Catia Sternini, MD

Professor, Vatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at UCLA

Dr. Sternini is Associate Director CURE: DDRCC, Director of the Morphology and Cell Imaging Core and Chair of the CURE Pilot and Feasibility Study Program. Her research program is concerned with the neuronal circuits that control gastrointestinal motility, the mechanisms that govern receptor-mediated responses in the enteric nervous system, and chemosensing in the gastrointestinal tract. Currently, the main lines of her research include: (1) trafficking and signaling of G protein-coupled receptors induced by physiological and pathophysiological events with an emphasis on µ opioid receptor, the target of opiate analgesics used for pain control, which mediates opioid bowel syndrome and tolerance, and (2) role of taste signaling molecules in the regulation of gastrointestinal functions and feeding behavior. Her group was the first to demonstrate that opiates differing in their ability to induce tolerance also differ in their efficiency to induce µOR trafficking, a process that regulates receptor signaling and function, and that chronic opiate treatment may affect ligand ability to induce receptor endocytosis depending upon changes in the expression of trafficking proteins. The findings of ligand-selective and stimulation-dependent µ opioid receptor internalization in enteric neurons are of importance for understanding the mechanisms underlying intracellular adaptations induced by prolonged activation of µ opioid receptors, which hamper the use of opiates as analgesics and contributes to the development of the opioid bowel syndrome.  Another focus of her research is on the role of taste signaling molecules as chemosensors in the gut mucosa, which are likely to modulate gut function and food intake through the release of signaling molecules by enteroendocrine cells, with emphasis on bitter taste receptors, a putative side of defense from potentially toxic substances, drugs and pathogens. The recent discovery that taste receptors for sweet and bitter are expressed throughout the body and not only in the tongue has given rise to the concept of a broader role for these receptors beyond “taste”. The finding that taste signaling molecules are expressed by distinct populations of mucosal cells, including enteroendocrine cells, which synthesize peptides affecting motility, secretion, satiety and hunger, and that bitter taste receptors are regulated by feeding and different diets, support the concept that they participate in the functional detection of intraluminal content and might serve as regulators of diet-induced responses as well as defense mechanisms toward toxins and bacteria.