Author
Marjorie K. Jeacock
Bio: Marjorie K. Jeacock is an academic researcher from Imperial College London. The author has contributed to research in topics: Carbohydrate metabolism & Pyruvate carboxylase. The author has an hindex of 7, co-authored 10 publications receiving 114 citations.
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TL;DR: Acid and alkaline phosphatase activity was estimated in extracts of the whole placenta in order to determine if the activities of these enzymes differed from normal in placentae associated with toxaemia of pregnancy, intrauterine death, and other abnormal conditions.
25 citations
TL;DR: The results show that placental, glycogen is not the sole source of the lactic acid produced during incubation or of the excess lactate released under the influence of epinephrine and they provide evidence that the human placenta has its own specific metabolic pattern and isNot the biochemical equivalent of the liver.
17 citations
16 citations
TL;DR: The present study was designed to investigate some aspects of human placental carbohydrate metabolism in diabetes, in particular, lactate production, glucose uptake and glycogen breakdown in vitro, and the effect of adrenaline on these processes.
15 citations
TL;DR: The degree of inhibition was related to the time of preincubation of enzyme and 5-hydroxytryptamine and to the concentration of added pyridoxal phosphate, the co-factor for decarboxylation of 5- hydroxytryptophan.
13 citations
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180 citations
130 citations
26 May 2014
TL;DR: The data suggest that androgen receptor (AR) signaling can promote prostate cancer through the upregulation of G6PD and therefore, the flux of sugars through the pentose phosphate pathway, and support a vital role for other metabolic pathways in prostate cancer cell growth and maintenance.
Abstract: Regulation of the pentose phosphate pathway by an androgen receptor–mTOR-mediated mechanism and its role in prostate cancer cell growth
122 citations
TL;DR: The insulin-regulatable GLUT4 is expressed in the cytosol of first trimester ST compatible with a role forGLUT4 in placental glucose transport in early pregnancy, and the placental expression pattern of GLUT isoforms in earlyregnancy is distinct from that later in pregnancy.
Abstract: BACKGROUND: Placental glucose transport mechanisms in early pregnancy are poorly understood. The aims of this study were to investigate the expression of glucose transporter (GLUT) isoforms 1, 3 and 4 in first trimester villous tissue, to assess the effects of insulin on glucose uptake and compare them with term. METHODS: The expression of GLUT isoforms was investigated using immunohistochemistry, Western blot and reverse transcription (RT) ‐PCR in trophoblast tissue from terminations at 6 ‐ 13 weeks gestation and term. The effects of insulin (300 ng/ml, 1 h) on glucose uptake were studied in villous fragments. RESULTS: In the first trimester, GLUT1 and GLUT3 were present in the microvillous membrane and the cytotrophoblast, and GLUT4 in perinuclear membranes in the cytosol of the syncytiotrophoblast (ST). GLUT4 protein (48 kDa) and mRNA were identified in trophoblast homogenates. Whereas GLUT1 was expressed abundantly in term placenta, the expression of GLUT3 and 4 was markedly lower at term compared with first trimester. Insulin increased glucose uptake by 182% (n 5 6, P< 0.05) in first trimester fragments, but not in term fragments. CONCLUSIONS: The insulin-regulatable GLUT4 is expressed in the cytosol of first trimester ST compatible with a role for GLUT4 in placental glucose transport in early pregnancy. The placental expression pattern of GLUT isoforms in early pregnancy is distinct from that later in pregnancy.
121 citations
106 citations