Raynald Bergeron, PhD
Associate Professor of Kinesiology
Raynald Bergeron received his PhD in exercise physiology from the
University of Montreal in 1997. His doctoral work under the supervision of Dr
Jean-Marc Lavoie focused on the role of liver metabolism in the modulation of
endocrine responses such as during elevated delivery of free fatty acids into the
hepatic portal circulation. He then pursued his academic training in the laboratory of Dr
Gerald I. Shulman at Yale University School of Medicine. As a post-doctoral fellow in Dr
Shulman�s lab, his work supported a role for AMP-activated protein kinase (AMPK) in the
regulation of glucose transport and mitochondrial biogenesis in skeletal muscle. Dr
Bergeron then joined Merck Research Laboratories in 2001 where, as a senior research
biochemist, he played an active role in bringing Januvia®, the first DPP-IV inhibitor
to the market. He also was a leader of the research team whose efforts is to develop
a pharmacological activator of AMPK activator for the treatment of diabetes. In 2006,
he joined the department of Kinesiology of the University of Montreal where he is now
associate professor. He became member of the MDRC in 2007.
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Selected Scientific Contributions
Dr Bergeron�s work, as well as work from other scientists, showed
that AMPK is activated during muscle contraction and contributes to skeletal muscle
contraction-induced glucose transport in muscles primarily composed of fast twitch
muscle fibers and that this was an insulin-dependant event as wortmannin did not
suppress contraction mediated elevation of glucose transport. The contribution of
acute AMPK activation to glucose transport was shown to be active in both normal as
well as insulin resistant rats (fa/fa). This work supported that AMPK-induced
stimulation of glucose transport was intact in insulin resistant animals suggesting
that this cellular pathway could be exploited pharmacologically to improve defective
muscle glucose transport in T2DM.
Using an analog of creatine (�-GPA) leading to chronic activation
of AMPK, Dr Bergeron also demonstrated that this pathway was associated with skeletal
muscle mitochondrial biogenesis. This finding was later confirmed with the use of
AMPKa2 muscle specific dominant negative mice.
As a scientist at Merck Research Laboratories, Dr Bergeron explored
a vast range of animal models of insulin resistance and diabetes. Those models were
used to validate and develop pharmacological tools for diabetes targets including AMPK,
PPAR, glycogen phosphorylase, glucokinase, acetyl-CoA carboxylase, stearyl-CoA
desaturase-1. More specifically, he recently highlighted the beneficial effects of PPARa
selective agonist treatment on glucose metabolism and insulin secretion in Zucker
Diabetic Fatty (ZDF) rats, a common diabetes animal model.
Current projects in the laboratory fall into three areas:
Contractile activity of skeletal muscle: Mechanisms
leading to improved muscle glucose metabolism in insulin resistant models.
Studies focusing on the interaction between reactive oxygen species being generated
during acute muscle contraction and AMPK activation in the modulation of glucose
transport and metabolism are being conducted. A colony of AMPKa1 KO mice is being
used to investigate this research area.
Effect of physical activity on insulin secretion in
diabetes prone individuals. Although the effects of regular physical activity
on peripheral insulin sensitivity are well documented, outcomes on insulin secretion
are not clear. Using ZDF rats being physically trained on a voluntary basis in wheel
cages, we have developed a model to study both in vivo as well as in vitro
(isolated islets) dynamics of insulin secretion in response to physical activity in
a rat strain with a high genetic propensity to develop diabetes. Studies focusing on
the role of oxidative stress in relationship with islet substrate metabolism in the
modulation of this training effect on the �-cells are underway.
Study of interactions between exercise training and
antihyperglycemic agents on glucose control. Dr Bergeron�s laboratory is
currently developing new diabetes animal models to diversify observations and gain
more confidence in the relevance of such models to the human disease. Those models
will be used to better investigate potential benefits and adverse effects of combining
physical activity and antihyperglycemic pharmacological agents under development as
more and more diabetic patients become active, as recommended by health professionals,
while taking medications.