Dr. Johnson is a Full Professor in the Department of Cellular and Physiological Sciences, in the Faculty of Medicine at the University of British Columbia. He is Leader of the Life Sciences Institute Diabetes Research Group, consisting of 8 laboratories and >70 staff/trainees.
He is also helping to start up and direct a new academic-industry hybrid type 2 diabetes research institute in Oxford funded by Novo Nordisk. He will do this while maintaining his academic laboratory at UBC.
His research group at UBC studies the pathophysiology and signalling mechanisms underlying diabetes, obesity, longevity, heart disease, Alzheimer's disease and pancreatic cancer. He is Editor-in-Chief of Islets and serves on the Editorial Boards of Diabetes and of Endocrinology.
Industry Expertise (4)
Areas of Expertise (5)
2016 Diabetes Canada Young Scientist Award (professional)
Diabetes Canada established the Young Scientist Award in 1987 for the purpose of encouraging, by appropriate recognition, outstanding research conducted in Canada by young scientists in the field of diabetes. This award continues today with the support of the CH Best Research Fund of Canadian Diabetes Association.
Visiting Scholar – Harris Manchester College, Oxford University (professional)
Visiting Professor of Integrated Physiology, Oxford University (personal)
Killam Research Fellowship (professional)
Researcher of the Year, Department of Cellular and Physiological Sciences, University of British Columbia (professional)
Murray L Barr Award, Canadian Association for Anatomy Neurobiology and Cell Biology (professional)
Washington University Medical Cente: Post-doctoral Fellowship 2004
Washington University School of Medicine: Fellow of the Lucille P. Markey Pathway, Human Pathobiology 2003
University of Alberta: Ph.D., Physiology and Cell Biology 2000
Lakehead University: HBKin, Kinesiology 1996
- Professor LSI Diabetes Research Group University of British Columbia
Obesity is a principal risk factor for type 2 diabetes, and elevated fatty acids reduce beta-cell function and survival. An unbiased proteomic screen was used to identify targets of palmitate in beta-cell death. The most significantly altered protein in both human islets and MIN6 beta-cells treated with palmitate was carboxypeptidase E (CPE). Palmitate reduced CPE protein levels within 2 h, preceding endoplasmic reticulum (ER) stress and cell death, by a mechanism involving CPE translocation to Golgi and lysosomal degradation. Palmitate metabolism and Ca(2+) flux were also required for CPE proteolysis and beta-cell death. Chronic palmitate exposure increased the ratio of proinsulin to insulin. CPE null islets had increased apoptosis in vivo and in vitro. Reducing CPE by approximately 30% using shRNA also increased ER stress and apoptosis. Conversely, overexpression of CPE partially rescued beta-cells from palmitate-induced ER stress and apoptosis. Thus, carboxypeptidase E degradation contributes to palmitate-induced beta-cell ER stress and apoptosis. CPE is a major link between hyperlipidemia and beta-cell death pathways in diabetes.
Insulin 2 (INSULIN), but not Insulin 1, is produced locally in the adult brain; circulating insulin can be reduced without sustained changes in glucose homeostasi; fasting hyperinsulinemia is required for diet-induced obesity and its complications; insulin controls Ucp1 in white adipose tissue and energy expenditure
Hyperinsulinaemia is associated with obesity but its causal role in the onset of obesity remains controversial. In this study, we tested the hypothesis that transient attenuation of diet-induced insulin hypersecretion in young mice can provide sustained protection against obesity throughout adult life...
The proteins that coordinate complex adipogenic transcriptional networks are poorly understood. 14-3-3ζ is a molecular adaptor protein that regulates insulin signalling and transcription factor networks. Here we report that 14-3-3ζ-knockout mice are strikingly lean from birth with specific reductions in visceral fat depots. Conversely, transgenic 14-3-3ζ overexpression potentiates obesity, without exacerbating metabolic complications...
Beta cell death is a hallmark of diabetes. It is not known whether specific cellular stresses associated with type 1 or type 2 diabetes require specific factors to protect pancreatic beta cells. No systematic comparison of endogenous soluble factors in the context of multiple pro-apoptotic conditions has been published...