptor [RXRs]) and mitogen-activated protein kinases (MAPKs) play crucial roles during embryonic development, and their suppression or activation has been shown as a determinant of the fate of embryonic organogenesis. We studied the activation of RARs and MAPKs in embryonic day 12 (E12) in embryos of rats under normal, diabetic, and diabetic treated with resveratrol ([RSV]; 100 mg/kg body weight) conditions. We found downregulation of RARs and RXRs expressions as well as their DNA-binding activities in the embryos exhibiting developmental delays due to diabetes. Furthermore, the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 was decreased and phosphorylation of c-Jun N-terminal kinase (JNK) 1/2 and p38 was increased. Interestingly, embryos of diabetic rats treated with RSV showed normalized patterns of RARs, RXRs, neuronal markers, and ERK, JNK and p38 phosphorylation.

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Long-term effects of diabetes during pregnancy on the offspring

Abstract: Children born to mothers with gestational diabetes seem to be at risk for obesity and metabolic disturbances.

Cited by 50 publications

References 38 publications

Predominant Role of GIP in the Development of a Metabolic Syndrome-like Phenotype in Female Wistar Rats Submitted to Forced Catch-up Growth

Predominant Role of GIP in the Development of a Metabolic Syndrome-like Phenotype in Female Wistar Rats Submitted to Forced Catch-up Growth

Placental infiltration of inflammatory markers in gestational diabetic women

Resveratrol Prevents Impairment in Activation of Retinoic Acid Receptors and MAP Kinases in the Embryos of a Rodent Model of Diabetic Embryopathy

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