Identifying the pregnancy at risk for intrauterine growth retardation: Possible usefulness of the intravenous glucose tolerance test

Sokol, Robert J.; Kazzi, George M.; Kalhan, Satish C.; Pillay, Sasi K.

doi:10.1016/0002-9378(82)90658-5

Cited by 38 publications

(15 citation statements)

References 14 publications

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“…Maternal hypoglycemia did not influence the macrosomia rate in female infants, but it decreased the rate of macrosomia in the male infants. Although gender-specific risk for SGA has not been identified previously, fetal growth restriction was observed in patients with hypoglycemia in previous studies [8][9][10][11][12]. According to most studies, the risk of SGA is significantly higher in neonates born to mothers with low GCT [13,14].…”

Section: Discussionmentioning

confidence: 88%

Maternal hypoglycemia on 50 g glucose challenge test: outcomes are influenced by fetal gender

Topçu

İskender

Çelen

et al. 2016

Journal of Perinatal Medicine

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Section: Discussionmentioning

confidence: 88%

Maternal hypoglycemia on 50 g glucose challenge test: outcomes are influenced by fetal gender

Topçu

İskender

Çelen

et al. 2016

Journal of Perinatal Medicine

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“…However, much less information is available on the interaction between maternal metabolism and FGR. Some authors have reported a link between reduced birth weight and low glucose and insulin levels after glucose load (22,25,37,39). Caruso et al (11) have shown, with the hyperinsulinemic euglycemic clamp, an increase in insulin sensitivity in eight mothers with unexplained FGR newborns.…”

Section: Discussionmentioning

confidence: 98%

“…In addition, it has been observed that, post-glucose load, plasma insulin and glucose levels are lower in women with FGR fetuses than in women with a normal growing fetus (22,25,37,39).…”

mentioning

confidence: 99%

Elevated insulin sensitivity and β-cell function during pregnancy in mothers of growth-restricted newborns

Dalfrà

Pacini

Parretti

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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The "Barker hypothesis" suggests that low birth weight might predict future risk of developing obesity, cardiovascular disease, and type 2 diabetes. Identification of the causes of fetal growth restriction (FGR) is critical for preventive and management strategies. Some studies indicate that maternal carbohydrate metabolism might be involved in FGR development. We aimed to evaluate, in a large number of normotensive pregnant women with normal glucose tolerance, the effect of insulin sensitivity and β-cell function on unexplained fetal growth. A total of 1,814 Caucasian pregnant women with normal prepregnancy body mass index were tested with a 75-g, 2-h glucose load (24-28 gestation wk). Insulin sensitivity was evaluated with fasting (QUICKI) and dynamic index (OGIS) and β-cell function with a modified insulinogenic index as ΔAUC(insulin)/ΔAUC(glucose) and disposition index. FGR was a birth weight below the 5th percentile for gestational age. FGR developed in 99 (5.5%) pregnant women that showed significantly higher QUICKI, OGIS, insulinogenic, and disposition index with respect to women with normal-weight babies (P < 0.0001). By using multiple regression analysis in the FRG group, QUICKI and OGIS appeared as significant independent variables (P < 0.0001 and P < 0.0366, respectively). We conclude that elevated insulin sensitivity seems to be one of the factors involved in determining unexplained fetal growth retardation; its assessment, even only in the fasting state, could be useful to guide any possible monitoring and therapeutic strategies to reduce fetal complications.

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“…A similar difference in glucose levels was not seen when thiamine deficiency [13] or biotin deficiency alone was investigated. Low maternal glucose levels have been associated with small for gestational age infants in animals and in humans [14]. Therefore, the finding that glucose levels were decreased in experimental dams from Group 2 may point to a mechanism whereby poor fetal growth could be explained on the basis of lack of fetal nutrients alone [9].…”

Section: Discussionmentioning

confidence: 97%

Intrauterine growth retardation caused by dietary biotin and thiamine deficiency in the rat

1985

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The effects on fetal development of maternal biotin deficiency, alone and in conjunction with thiamine deficiency, were investigated in rats. Fetuses from dams given biotin-deficient diet throughout gestation demonstrated only some characteristics of intrauterine growth retardation (IUGR) including abnormal liver weight and a higher brain/liver ratio. However, fetuses from dams given biotin-thiamine-deficient diet and daily pyrithiamine (a thiamine antagonist used to insure thiamine deficiency) injections demonstrated severe IUGR along all of the fetal parameters investigated. We conclude that biotin and thiamine deficiency during intrauterine growth of the fetus may be partially responsible for the development of IUGR, a frequent concomitant of fetal alcohol syndrome.

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Identifying the pregnancy at risk for intrauterine growth retardation: Possible usefulness of the intravenous glucose tolerance test

Cited by 38 publications

References 14 publications

Maternal hypoglycemia on 50 g glucose challenge test: outcomes are influenced by fetal gender

Maternal hypoglycemia on 50 g glucose challenge test: outcomes are influenced by fetal gender

Elevated insulin sensitivity and β-cell function during pregnancy in mothers of growth-restricted newborns

Intrauterine growth retardation caused by dietary biotin and thiamine deficiency in the rat

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