Dr. Haqq's clinical translational research has centered on the neuroendocrinology of energy balance in childhood obesity. We have demonstrated that children with PWS have unusual biochemical features that may explain their uncontrollable appetites and excess weight gain. Foremost among these is a paradoxical elevation of ghrelin, an appetite-stimulating hormone. Dietary or pharmacologic approaches to therapy based on reducing ghrelin levels or limiting ghrelin action might prevent or reverse obesity in children with PWS.
For reasons unknown, some obese individuals are protected from developing metabolic co-morbidities such as glucose intolerance and cardiovascular disease. PWS provides a unique model that may help to explain this phenomenon of the “healthy obese” patient. Studies from our laboratories showed that PWS is associated with relative hypoinsulemia and hypersensitivity to insulin action, associated with hyperadiponectinemia, low levels of interleukin 6 and C-reactive protein, and relatively low visceral fat deposition. The relative insulin sensitivity may protect children and adults with PWS from development of metabolic co-morbidities. Preliminary ongoing studies suggest that the preservation of insulin sensitivity might be explained by the differential patterns of fat distribution in PWS and other obese subjects. Ongoing studies of the developmental changes in fat distribution in PWS and non-syndromic obesity may shed new light on the pathogenesis of insulin resistance and life-threatening metabolic complications of obesity.
Further translational clinical research goals include understanding the regulation of ghrelin and other neuropeptides’ (adiponectin, adropin, obestatin, Peptide YY, leptin) in the context of childhood disorders of energy balance including PWS and general childhood obesity.
Most recent work focuses on the characterization of autonomic nervous system (ANS) dysfunction in childhood obesity and examination of the relationship between ANS dysfunction, body fat distribution and metabolic profile in obese children. To further elucidate this relationship, ANS function in obese children will be compared to children with a unique genetic model of obesity and ANS dysfunction called Prader-Willi Syndrome (PWS).
Dr. Haqq has assumed leadership roles in the general pediatric endocrine community. She has served on the international Pediatric Endocrine Society (PES) Obesity Committee and the Drug and Therapeutics Committee. Through her involvement in these committees, she has contributed to the development of several manuscripts that provide state of the art reviews and practice guidelines for pediatric endocrinologists in areas of management of type I and type 2 diabetes and childhood obesity. Her current research efforts are supported by Canadian Institutes of Health Research (CIHR) operating grants and project grants from the Foundation for Prader-Willi Research (FPWR), the Prader-Willi Syndrome Association of Alberta, the Alberta Diabetes Institute and Women & Children’s Health Research Institute, University of Alberta.
Master of Health Science