IGPNS Faculty Mentors

Michael W. Pariza, Ph.D.

Michael W. Pariza, Ph.D.Wisconsin Idea Fellow

Food Microbiology and Toxicology
1925 Willow Drive Rm 176
Madison, WI 53706
608-263-7777
mwpariza@facstaff.wisc.edu

Emphasis Groups:
Biochemical & Molecular Nutrition
Human Nutrition

Principal Research Interest:
Dietary anticarcinogens; biological significance of conjugated linoleic acid.

Research Summary:

CLA is the acronym for a class of positional and geometric conjugated dienoic isomers of linoleic acid. We coined the term in 1987 when we reported biological activity (i.e., anticarcinogenic activity) associated with CLA produced from linoleic acid by base-catalyze disomerization. Since then substantial interest has developed in the biochemical actions of CLA and its potential application to foods, feeds and pharmaceuticals (for a current listing of scientific literature on CLA throughout the world since 1987, see http://www.wisc.edu/fri/clarefs.htm).

Dietary CLA has been shown to affect body composition (reduction in body fat, enhancement of fat free mass) in a number of animal species including mice, rats, and pigs. CLA exerts direct effects on adipocytes, which are the principal sites of fat storage, and skeletal muscle cells, which are the principal sites of fat combustion. We found that adding CLA to the culture medium of mouse 3T3-L1 adipocytes produced a dose-dependent reduction in lipoprotein lipase activity, and apparently induced lipolysis as well in this cell line. Additionally, elevated carnitine palmitoyltransferase activity. Evidence was also presented indicating that CLA enhanced whole body protein accretion. Based on these findings we proposed that the physiological mechanism of body fat reduction in mice by CLA involved inhibition of fat storage in adipocytes coupled with both elevated b-oxidation in skeletal muscle as well as an increase in skeletal muscle mass, effected in part via protection of skeletal muscle by CLA from immune-induced catabolism.

Our current research focuses on further defining the molecular mechanisms of action of the various CLA isomers.

Representative Publications:

Li G, Dong B, Butz DE, Park Y, Pariza MW, Cook ME. NF-kappaB independent inhibition of lipopolysaccharide-induced cyclooxygenase by a conjugated linoleic acid cognate, conjugated nonadecadienoic acid.Biochim Biophys Acta. 2006 Sep;1761(9):969-72.

Park Y, Yang H, Storkson JM, Albright KJ, Liu W, Lindsay RC, Pariza MW. Controlling acrylamide in French fry and potato chip models and a mathematical model of acrylamide formation: acrylamide: acidulants, phytate and calcium. Adv Exp Med Biol. 2005;561:343-56.

Park Y, Storkson JM, Liu W, Albright KJ, Cook ME, Pariza MW. Structure-activity relationship of conjugated linoleic acid and its cognates in inhibiting heparin-releasable lipoprotein lipase and glycerol release from fully differentiated 3T3-L1 adipocytes. J Nutr Biochem. 2004 Sep;15(9):561-8.

Kang K, Miyazaki M, Ntambi JM, Pariza MW. Evidence that the anti-obesity effect of conjugated linoleic acid is independent of effects on stearoyl-CoA desaturase1 expression and enzyme activity. Biochem Biophys Res Commun. 2004 Mar 12;315(3):532-7.

Kang K, Liu W, Albright KJ, Park Y, Pariza MW. trans-10,cis-12 CLA inhibits differentiation of 3T3-L1 adipocytes and decreases PPAR gamma expression. Biochem Biophys Res Commun. 2003 Apr 11;303(3):795-9.