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Raymond Rodriguez
Director,
Center of Excellence in Nutritional Genomics,
University of California Davis
Davis, CA, USA
Nutritional Genomics
Monday, September 13, 2010
10:30 - 11:00 am
Abstract:
The mechanisms by
which nutrient and
non-nutrient
bioactives influence
long-term health
outcomes are not
well understood. For
example, how do
low-potency dietary
signals regulate
thousands of genes
in hundreds of
pathways to reduce
disease risk? Do
dietary signals
interact with the
genome randomly, or
are these
interactions
targeted in a regio-specific
fashion? While the
genomic revolution
has provided an
array of powerful
analytical tools to
investigate human
health, many
researchers continue
to use reductionist
approaches to study
complex diet-genome
interactions.
Researchers have
focused too intently
on isolating
individual food
bioactive at the
expense of
discovering novel
synergistic effects
of combinations of
dietary signals.
Researchers have
also relied too
heavily on genetic
theories of disease,
ignoring important
genetic modifiers
such as nutrition,
lifestyle, exercise
and epigenetics —
factors that make
human health a
complex system. As a
complex system,
human physiology
consists of networks
genes, proteins and
metabolites that are
interconnected in
interdependent at
the boundary between
deterministic
processes and
chaotic (i.e.,
unpredictable)
processes. In
response to
nutritional stress,
adaptive,
self-organizing
molecular and
cellular responses
emerge to return the
network to
homeostasis. Such
behaviors are called
nutridynamical
systems or
time-dependent
molecular and
cellular states that
emerge in response
to small changes in
nutritional input.
For one type of
nutritional input,
self-organizing,
adaptive behaviors
can emerge that
return the network
to homeostasis while
other kinds of
inputs can produce
chaotic behaviors
can prolong the
return to
homeostasis. The
latter may increase
the chances that a
chaotic, or disease
state, will emerge.
The difficulty in
integrating dietary
signaling with
current genetic
control and signal
sensing mechanisms
is the lack of
regulatory models
that incorporate
diet-influenced
phase transitions
and other non-linear
effects.
Diet-informed
epigenetic
modifications of
chromatin could
represent a new
regulatory motif
with the potential
to produce large
changes in gene
expression in
response to
low-potency dietary
signals.
Biography
Dr. Rodriguez is a professor in the Department of Molecular & Cellular Biology in the College of Biological Sciences at the University of California, Davis. After receiving his Ph.D. at the University of California, Santa Cruz in 1974, he was an A.P. Giannini Foundation Fellow in the laboratory of Herbert W. Boyer at UC San Francisco Medical Center where he helped develop many of the molecular cloning technologies that now serve as the foundation of the modern biotechnology industry. Dr. Rodriguez joined the faculty at the UC Davis in 1977 and is actively involved in research and teaching at the undergraduate and graduate level. Dr. Rodriguez has been actively involved in all aspects of biotechnology as well as and holds 17 patents. In 2003 he became director of the Center of Excellence for Nutritional Genomics, a multi-investigator, multi-institutional research program to study the impact of diet-genome interactions on human health. He has published numerous articles and books on molecular biology and biotechnology and is currently working on a new book entitled, Dietary Regulation of Gene Expression and its Impact on Human Health. His current research focus is nutritional epigenomics or the study of how plant-based dietary factors alter human gene activity by chromatin modification.
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Raymond Rodriguez's ABIC 2010
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