"We discovered that the neural pathways that carry OT to its sites of action in the brain don't mature until a few weeks after birth in rats," Rinaman reported, "and we've also found that OT contributes to the well-known effect of dehydration to inhibit food intake in mature rats and mice, but not in baby rats."
Now, she said "we (with University of Pittsburgh research colleagues Janet Amico and Regis Vollmer) have shown that 'dehydration anorexia' is virtually absent in mice that have been genetically engineered to eliminate OT." That is, so-called OT-null mice ate their regular amount of food even when they were dehydrated, which normally reduces the amount eaten. This followed earlier work where the ability of dehydration to inhibit food intake in rats was attenuated by blocking central OT receptors.
"These and other findings support the view that OT is a key signaling peptide in hypothalamic control of adaptive responses to dehydration," Rinaman said, as well as that "the hindbrain appears to be a key target region through which the effects of OT are exerted."
Rinaman is speaking at the American Physiological Society's 2005 Conference, "Neurohypophyseal Hormones: From Genomics and Physiology to Disease," plus the latest developments toward clinical applications, July 16-20 in Steamboat Springs, Colorado.
Next steps will consider if OT's role is situation-specific
Rinaman said she and her colleagues are interested in determining "the special role that OT may have to control food intake under certain situations, but not in others. We think that oxytocin might normally act in the brain to inhibit intake only in certain types of feeding or drinking situations. If we can pinpoint the types of situations, we'll learn more about how OT and other peptides may function under unique environmental conditions."
"Oxytocin and ingestive behavior." Linda Rinaman, University of Pittsburgh. NIH grant.
Rinaman is participating in the symposium "Central release and actions of NH hormones," chaired by Quentin Pittman of University of Calgary, Canada, and Larry Young, Emory University School of Medicine.
Arrangements for on-site interviews, or telephone interviews during the meeting, can be through APS from Mayer Resnick (cell: 301.332.4402; office 301.634.7209, or mresnick@the-aps.org).
Sponsorships. The American Physiological Society thanks the following sponsors for their generous support of the conference: Astellas Pharmaceuticals Inc., GlaxoSmithKline Pharmaceuticals, NIH/NIDDK, Wyeth Research and Olympus America Inc.
Three APS Journals call for papers. In conjunction with the conference, three American Journal of Physiology (AJP) editions – AJP-Regulatory, Integrative and Comparative Physiology, AJP-Endocrinology and Metabolism, and AJP-Renal Physiology – have called for related papers for publication. The deadline for all editions is October 1, 2005.
The American Physiological Society was founded in 1887 to foster basic and applied bioscience. The Bethesda, Maryland-based society has more than 10,000 members and publishes 14 peer-reviewed journals containing almost 4,000 articles annually.
APS provides a wide range of research, educational and career support and programming to further the contributions of physiology to understanding the mechanisms of diseased and healthy states. In May 2004, APS received the Presidential Award for Excellence in Science, Mathematics and Engineering Mentoring (PAESMEM).