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Bruce  Verchere - Diabetes Canada. Vancouver, BC, CA

Bruce Verchere Bruce  Verchere

Professor in the Departments of Surgery and Pathology & Laboratory Medicine | Diabetes Canada

Vancouver, BC, CANADA

Specializes in childhood diabetes research






DREAM Symposium 2013 Keynote - Dr. Bruce Verchere




Bruce Verchere is a Professor in the Departments of Surgery and Pathology & Laboratory Medicine at the University of British Columbia in Vancouver, Canada. He is head of the Canucks for Kids Fund Childhood Diabetes Laboratories at BC Children’s Hospital and holds the Irving K Barber Chair in Diabetes Research.

He obtained his PhD in Physiology from UBC in 1991, then pursued post-doctoral fellowship training in islet biology in Seattle and Geneva before returning to Vancouver in 1997.

His research focuses on the pancreatic islet and aims to understand how beta cell death and dysfunction arises in diabetes and following transplantation, with particular focus on islet amyloid and inflammation, and with the goal of developing therapeutic approaches for enhancing beta cell survival and function in diabetes.

He was awarded the Diabetes Canada Young Scientist Award in 2006 and a Queen Elizabeth II Diamond Jubilee medal for diabetes research and service in 2012.

In recent years he has served on a number of advisory and editorial boards, including the Diabetes Canada Board of Directors and National Research Council; the Institute Advisory Board for the Canadian Institutes of Health Research (CIHR) Institute of Nutrition, Metabolism and Diabetes; on the editorial boards of the Canadian Journal of Diabetes, Diabetes, and Endocrinology; as an associate editor of the journals Islets and Diabetologia; and as chair of grant review panels for the CIHR, JDRF, and NIH.

Industry Expertise (5)

Health and Wellness



Health Care - Services

Training and Development

Areas of Expertise (4)


Type 1 Diabetes

Type 2 Diabetes

Insulin-Producing Beta Cells

Accomplishments (5)

Geoffrey L Hammond Lectureship (professional)


BC Children’s Hospital

Award of Excellence in Mentoring Early Career Faculty (professional)


UBC Faculty of Medicine

Queen Elizabeth II Diamond Jubilee Award (professional)



Young Scientist Award (professional)


Diabetes Canada

Health Research Senior Scholar Award (professional)


Michael Smith Foundation

Education (3)

University of British Columbia: PhD, Dept of Physiology 1991

University of Washington and VA Medical Cente: Post-doctoral fellowship 1996

University of Geneva, Geneva Switzerland: Post-doctoral fellowship 1997

Affiliations (2)

  • University of British Columbia Department of Surgery Department of Pathology & Laboratory Medicine Professor
  • Canucks for Kids Fund Childhood Diabetes Laboratories

Media Appearances (1)

$27 million boost to UBC research into health, sustainability, IT

University of British Columbia  online


“This investment in UBC has the potential to bring significant social and economic benefits to all British Columbians.” Among the funded projects is the Canucks for Kids Fund Childhood Diabetes Laboratories, led by UBC diabetes researcher Bruce Verchere at BC Children’s Hospital, an agency of the Provincial Health Services Authority. A $3.2 million funding investment in new state-of-the-art technology will help further research into diabetes prediction, treatment and prevention.

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Articles (5)

Improving glycemic control in type 2 diabetes: stimulate insulin secretion or provide beta-cell rest?

Diabetes Obes Metab.


Type 2 diabetes (T2D) is characterized by a gradual decline of pancreatic beta cell function that determines the progressive course of the disease. While beta-cell failure is an important contributor to hyperglycemia, chronic hyperglycemia itself is also detrimental for beta-cell function, likely by inducing prolonged secretory stress on the beta cell as well as through direct glucotoxic mechanisms that have not been fully defined. For years, research has been carried out in search of therapies targeting hyperglycemia that preserve long-term beta-cell function in T2D, a quest that is still ongoing. Current strategies aim to improve glycemic control either by promoting endogenous insulin secretion, such as sulfonylureas, or by mechanisms that may impact the beta cell indirectly, for example providing beta-cell rest through insulin treatment. Although overall long-term success is limited with currently available interventions, in this review we argue that strategies that induce beta-cell rest have considerable potential to preserve long-term beta-cell function. This is based on laboratory-based studies involving human islets as well as clinical studies employing intensive insulin therapy, thiazolidinediones, bariatric surgery, short-acting glucagon-like peptide (GLP)-1 receptor agonists, and a promising new class of diabetes drugs, sodium-glucose linked transporter (SGLT)-2 inhibitors. Nevertheless, a lack of long-term clinical studies that focus on beta-cell function for the newer glucose-lowering agents as well as commonly used combination therapies preclude a straightforward conclusion; this gap in our knowledge should be a focus of future studies.

