Insulin‐Induced Hypoglycemia in Pregnant Diabetics

Stangenberg, Magnus; Persson, Bengt; Stånge, Lars; Carlström, Kjell

doi:10.3109/00016348309155801

Cited by 19 publications

(13 citation statements)

References 24 publications

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“…A decrease in FHR variability was observed as well as an increased frequency of fetal movements accompanied by FHR accelerations [87,88]. In other studies, fetuses tolerated well glucose levels as low as 2.5 mmol/l [56,89].…”

Section: Studies In Humansmentioning

confidence: 80%

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Maternal hypoglycemia during pregnancy in type 1 diabetes: maternal and fetal consequences

Braak

Evers

Erkelens

et al. 2002

Diabetes Metabolism Res

139

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There is strong evidence that the avoidance of hyperglycemia is essential inoptimizing pregnancy outcome in type 1 diabetes. The price to pay is a striking increase in severe hypoglycemia (SH), defined as episodes requiring help from another person. During type 1 diabetic pregnancy, occurrence rates of SH up to 15 times higher as in the intensively treated group of the Diabetes Control and Complications Trial (DCCT) are reported. Blood glucose (BG) treatment targets differ considerably between clinics; some authors advocate lower limits as low as 3.3 mmol/l. Improved glycemic control and/or recurrent hypoglycemia (i.e. BG <3.9 mmol/l) may result in impairment of glucose counterregulatory responses. Also, glucose counterregulation may be altered by pregnancy itself. Short-acting insulin analogs may help reduce hypoglycemia with preservation of good glycemic control, but their use during pregnancy has yet to be proven safe.Several clinical studies did not establish an association between maternal hypoglycemia and diabetic embryopathy. However, animal studies clearly indicate that hypoglycemia is potentially teratogenic during organogenesis. Increased rates of macrosomia continue to be observed despite near normal HbA(1c) levels. This may, at least in part, be the result of rebound hyperglycemia elicited by hypoglycemia. Exposure to hypoglycemia in utero may have long-term effects on offspring including neuropsychological defects. It is yet unclear to what extent the benefits of tight glycemic control balance with the increased risk of (severe) hypoglycemia during type 1 diabetic pregnancy. Efforts must be made to avoid low BG, i.e. <3.9 mmol/l, when tightening glycemic control.

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Section: Studies In Humansmentioning

confidence: 80%

“…Studies on the responses of the fetus during experimentally induced hypoglycemia are inconsistent [56,[87][88][89][90]. A decrease in FHR variability was observed as well as an increased frequency of fetal movements accompanied by FHR accelerations [87,88].…”

Section: Studies In Humansmentioning

confidence: 99%

Maternal hypoglycemia during pregnancy in type 1 diabetes: maternal and fetal consequences

Braak

Evers

Erkelens

et al. 2002

Diabetes Metabolism Res

139

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“…In human pregnancies complicated by maternal diabetes, standard practice involves tight glycemic control to avoid the severe morbidities and mortalities associated with hyperglycemia in utero (55). Implementation of these practices has increased bouts of maternal hypoglycemia, leading to fetal hypoglycemia and hypoinsulinemia (47), which in turn produces changes in fetal heart rate and movement (2,10,28,32,52), as well as increased surfactant in the amniotic fluid (62). The implication of these studies is that fetal AMCs are capable of responding to hypoglycemia with inappropriately timed catecholamine secretion.…”

Section: Discussionmentioning

confidence: 99%

Low glucose sensitivity and polymodal chemosensing in neonatal rat adrenomedullary chromaffin cells

