Department of Biochemistry and Biomedical Sciences

Professor, Department of Pediatrics
3A42 Health Sciences Centre McMaster University
Tel: 905-521-2100 ext. 75644
Email: satkins@mcmaster.ca
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Research

• Metabolism and Toxicology

Nutritional biochemistry and applied nutrition related to skeletal development during growth and in pediatric diseases. Dr. Atkinson is a nutritional scientist whose research interests encompass studies of the nutritional and endocrine regulation of growth processes, with a focus on skeletal development. Her clinical research has identified abnormalities in growth and bone development associated with disease or drug (e.g. steroids) therapies in children with disorders such as prematurity, leukemia, cystic fibrosis or epilepsy. Studies in children and an animal model have investigated the potential of anabolic agents such as nutrition, calcitriol, growth hormone, or insulin-like growth factor to preserve normal growth processes in target disease pediatric populations. Insights into the functional aspects of bone metabolism are assessed by bone histomorphometry, bone mass and body composition by dual energy x-ray absorptiometry, bone strength testing and measurements of bone bi markers such as osteocalcin, IGF-I, IGF binding protein and cross-linked C-telopeptide of type 1 collagen. Using standard and mini pigs as animal models, current research focuses on the mechanisms by which steroid drugs alter bone metabolism during early development and the potential for osteoanabolic agents such as recombinant growth factors such as (growth hormone or IGF-I), bisphosphate drugs or calcitriol to attenuate the catabolic effects of the steroids on normal bone growth. The long term objective of this area of research is to extend knowledge of how physiological mechanisms affecting mineral utilization change from infancy and throughout development, the impact of disease and drugs on these processes, and possible nutritional or pharmacological interventions that will ameliorate any abnormalities that might impede a child's genetic potential to achieve peak bone mass, a key factor in prevention of adult-onset osteoporosis.

Selected Publications

• Dexamethasone-induced abnormalities in growth and bone metabolism in piglets are partially attenuated by growth hormone with no synergistic effect of insulin-like growth factor-I. Ward, WE, Donovan, SM, Atkinson, SA. Pediatr Res 1998;44:215-221.
• Bone metabolism and circulating IGF-I and IGFBPs in dexamethasone-treated preterm infants. Ward WE, Atkinson SA, Donovan S, Paes B. Early Human Develop 1999; 56:127-141.
• Comparative response in growth and bone status to three dexamethasone treatment regimens in infant piglets. Guo, C-Y, Ward W, Cairns P, Atkinson SA Pediatr Res 2000;48:1-6.
• Calcium competes with zinc for a channel mechanism on the brush border membrane of piglet intestine. Bertolo RF, Bettger W, Atkinson S.A. J Nutr Biochem 2001;12(2):66-72.
• Elevated intact parathyroid hormone is associated with reduced bone resorption in infant piglets receiving oral dexamethasone for 15 days. Guo C-Y, Weiler H, Atkinson SA. J Biology of the Neonate 2001;80:195-199.
• Long term valproate and lamotrigine treatment may be a marker for reduced growth and bone mass in children with epilepsy. Guo C-Y, Ronen GM, Atkinson SA Epilepsia 2001;42(9):1141-47.
• Hypomagnesemia associated with chemotherapy in children treated for acute lymphoblastic leukemia: possible mechanisms. Guo CY, Atkinson SA, Halton J, Barr RD. Oncology Reports 2003;10:In press.