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Loss of prohormone convertase 2 promotes beta cell dysfunction in a rodent transplant model expressing human pro-islet amyloid polypeptide


2016 Islet amyloid has been recognized as a pathological entity in type 2 diabetes since the turn of the century. It has as its unique component the islet beta-cell peptide islet amyloid polypeptide (IAPP), or amylin, which is cosecreted with insulin. In addition to this unique component, islet amyloid contains other proteins, such as apolipoprotein E and the heparan sulfate proteoglycan perlecan, which are typically observed in other forms of generalized and localized amyloid. Islet amyloid is observed at pathological examination in the vast ...

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Cellular mechanisms of CCL22-mediated attenuation of autoimmune diabetes

J Immunol.


Autoimmune destruction of insulin-producing β cells in type 1 diabetes and islet transplantation involves a variety of immune pathways but is primarily mediated by self-reactive T cells. Chemokines can modulate local immune responses in inflammation and tumors by recruiting immune cells. We have reported that expression of the chemokine CCL22 in pancreatic β cells in the NOD mouse prevents autoimmune attack by recruiting T regulatory cells (Tregs), protecting mice from diabetes. In this study we show that invariant NKT cells are also recruited to CCL22-expressing islet transplants and are required for CCL22-mediated protection from autoimmunity. Moreover, CCL22 induces an influx of plasmacytoid dendritic cells, which correlates with higher levels of IDO in CCL22-expressing islet grafts. In addition to its chemotactic properties, we found that CCL22 activates Tregs and promotes their ability to induce expression of IDO by dendritic cells. Islet CCL22 expression thus produces a tolerogenic milieu through the interplay of Tregs, invariant NKT cells, and plasmacytoid dendritic cells, which results in suppression of effector T cell responses and protection of β cells. The immunomodulatory properties of CCL22 could be harnessed for prevention of graft rejection and type 1 diabetes as well as other autoimmune disorders.

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Death and dysfunction of transplanted β-cells: lessons learned from type 2 diabetes?



β-Cell replacement by islet transplantation is a potential curative therapy for type 1 diabetes. Despite advancements in islet procurement and immune suppression that have increased islet transplant survival, graft function progressively declines, and many recipients return to insulin dependence within a few years posttransplant. The progressive loss of β-cell function in islet transplants seems unlikely to be explained by allo- and autoimmune-mediated mechanisms alone and in a number of ways resembles β-cell failure in type 2 diabetes. That is, both following transplantation and in type 2 diabetes, islets exhibit decreased first-phase glucose-stimulated insulin secretion, impaired proinsulin processing, inflammation, formation of islet amyloid, signs of oxidative and endoplasmic reticulum stress, and β-cell death. These similarities suggest common mechanisms may underlie loss of insulin production in both type 2 diabetes and islet transplantation and point to the potential for therapeutic approaches used in type 2 diabetes that target the β-cell, such as incretin-based therapies, as adjuncts for immunosuppression in islet transplantation.

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Resident macrophages mediate islet amyloid polypeptide-induced islet IL-1β production and β-cell dysfunction



IL-1 blockade attenuates islet amyloid polypeptide-induced proinflammatory cytokine release and pancreatic islet graft dysfunction. Islet amyloid polypeptide (IAPP) aggregates to form amyloid fibrils in patients with type 2 diabetes and acts as a potent stimulus for interleukin (IL)-1β secretion by bone marrow-derived macrophages. We sought to determine the contribution of resident islet macrophages to IAPP-induced inflammation and β-cell dysfunction. In cultured islets, macrophages (F4/80(+)CD11b(+)CD11c(+) cells) were required for IAPP-induced mRNA expression of the proinflammatory cytokines IL-1β, tumor necrosis factor-α, and IL-6 and the anti-inflammatory cytokines IL-10 and IL-1 receptor antagonist. Moreover, IAPP-induced IL-1β synthesis and caspase-1 activation were detected in macrophages but not other islet cell types. Transgenic mice with β-cell human IAPP (hIAPP) expression had impaired glucose tolerance, elevated islet Il1b mRNA, and decreased Il10 and Il1rn expression following high-fat feeding. Islet macrophages were the major source of these transcripts and expressed increased cell surface Ly6C and CD11c in hIAPP transgenic mice. Clodronate liposome-mediated depletion of islet macrophages improved glucose tolerance and blocked proinflammatory gene expression in hIAPP-expressing mice, despite increasing the amount of islet amyloid. These data provide the first evidence that IAPP aggregates skew resident islet macrophages toward a proinflammatory phenotype and suggest a mechanism by which anti-inflammatory therapies may protect β-cells from IAPP-induced islet dysfunction.

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