Livermore

Piskuric

Buttigieg

et al. 2011

American Journal of Physiology-Cell Physiology

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Livermore S, Piskuric NA, Buttigieg J, Zhang M, Nurse CA. Low glucose sensitivity and polymodal chemosensing in neonatal rat adrenomedullary chromaffin cells. Am J Physiol Cell Physiol 301: C1104 -C1115, 2011. First published July 20, 2011 doi:10.1152/ajpcell.00170.2011Glucose is the primary metabolic fuel in mammalian fetuses, yet mammals are incapable of endogenous glucose production until several hours after birth. Thus, when the maternal supply of glucose ceases at birth there is a transient hypoglycemia that elicits a counterregulatory surge in circulating catecholamines. Because the innervation of adrenomedullary chromaffin cells (AMCs) is immature at birth, we hypothesized that neonatal AMCs act as direct glucosensors, a property that could complement their previously established roles as hypoxia and acid hypercapnia sensors. During perforated-patch, whole cell recordings, low glucose depolarized and/or excited a subpopulation of neonatal AMCs; in addition, aglycemia (0 mM glucose) caused inhibition of outward K ϩ current, blunted by the simultaneous activation of glibenclamidesensitive K ATP channels. Some cells were excited by each of the three metabolic stimuli, i.e., aglycemia, hypoxia (PO2 ϳ30 mmHg), and isohydric hypercapnia (10% CO2; pH ϭ 7.4). Using carbon fiber amperometry, aglycemia and hypoglycemia (3 mM glucose) induced robust catecholamine secretion that was sensitive to nickel (50 M and 2 mM) and the L-type Ca 2ϩ channel blocker nifedipine (10 M), suggesting involvement of both T-type and L-type voltage-gated Ca 2ϩ channels. Fura-2 measurements of intracellular Ca 2ϩ ([Ca 2ϩ ]i) revealed that ϳ42% of neonatal AMCs responded to aglycemia with a significant rise in [Ca 2ϩ ]i. Approximately 40% of these cells responded to hypoxia, whereas ϳ25% cells responded to both aglycemia and hypoxia. These data suggest that together with hypoxia and acid hypercapnia, low glucose is another important metabolic stimulus that contributes to the vital asphyxia-induced catecholamine surge from AMCs at birth. aglycemia; hypoglycemia; hypoxia; catecholamines; K ϩ current ALTHOUGH GLUCOSE IS THE PRIMARY metabolic fuel in the fetus, glycogenolysis and gluconeogenesis are absent in utero (27). As a result, fetuses are completely dependent on their mothers for the transplacental facilitated diffusion of glucose. During normal birth, this transport ceases, leading to a decrease in blood glucose (hypoglycemia) in the first few hours of life (26,30,39,51,54). In the newborn, hypoglycemia activates a counterregulatory surge in catecholamines and glucagon and a fall in insulin (11). These hormonal changes stabilize blood glucose by initiating glycogenolysis in liver hepatocytes (21,29). Despite this response, over 2% of newborns experience hypoglycemia and require clinical intervention (13), increasing the risk of brain damage (36). Moreover, premature infants, newborns of diabetic mothers, and neonates small-for-gestational age are at increased risk of hypoglycemia, which is one of the primary causes of increased n...

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“…Une bradycardie profonde, une tachycardie, une réduction de la variabilité ou une augmentation des accélérations peuvent être observées [29][30][31][32]. Le retour à l'euglycémie maternelle permet de restaurer la normalité du RCF [30][31][32]. Hyperglycémie (NP4).…”

Section: Conséquences Foetales Des Anomalies De Glycémie Maternelle (unclassified

Surveillance du travail dans les situations à risque

Houfflin‐Debarge

Closset

Deruelle

2008

Journal de Gynécologie Obstétrique et Biologie de la Reproducti

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Insulin‐Induced Hypoglycemia in Pregnant Diabetics

Cited by 19 publications

References 24 publications

Maternal hypoglycemia during pregnancy in type 1 diabetes: maternal and fetal consequences

Maternal hypoglycemia during pregnancy in type 1 diabetes: maternal and fetal consequences

Low glucose sensitivity and polymodal chemosensing in neonatal rat adrenomedullary chromaffin cells

Surveillance du travail dans les situations à risque

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