Sunday afternoon’s Physiology of Nervous System Detection of Hypoglycemia symposium will feature four lectures highlighting the latest research into the complex network of neurons involved in glucose homeostasis. The two-hour symposium begins at 2:15 p.m. in room 6DE.
Vanessa H. Routh, PhD
Vanessa H. Routh, PhD, Professor of Pharmacology, Physiology and Neurosciences at Rutgers New Jersey Medical School, will open the symposium with a 30-minute lecture titled “Brain Glucose Sensing Neurons in Hypoglycemia Detection.”
Dr. Routh will provide an overview of the mechanisms of glucose sensing in glucose-inhibited (GI) neurons and discuss the effects of oxidative stress on glucose sensing and hypoglycemia counterregulation. She also will explore the protective effects of the glutathione precursor N-acetylcysteine on hypoglycemia counterregulation and GI neuronal glucose-sensing after recurrent hypoglycemia.
“Impaired counterregulation following recurrent hypoglycemia is the major limiting factor in treating diabetes with insulin therapy,” Dr. Routh explained. “Our data suggest that antioxidant treatment can preserve hypoglycemia counterregulation after recurrent hypoglycemia or in type 1 diabetes.”
In their research, Dr. Routh and her colleagues work from the hypotheses that the maintenance of energy balance is a critical function of the brain, exploring specialized glucose-sensing neurons that sense and respond to nutrient and hormonal changes. They are investigating how the glucose sensitivity of hypothalamic glucose-sensing neurons is regulated.
The session’s second presenter, David H. McDougal, PhD, will present “Role of Astrocytes in the Central Nervous System Response to Hypoglycemia.” Dr. McDougal, Assistant Professor of Research at Louisiana State University’s Pennington Biomedical Research Center, is investigating the underlying causes of chronic hypoglycemia in diabetes patients.
The symposium will also feature a presentation from Jonathan N. Flak, PhD, who will discuss “Leptin-Regulated Neurons and Counterregulatory Response to Hypoglycemiatem Response to Hypoglycemia.” Dr. Flak, a Research Investigator of Internal Medicine-Metabolism, Endocrinology, and Diabetes at the University of Michigan Health System, received a 2017 Pathway to Stop Diabetes® research grant for his project “Targeting the VMN to Understand Hypoglycemia Pathogenesis.”
Casey Donovan, PhD
Casey Donovan, PhD, Professor of Biological Services at the University of Southern California, will close the session with a 30-minute lecture titled “Peripheral Hypoglycemic Detection at the Portal-Mesenteric Vein.” He will review how portal-mesenteric vein (PMV) glucosensors detect hypoglycemia, the impact of antecedent hypoglycemia on the sensors, and the mechanisms of PMV glucose detection.
Dr. Donovan, who has investigated PMV glucosensors for about two decades, said that while most experts acknowledge the role PMV glucosensors play in detecting slow-onset hypoglycemia (<-0.1mM/min), many fail to appreciate their clinical importance.
“It turns out they should be relevant because the vast majority of clinical hypoglycemic episodes happen slowly,” Dr. Donovan said. “In fact, many happen much more slowly than we study. The PMV glucosensors are not peripheral sensors in the sense that they are secondary. They probably provide a primary source of glucosensory input for most hypoglycemic episodes.”
During his presentation, Dr. Donovan will review and expand on work presented last year showing that PMV and central nervous system glucose-sensory inputs are integrated to yield the appropriate counterregulatory response. He will emphasize that work on the brain and peripheral glucose sensing shouldn’t be viewed in an “us versus them” context, but rather as a large, integrated network of glucose-sensing neurons defending against hypoglycemia.
“This type of neural network really characterizes many homeostatic systems, not just glucose homeostasis,” he said. “For example, when we talk about temperature regulation or blood pressure, these homeostatic systems all involve an exchange between peripheral and central sensors.”
