The "Metabolism and Disease" annual meeting theme will cover mitochondrial dysfunction, information transmission, signal transduction and cancer. There also will be a special workshop, titled “New Tools to Study Mitochondrial Function.” The meeting will be held April 9-13, 2011, in Washington, D.C. (Titled "Communications of the Metabolic State" in print version.)
|Barbara E. Corkey
Metabolic regulation represents the front line in the control of intermediary metabolism as well as transcriptional and protein synthetic adaptation to changes in the cellular environment. The increased sensitivity of analytical tools and recent advances in molecular genetics and imaging have fostered greater understanding of interconnections between metabolic networks and the diverse molecular mechanisms involved in cellular functions. As a result, “classical” intermediary metabolism has been found to be involved directly in signaling functions as diverse as apoptosis, cell growth and transcriptional control, which impact not only the single cell, but all basic physiological processes.
The 2011 American Society for Biochemistry and Molecular Biology annual meeting “Metabolism and Disease” theme consists of four symposia that focus attention on novel roles of mitochondria in diseases, metabolic communication among various organs, mechanisms of metabolic signal transduction within the cell and the rekindled awareness of the important role of metabolism in cancer.
The first symposium, titled “Mitochondrial Function and Disease,” will look at diseases directly related to mitochondrial dysfunction. Carlos Moraes (University of Miami) will discuss his experience with patients affected by mitochondrial oxidative phosphorylation disorders. He also will consider the various options that may improve respiration and ATP production in these patients’ cells.
Next, Siegfried Hekimi (McGill University) will present research that challenges our current thinking about the role of increased mitochondrial ROS production in aging.
And, finally, Orian Shirihai (Boston University) will discuss mitochondrial fission, fusion and networking and consider the heterogeneity of mitochondria in terms of structure and function and association with a number of diseases, including ischemia-reperfusion and nutrient-induced pancreatic β-cell dysfunction in diabetes.
Click here for more 2011 annual meeting thematic overviews.
For information on annual meeting registration, housing and abstract submission, click here.
The second symposium, titled “Metabolic Communication,” will focus on mechanisms by which metabolic information is transmitted from one organ to another via the extracellular thiol redox state, clock proteins and free fatty acids. Dean P. Jones (Emory University) will discuss the connection between the redox potential of plasma cysteine/cystine and the risk factors for cardiovascular disease, namely age, smoking, type 2 diabetes, obesity and alcohol abuse. Data show that the proinflammatory effects of the oxidized plasma redox state are due to a mitochondrial signaling pathway that is mediated through redox control of downstream effector proteins.
Molly S. Bray (University of Alabama at Birmingham) will then explain how biological rhythms profoundly influence energy homeostasis and also how carbohydrate or fat consumption at a given time of the day may influence health.
Metabolism and Disease
Session: Mitochondrial Function and Disease
• Beneficial Effects of Increased Mitochondrial Biogenesis in Aging, Carlos Moraes, University of Miami Miller School of Medicine
• Revisiting the Role of Mitochondrial ROS in Aging and Age-dependent Diseases Transfer Proteins, Siegfried Hekimi, McGill University
• Metabolic Regulation of Mitochondrial Dynamics, Orian Shirihai, Boston University
Session: Metabolic Communication
• Redox Analysis and Metabolic State, Dean P. Jones, Emory University
• The Role of Cell-specific Clocks in Metabolism and Disease, Molly S. Bray, University of Alabama at Birmingham
• Abdominal Obesity, Fatty Acids and Insulin Resistance, Richard Bergman, University of Southern California Keck School of Medicine
Session: Metabolic Signal Transduction
• Lipid Cycling as a Signal in β-cells, Marc Prentki, University of Montreal
• Signaling by ROS in β-Cells and Fat Cells, Barbara E. Corkey, Boston University School of Medicine
• NAD and Cofactors in the Control of Metabolism, Johan Auwerx, École Polytechnique Fédérale de Lausanne
Session: Metabolism and Cancer
• Metabolic Mutations that Cause Cancer, Craig B. Thompson, University of Pennsylvania
• Regulation of Tumor Cell Survival under Metabolic Stress, Tak W. Mak, University of Toronto
• Role of p53 in Metabolism and Invasion, Karen H. Vousden, Beatson Institute for Cancer Research
Workshop: New Tools to Study Mitochondrial Function
Chair: Orian Shirihai, Boston University
Lastly, Richard Bergman (University of Southern California) will talk about how free fatty acids, and the pattern of free fatty acid release, regulates glucose homeostasis. He also will examine the possible consequences of free fatty acid release on the sympathetic nervous system in the obese or insulin-resistant state.
The third symposium, titled “Metabolic Signal Transduction,” will concentrate on mechanisms by which metabolic changes within the cell are translated into signals that modulate functions, from secretion to metabolism to transcriptional regulation. Marc Prentki (University of Montreal) will discuss the biochemical basis of β-cell signaling in response to glucose, amino acids and fatty acids, as well as β-cell nutrient detoxification and the emerging role of glycerolipid/fatty acid cycling in these processes.
Next, Barbara E. Corkey (Boston University School of Medicine) will compare different fuel-induced signals in fat and β-cells with a focus on how the same signals subserve different cell-specific but complementary functions.
Johan Auwerx (École Polytechnique Fédérale de Lausanne) will then describe how protein acetylation-deacetylation reactions affect wide-ranging physiological processes, with a particular focus on the NAD dependent deacetylase SIRT-1. He will develop the concept that boosting cellular levels of NAD+ may ameliorate factors associated with the metabolic syndrome.
The fourth and final symposium, “Metabolism and Cancer,” will look at how altered metabolism can promote oncogenic pathways and tumor cell survival. Craig B. Thompson (University of Pennsylvania) will review his work on the role of glycolytic and Krebs cycle enzymes in controlling the production of metabolites with oncogenic or tumor suppression capabilities.
Next, Tak W. Mak (University of Toronto) will discuss how metabolic stress can influence various apoptotic pathways and cancer cell survival.
And, finally, Karen H. Vousden (Beatson Institute for Cancer Research in Glasgow) will discuss insights into the signaling and metabolic pathways involved in tumor cell invasion and the role played by p53 in metastasis.
We also have scheduled a workshop, titled “New Tools to Study Mitochondrial Function” and chaired by Orian Shirihai (Boston University). Speakers at this event will demonstrate new ways to monitor bioenergetics, mitochondrial function and ROS and mitochondrial dynamics (fusion, fission and morphology) in vivo.
Barbara E. Corkey (email@example.com) is director of the Obesity Research Center and a professor of medicine and biochemistry at the Boston University School of Medicine. Marc Prentki (firstname.lastname@example.org) is a professor of nutrition and biochemistry and Canada research chair in diabetes and metabolism at the University of Montreal.