David J. Hill


David Hill

PH.D. Oxford University
B.Sc. University of Nottingham
Office: Lawson Research Institute, Room 406
Phone: (519) 646-6100 Ext. 64716
E-mail: david.hill@lawsonresearch.com
See Publications by David Hill on PubMed

A major research theme is the hormonal control of growth and development, with a particular interest in the prenatal human. Recent studies have examined the ontogeny of expression, cellular location, and mechanism of action of peptide growth factors such as the insulinlike growth factors, fibroblast growth factors and transforming growth factor beta in the sheep, rat and human embryo or fetus. Particular interest has been taken in the interactions of endocrine hormones, such as growth hormone, placental lactogen and insulin, with the paracrine expression of growth factors, and nutritional availability and utilization during early growth. Studies utilize the tissue culture of animal and human connective tissue cell types, including myoblasts, fibroblasts and chondrocytes, hepatocytes, and isolated pancreatic islets of Langerhans. Hormone presence and action are investigated at the level of MRNA expression, peptide synthesis and release, receptorkinetics and cellular anabolic response.

Thyssen S, Arany E, Hill DJ. Ontogeny of regeneration of beta-cells in the neonatal rat after treatment with streptozotocin. Endocrinology. 2006 May;147(5):2346-56. Epub 2006 Feb 16.

Arany E, Strutt B, Romanus P, Remacle C, Reusens B, Hill DJ. Taurine supplement in early life altered islet morphology, decreased insulitis and delayed the onset of diabetes in non-obese diabetic mice. Diabetologia. 2004 Oct;47(10):1831-7. Epub 2004 Oct 21.

Joanette EA, Reusens B, Arany E, Thyssen S, Remacle RC, Hill DJ. Low-protein diet during early life causes a reduction in the frequency of cells immunopositive for nestin and CD34 in both pancreatic ducts and islets in the rat. Endocrinology. 2004 Jun;145(6):3004-13. Epub 2004 Mar 24.

Thompson A, Arany EJ, Hill DJ, Yang K. Glucocorticoid receptor expression is altered in pancreatic beta cells of the non-obese diabetic mouse during postnatal development. Metabolism. 2002 Jun;51(6):765-8.

Duvillie B, Currie C, Chrones T, Bucchini D, Jami J, Joshi RL, Hill DJ. Increased islet cell proliferation, decreased apoptosis, and greater vascularization leading to beta-cell hyperplasia in mutant mice lacking insulin. Endocrinology. 2002 Apr;143(4):1530-7.

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