The Infant of the Diabetic Mother

Tyrala, Eileen E.

doi:10.1016/s0889-8545(05)70253-9

Cited by 72 publications

(39 citation statements)

References 70 publications

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“…T-CHANNEL AND CARDIOMYOCYTE PROLIFERATION heart diseases, including hypertrophic cardiomyopathy (35), which has been linked to gestational diabetes of the women (36). In this study, we report data supporting the concept that these defects are directly correlated to poor maternal metabolic control.…”

supporting

confidence: 53%

T-Type Ca2+ Channels Are Involved in High Glucose–Induced Rat Neonatal Cardiomyocyte Proliferation

Zhang

Huang

et al. 2005

Pediatr Res

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Infants develop hypertrophic cardiomyopathy in~30% of diabetic pregnancies. We have characterized the effects of glucose on voltage-gated T-type Ca 2ϩ channels and intracellular free calcium concentration, [Ca 2ϩ ] i in neonatal rat cardiomyocytes. We found that T-type Ca 2ϩ channel current density increased significantly in primary culture neonatal cardiac myocytes that were treated with 25 mM glucose for 48 h when compared with those that were treated with 5 mM glucose. Diabetes is one of the most common medical complications seen in pregnancy. Approximately 3-10% of pregnant women have disorders of glucose intolerance (1). This disease affects the fetal cardiovascular system in many ways, both directly and indirectly. The risk for congenital heart disease in infants of diabetic mothers (IDM) is reported to be 5 times higher than in the general population (2). It has been estimated that 30% of IDM have cardiomegaly, only a few of which develop congestive heart failure (1). Diabetic hypertrophic cardiomyopathy has been associated with poor maternal glucose regulation; however, recent studies indicate that cardiac hypertrophy can be attributed to a more complex mechanism possibly including Ca 2ϩ overload (3-5), which may result from an elevated expression of voltage gated Ca 2ϩ channels.Two well-documented voltage gated Ca 2ϩ channels found in fetal and neonatal hearts are the L-type and T-type Ca 2ϩ channels (6 -8). The L-type Ca 2ϩ channels become more abundant as some organisms develop into adulthood (8 -10); however, T-type Ca 2ϩ channels are down-regulated or disappear in adult animals (6,(11)(12)(13)(14). The density of T-type Ca 2ϩ channels is predominant only in pacemaker cells of the sinoatrial node and the Purkinje fibers (15,16). The physiologic role of the T-type Ca 2ϩ channel has been postulated to be involved in the cell cycle during proliferation (17); therefore, we expect to see an increase in T-type Ca 2ϩ channel activity in glucoseinduced neonatal hypertrophic cardiomyopathy secondary to cell proliferation.We hypothesized that T-type calcium currents would be increased in response to high glucose. We found that this indeed was the case and that many of the effects of high glucose were prevented by manipulations that reduced T-type calcium currents. METHODSCell preparation. Neonatal ventricular myocytes were prepared from the hearts of 4-d-old Charles River rats using a previously described protocol Received April 20, 2004; accepted September 3, 2004

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supporting

confidence: 53%

T-Type Ca2+ Channels Are Involved in High Glucose–Induced Rat Neonatal Cardiomyocyte Proliferation

Zhang

Huang

et al. 2005

Pediatr Res

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“…In humans, fetal insulin acts primarily at the level of the adipocyte to stimulate growth. For example, macrosomia associated with fetal hyperinsulinism is largely the result of increased fat body mass [12,23,24]. Thus, it would be predicted that fat cell mass should be impaired in the absence of IRs.…”

Section: Discussionmentioning

confidence: 99%

Lack of insulin receptors affects the formation of white adipose tissue in mice. A morphometric and ultrastructural analysis

et al. 1998

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Insulin receptors (IRs) mediate insulin action upon target cells [1]. Disorders of IR function are a well established, albeit rare, cause of insulin resistance and diabetes mellitus [2±4]. In mice, targeted ablation of IR expression results in lethal diabetic ketoacidosis [5±7]. Unlike children with homozygous nonsense mutations of the IR gene, IR ±/± mice do not develop substantial growth retardation, fasting hypoglycaemia, or signs of hyperandrogenism.The lack of gross growth retardation in IR ±/± mice is an unexpected finding. To understand better the causes of this apparent discrepancy between the human paradigm and the mouse model, we have recently performed genetic crosses of IR ±/± mice with mice lacking insulin-like growth factor-1 (IGF-1) receptors (IGF-1Rs) and . The results of these experiments indicate that IRs do indeed affect embryonic growth. The growth-promoting actions of IRs occur in response to IGF-2, rather than insulin, binding. The interaction between IRs and IGF-2 plays an important role during the last phase of mouse gestation. Based on these data, we have suggested that the lack of a growth-retarded phenotype in IR ±/± mice may be due to the shorter duration of mouse gestation Diabetologia (1998) 41: 171±177

