Alan G. Watts
Department of Biological Sciences
Fellow, American Association for the Advancement of Science (AAAS)
Past-President, The Society for the Study of Ingestive Behaviors
- Systems neuroscience
- Neural control of metabolism
- Ingestive behaviors
- Diabetes & Obesity
Research OverviewThe increasing prevalence of obesity has pathological consequences for the health of populations in many countries, both developed and less well developed. In particularly, obesity is often associated with type 2 diabetes (T2D) and cardiovascular disease. For many years the brain's role in generating obesity and diabetes went more or less unrecognized. But much work during the past 25 years has quite clearly identified the brain as both a driver and a target of the complications of obesity and diabetes.
The brain controls eating behavior, and has major influences on the release of energy-controlling hormones, and on liver, pancreatic, gut, and fat (adipose) tissue function. But it also responds, often detrimentally, to the consequences of obesity and T2D. For example, hyperglycemia, hypoglycemia, hyperinsulinemia, insulin resistance, dyslipidemia, and increased inflammatory signals all take their toll on brain function, and in some cases lead to cognitive impairment and increased incidence of Alzheimer?s disease.
To control energy balance and metabolism the brain receives a large number of powerful signals from the environment, the gut, and the bloodstream that it uses to organize appropriate behavioral autonomic, and endocrine functions. In diseases states these functions can be inappropriate and detrimental. The goal of my work is to determine the functional organization of the brain networks that organize and control energy metabolism in response to these signals.
In particularly we are interested in how the brain controls glucose metabolism (particularly in the liver and pancreas), adipose tissue function, and eating behavior. Our overall goal is to understand how the brain is organized to control these key functions and how they change with diabetes and obesity. To do this we use a range of physiologically centered manipulations, selective methods to disrupt the functions of specific neuronal pathways, and sophisticated neural tracing that can reveal the organization of neural connections in exquisite detail.
My full PubMed publication list is here
Hedco Neuroscience Building, Rm 416
3641 Watt Way
Los Angeles, CA 90089
- BSc (Hons): University of Wales, UK
- D.Phil: University of Oxford, UK
- Post-Doc: Salk Institute, La Jolla, CA
Selected PublicationsView a complete PubMed searchView a complete Google Scholar search
Jokiaho, A J., Donovan, C.M. & Watts, A.G. (2014). The rate of fall of blood glucose during hypoglycemia determines the necessity of forebrain-projecting catecholaminergic neurons for male rat adrenomedullary responses. Diabetes 68: 2854-65.PubMed
- Watts, A.G. (2014) How do we know if the brain is wired for type 2 diabetes? Current Diabetes Reports 14: 465. PubMed
- Watts, A.G. & Khan, A.M. (2013) Identifying links in the chain: The dynamic coupling of catecholamines, peptide synthesis, and peptide release in hypothalamic neuroendocrine neurons. Advances in Pharmacology 68: 421-444. PubMed
- Kaminski, K.L. & Watts, A.G. (2012) Intact catecholamine inputs to the forebrain are required for appropriate regulation of CRH and vasopressin gene expression by corticosterone in the rat paraventricular nucleus. J. Neuroendocrinology 24: 1517-1526. PubMed
- Khan, A.M., Kaminski, K.L., Sanchez-Watts, G., Ponzio T.A., Kuzmiski, J.B., Bains, J.S., & Watts, A.G. (2011) MAP kinases couple hindbrain-derived catecholamine signals to hypothalamic adrenocortical control mechanisms during glycemia-related challenges. J. Neuroscience 31: 18479 â18491. PubMed
- Watts, A.G. & Donovan, C.M. (2010) Sweet talk in the brain: glucosensing, neural networks, and hypoglycemic counterregulation. Frontiers in Neuroendocrinology 31: 32-43. PubMed