February 26, 2004
Feeding behavior: Studying how the cycles and signals work
A table set with china, linen, silverware, and flowers is a civilized garnish for a basic survival mechanism: feeding. Hunger prods people and animals to seek life-sustaining energy in the form of food. Loss of appetite, if it goes unabated, can be deadly. Overeating endangers health, too.
To stay well, the body has to balance its energy and nutrient intake, both short term and long term, and its energy and nutrient expenditures. For most animals and for most of human history, food has not always been easy to get. That’s why the body protects its energy stores from famine. To further complicate matters, bearing offspring also taps into energy stores.
Because eating is central to the continuation of the individual and the species, people and animals have evolved many physiological mechanisms that initiate feeding behaviors. Mammals have an array of controls, regulators, feedback
mechanisms, and internal signals that spell hunger, cravings, and satiety and that inventory the body’s nutrient stores. Many signals act on the brain and the gut to set off hunger pangs and to drive appetite and eating.
How the nervous system integrates feeding behaviors, using up nutrients, and maintaining body weight, and how this circuitry strives to achieve a metabolic steady state, are the research interests of this year’s WWAMI Science in Medicine lecturer, Dr. W. Sue Ritter. She is a professor of veterinary and comparative anatomy, pharmacology and physiology at Washington State University’s College of Veterinary Medicine. She is also a researcher in WSU’s Programs in Neuroscience, and its Center for Reproductive Biology. Ritter has taught first-year UW medical students in the WWAMI Program at the University of Idaho/Washington State University.
Ritter will speak on “Feeding Your Hungry Brain” at noon, Thursday, March 11, in Hogness Auditorium, room A-420 of the Health Sciences Center. Her lecture is free and open to all interested persons.
Ritter studies the role of the brain’s glucose-sensing cells and the neural pathways that link these receptor cells to control sites in the brain. The brain requires glucose as its metabolic fuel. The brain can’t store glucose, but has an early warning when its fuel tanks are nearing empty. Because glucose deprivation can be lethal, sensitive detectors fire off powerful nerve, hormonal and behavioral control signals to try to restore normal glucose levels. The crisis intervention includes increased adrenal medullary secretion, increased corticosterone and glucagon secretion, and increased food intake. Ritter’s laboratory results suggest that catacholamine neurons in the hindbrain are essential mediators for these responses, and couple glucoreceptor cells to neurons in the forebrain and the spine.
Ritter went on to note that deficits in glucoreceptor function are life threatening and could be part of the pathology behind a condition observed in some diabetes patients on intensive insulin therapy, in which their brains don’t respond to stave off low blood sugar. As a consequence, these patients can experience autonomic failure, which can weaken the circulatory, respiratory, digestive, and body temperature regulating systems. It is thought that previous episodes of very low blood sugar cause brain receptors to become less responsive to subsequent drops in blood glucose levels.
Glucoreceptive cells, which drive appetite, may also be one of the contributors to disorders of body weight regulation, according to Ritter.
She also studies the responses of the female reproductive system to glucose deficits. Chronic glucose deficits suppress the natural cycle in which female mammals come into seasonal receptivity to mating. Ritter’s team is examining the locus of the glucose-sensing cells that determine the need for this suppression, and hopes to identify the associated neurons that link the glucose-sensing cells to parts of the brain that control estrus, or the fertile time during which the female can mate.
Ritter wrote that she “came upon the field of neuroscience by walking around during my last semester of undergraduate school and bumping into it.” She had changed career interests three or four times in school, then took a semester off to work. She ended up as a helper in the lab of a sleep physiologist, who insisted that she read journal articles, invited her on pediatric neurology rounds, gave her Marie Curie’s biography to read, and introduced her to science graduate students. The mentorship put her on the path to becoming a neuroscientist, and gave her the will to persevere despite others who discouraged women in science.
Ritter described what brought her to her studies of the physiology of hunger: “I have always been fascinated by the grasp of biological need on brain function. I’ve studied this through the narrower question of how an animal’s need for glucose is detected and translated into neural signals that orchestrate the multiple levels of response required to reduce that need. Detection of glucose deficit activates systems that seemingly or maybe actually commandeer the animal’s entire response network. The animal’s life is instantly reorganized, priorities are dramatically altered, sensation is redirected, physiology is changed from cells to systems, and reproductive capacity is put on hold. The animal is driven to find and consume food, while its physiology meters out the remaining metabolic fuels. This is amazing. How does it happen?”
Ritter will look at that question during her March 11 Science in Medicine talk.
Each year the UW School of Medicine sponsors an outstanding scientist from one of the other five universities in the WWAMI (Washington, Wyoming, Alaska, Montana, and Idaho) regionalized medical education program to come to the UW to give a presentation on his or her research and to meet with UW faculty, fellows, and students.