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“…Os resultados obtidos neste trabalho permitem a compreensão dos achados clínicos de Gluck e Kulovich 12 de que os recém-nascidos de mães diabéticas das classes A, B e C de White 4 têm atraso na maturidade pulmonar. A associação dos achados clínicos de maior incidência de SDR nos recém-nascidos de mães diabéticas 17,19 com os resultados deste experimento sugere que pulmões grandes e com baixa concentração de PG e PI sejam a causa da maior incidência desta patologia nesse grupo de recém-nascidos. Os animais com diabete moderado simulam o diabete gestacional humano e o diabete clínico de curta duração, que se associam à macrossomia fetal, à menor produção de surfactante pulmonar e à maior incidência de SDR.…”

Section: Hallman E Teramo 18unclassified

“…A causa desse amadurecimento pulmonar acelerado deve ser a hipoinsulinemia fetal, pois os pâncreas dos fetos com diabete grave têm ilhotas aumentadas de tamanho mas não têm células insulino-positivas, evidenciando falência funcional do pâncreas 15 . Os resultados deste trabalho corroboram a afirmação de Tyrala 19 de que as diabéticas das classes F e R de White 4 têm aceleração da maturidade pulmonar fetal e menor incidência de SDR.…”

Section: Hallman E Teramo 18unclassified

Perfil Fosfolipídico Pulmonar em Recém-nascidos de Ratas Diabéticas

Rudge¹,

Calderon²,

Ramos³

et al. 2001

Rev. Bras. Ginecol. Obstet.

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RESUMO Objetivo: avaliar as repercussões do diabete materno sobre o perfil fosfolipídico pulmonar de fetos de ratas com diabete moderado e grave pelas dosagens de lecitina (L), esfingomielina (E), fosfatidil-glicerol (PG), fosfatidil-inositol (PI) e relações L/E e PG (0,155 g; 6,8 e 6,7 µg/mL), e as mesmas relações L/E (2,2) e PG/PI (2,0); os pulmões dos filhotes das ratas com diabete grave tiveram menor peso (0,145 g), os mesmos valores das relações L/E (1,9) e PG/PI (2,1) e menor valor de PI (5,1 µg/mL) que o grupo controle. Conclusões: 1) o retardo do amadurecimento pulmonar dos recém-nascidos de ratas com diabete moderado é explicado pelo maior peso pulmonar associado à menor concentração de PG e PI. Entretanto, permanece sem explicação o fato de que uma patologia, que se caracteriza por hiperglicemia materna, possa atrasar a maturidade pulmonar nas diabéticas gestacionais e nas clínicas de curta duração, e acelerá-la nas diabé-ticas clínicas com vasculopatia [2][3][4][5][6] . Alguns especulam sobre a influência dos quadros hipertensivos e da vasculopatia como fatores aceleradores da maturidade pulmonar fetal nessas gestantes diabéticas.O perfil fosfolipídico pulmonar, que consiste na determinação da relação lecitina/esfingomielina (L/E) e de fosfatidil-inositol (PI) e fosfatidilglicerol (PG) no líquido amniótico, aumenta a acurácia do diagnóstico de maturidade pulmonar em diabéticas 7 . O surfactante maduro, isto é, o que contém PG, tem melhor propriedade estabilizadora do alvéolo 8 , sendo a sua determinação o método preditivo acurado da maturidade pulmonar fetal.Vários trabalhos experimentais in vivo e in vitro foram feitos para analisar o efeito do diabete sobre a maturidade pulmonar fetal 6 , sendo que os in vivo trazem respostas mais adequadas. Os filhotes de macacas rhesus diabéticas têm menor habilidade em sintetizar, estocar e liberar a lecitina 9 e os de coelhas diabéticas, menor quantidade de surfactante no lavado pulmonar 10 . O pulmão dos fetos de ratas diabéticas tem imatu-

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The Infant of the Diabetic Mother

Cited by 72 publications

References 70 publications

T-Type Ca2+ Channels Are Involved in High Glucose–Induced Rat Neonatal Cardiomyocyte Proliferation

T-Type Ca2+ Channels Are Involved in High Glucose–Induced Rat Neonatal Cardiomyocyte Proliferation

Lack of insulin receptors affects the formation of white adipose tissue in mice. A morphometric and ultrastructural analysis

Perfil Fosfolipídico Pulmonar em Recém-nascidos de Ratas Diabéticas

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