Here's a new paper out in Nature Neuroscience that explores the ability of the hypothalamus to sense the nutritional status of the body and modulate hunger in response.Malonyl-coenzyme A is a very interesting protein that has recently been proposed to play a central role in this pathway. Malonyl-CoA in the brian is induced by feeding and is suppressed by fasting. Here the authors treated rats with a virus encoding a protein that breaks down malonyl Co A, which resulted in rats that chronically had too little malonyl-CoA in their hypothalamus. This caused a major disruption in nutrient sensing in the hypothalamus, and led to hyperphagia and obesity in the rats. This raises the question of whether defective nutrient sensing might play a role in hyperphagia in PWS.
Molecular disruption of hypothalamic nutrient sensing induces obesity
He W, Lam TKT, Obici S & Rossetti L. Nature Neuroscience 9, 227 - 233 (2006)
Theresa Strong
Theresa V. Strong, Ph.D., received a B.S. from Rutgers University and a Ph.D. in Medical Genetics from the University of Alabama at Birmingham (UAB). After postdoctoral studies with Dr. Francis Collins at the University of Michigan, she joined the UAB faculty, leading a research lab focused on gene therapy for cancer and directing UAB’s Vector Production Facility. Theresa is one of the founding members of FPWR and has directed FPWR’s grant program since its inception. In 2016, she transitioned to a full-time position as Director of Research Programs at FPWR. She remains an Adjunct Professor in the Department of Genetics at UAB. She and her husband Jim have four children, including a son with PWS.
