Bioacoustics Research Lab
University of Illinois at Urbana-Champaign | Department of Electrical and Computer Engineering | The Department of Bioengineering  Monday, December 11th, 2017
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1999 ROT Retreat Schedule

Saturday, January 23, 1999

8:30 am - 1:30 pm

1005 Beckman Institute


8:30 - 8:50: Registration and refreshments

8:50 - 9:00: Introductions and Introductory Remarks

9:00 - 9:40: Ronald W. Hart, PhD, National Center for Toxicological Research, Food and Drug Administration, Jefferson, Arkansas "Influencing Carcinogenicity/Anticarcinogenicity by Overnutrition and Caloric Restriction" ABSTRACT BELOW.

9:40 - 10:00: Ying Huang (Advisor: Professor J. Katzenellenbogen)

Introduced by Inho Choi

10:00 - 10:20: Karen A. Topp (Advisor: Professor O'Brien)

Introduced by Ying Huang

10:20 - 10:40: Inho Choi (Advisor: Professor B. Katzenellenbogen)

Introduced by Karen Topp

10:40 - 11:00: Babak Behnia (Advisor: Professor Webb)

Introduced by Michael Aref

11:00 - 11:15: Break

11:15 - 11:35: Rachel Konda-Sundheim (Advisor: Professor Clarkson)

Introduced by Babak Behnia

11:35 - 11:55: Ramji Rajendran (Advisor: Professor B. Katzenellenbogen)

Introduced by Rachel Konda-Sundheim

11:55 - 12:15: Kara C. Sorensen (Advisor: Professor Kitchell)

Introduced by Ramji Rajendran

12:15 - 12:35: Joseph Tan (Advisor: Professor Frizzell)

Introduced by Kara C. Sorensen

12:35 - 12:55: Michael Aref (Advisor: Professor Wiener)

Introduced by Joseph Tan

12:55 - 1:00: Closing Remarks

1:00: Light Lunch


Ronald W. Hart, PhD

National Center for Toxicological Research

Food and Drug Administration

Jefferson, Arkansas

"Influencing Carcinogenicity/Anticarcinogenicity by Overnutrition and Caloric Restriction"


Carcinogenicity is characterized by a set of complex endpoints, which appear as a series of molecular events. Many of these events can be modified by caloric intake. Since most of these processes determine an organism's ability to cope with various environmental stressors, it is not surprising that a relationship (in the presence of a constant nutrient density) exists between caloric intake and time to tumor. Our studies have clearly shown that the greater the body weight (generally in rodents directly related to extent of caloric intake) the higher the incidence of spontaneous tumor occurrence, the greater the susceptibility to chemical carcinogens and the shorter the life span. We have focused our attention on the questions of how and to what extent does caloric intake modify those homeostatic processes believed to be critical in determining the ability of an organism to cope with endogenous and exogenous stress such as chemical, physical and biological carcinogens.

The response of an organism can be classified into four (4) categories - physiological, metabolic, molecular and cellular.

We have found, from a physiological perspective, that body temperature in rodents is decreased by 0.5 to 1.8 C, while water consumption is increased by 40 to 80% as is running activity, however, metabolic output per gram of lean body mass is not altered, with decreasing caloric intake. Reproductive capacity declines whereas the ECG waveform is preserved as caloric intake is decreased. Alterations in these and other physiological functions suggests that energy intake serves as a signal to up-regulate or down-regulate functions related to the flight or fright response observed in placental mammals.

A number of key metabolic pathways are altered as a function of caloric intake despite the observation that food consumption per gram lean body mass remains similar due to decreased body weight with decreased caloric intake. Pharmacological compartmentalization, however, is altered. As caloric intake declines, changes occur in the expression of a number of drug metabolizing enzymes, with the most striking effect being seen on sex-specific, growth-hormones dependent liver enzymes. Additionally, oxidation stress (free radical production) appears to decrease as a function of caloric intake and antioxidant activity increases concurrent with an up-regulation in the activity of a number of key enzymes of intermediary metabolism.

A number of molecular processes also change with changes in energy consumption. Our studies have shown that regardless of the source of DNA damage, DNA repair is preserved and/or enhanced as caloric consumption decreases. In addition, the fidelity of DNA replication increases and oncogene expression is stabilized, P53 gene expression is increased as a function of the decrease in circulating glucose and apoptosis is elevated by up to 500%.

At the cellular level, cellular proliferation is decreased proportionate to energy intake in some but not all tissues. Studies both in our laboratory and associate laboratories have also shown an enhancement in immune capacity, changes in IGF1, and accelerated rates of wound healing proportionate with declines in energy consumption. Our most recent findings, however, have shown that the benefits associated with decreases in caloric intake only occur in the presence of sufficient nutrient density. In the absence of proper nutrition, sensitivity to carcinogens appears to be enhanced. These observations have led us to conclude that response to a decrease in caloric intake involves an up-regulation of those processes that modulate the response of organisms to a wide range of environmental stressors.



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