Gene/Protein
Disease
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Drug
Enzyme
Compound
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Gene/Protein
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Target Concepts:
Gene/Protein
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Query: EC:4.1.1.49 (
phosphoenolpyruvate carboxykinase
)
4,654
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The activity of enzymes with a regulatory function in the pathways of glycolysis, glyconeogenesis and NADP-generation, and the tissue content of DNA, protein, glycogen, triglycerides (TG), phospholipids (PL), cholesterol and dry matter were investigated in placentas from deliveries accompanied by fetal distress as a result of umbilical cord compression or placental dysfunction in toxemic pregnancies. In placentas from cases of fetal distress due to umbilical cord compression, there was increased activity of pyruvate kinase, 6-phosphogluconate dehydrogenase and NADP-malate dehydrogenase, and decreased activity of
phosphoenolpyruvate carboxylase
. The activity of aspartate aminotransferase was unchanged, and that of glucose-6-phosphate dehydrogenase was slightly elevated. The tissue content of dry matter, DNA, TG and PL was increased, whereas the protein, cholesterol and glycogen concentrations remained unaltered. In placentas from deliveries accompanied by fetal distress due to placental dysfunction, pyruvate kinase, when calculated per mg protein, was the only enzyme with decreased activity. TG, PL, glycogen and dry matter content were increased, DNA concentration was decreased, and protein and cholesterol remained unchanged. It is suggested that the divergent placental metabolic patterns found in the two fetal distress groups are related to the different levels of disturbed oxygen passage along the
uterus
-placenta-fetus axis.
...
PMID:The placenta in intrauterine fetal deprivation. II. Biochemical profile of placentas from deliveries associated with fetal distress. 735 17
To characterize long-term actions and interactions of growth hormone (GH) and insulin-like growth factor-II (IGF-II) on postnatal body and organ growth, hemizygous
phosphoenolpyruvate carboxykinase
(
PEPCK
)-human IGF-II transgenic mice were crossed with hemizygous
PEPCK
-bovine GH transgenic mice. The latter are characterized by two-fold increased serum levels of IGF-I and exhibit markedly increased body, skeletal and organ growth. Four different genetic groups were obtained: mice harbouring the IGF-II transgene (I), the bGH transgene (B), or both transgenes (IB), and non-transgenic controls (C). These groups of mice have previously been studied for circulating IGF-I levels (Wolf et al., 1995a), whereas the present study deals with body and organ growth. Growth curves (week 3 to 12) were estimated by regression with linear and quadratic components of age on body weight and exhibited significantly (p < 0.001) greater linear coefficients in B and IB than in I and C mice. The linear coefficients of male I and C mice were significantly (p < 0.001) greater than those of their female counterparts, whereas this sex-related difference was absent in the bGH transgenic groups. The weights of internal organs as well as the weights of abdominal fat, skin and carcass were recorded from 3.5- to 8-month-old mice. In addition, organ weight-to-body weight-ratios (relative organ weights) were calculated. Except for the weight of abdominal fat, absolute organ weights were as a rule significantly greater in B and IB than in I and C mice. IGF-II overproduction as a tendency increased the weights of kidneys, adrenal glands, pancreas and
uterus
both in the absence and presence of the bGH transgene. Analysis of relative organ weights demonstrated significant (p < 0.05) effects of elevated IGF-II on the relative growth of kidneys (males and females) and adrenal glands (females), confirming our previous report on organ growth of
PEPCK
-IGF-II transgenic mice. In females, IGF-II and GH overproduction were additive in stimulating the growth of spleen and
uterus
, providing evidence for tissue-specific postnatal growth promoting effects by IGF-II in the presence of elevated IGF-I.
...
PMID:Actions and interactions of growth hormone and insulin-like growth factor-II: body and organ growth of transgenic mice. 916 69