University of California, Riverside

School of Medicine

Faculty Biographies

School of Medicine: Nicholas V. DiPatrizio

Nicholas V. DiPatrizio

Nicholas V. DiPatrizio

Assistant Professor of Biomedical Sciences

Nicholas V. DiPatrizio

University of California, Riverside
Riverside, CA 92521
Tel: (951) 827-7252
Office: 215 School of Medicine Research Building

Education and Training

  • B.A., Psychology, Temple University, 2001
  • Ph.D., Neuroscience, Drexel University College of Medicine, 2008
  • Postdoctoral Fellow, University of California, Irvine, School of Medicine, 2014

Research Summary

The DiPatrizio laboratory is dedicated to elucidating the integrative neurobiology and physiology that controls food reward, sensory processing, and energy balance. A combination of state-of-the-art analytical (i.e., ultra-performance liquid chromatography/tandem mass spectrometry), genetic (i.e., first-of kind genetic mutant mice with conditional organ-selective knockout of cannabinoid CB1Rs), surgical, biochemical, molecular, pharmacological, and behavioral tools are employed to achieve these goals. Importantly, our research program investigates the molecular and neural underpinnings of obesity and hedonic eating, which are suggested to share characteristics with addictive and compulsive behaviors. This work will support the discovery and development of novel therapeutic strategies to safely treat obesity, cardiovascular disease, and diabetes.

The Big Picture

Humans and other mammals have an adaptive advantage in seeking and ingesting palatable fat-rich foods, which are nutritionally vital, but are generally scarce in natural habitats. The same biological processes that supported survival under feast-or-famine conditions in the past, however, can become maladaptive in contemporary societies where fatty foods are readily available and the energy necessary to find them is minimal. This presumably innate drive to consume energy-rich foods can contribute to obesity and associated metabolic disorders, which place an enormous burden on our health care system, and reduce longevity and quality of life. Despite promising advances in the field made to date, the molecular and neural mechanisms that control dietary fat preference and compulsive eating – among many complex behaviors – remain largely unknown. Consequently, it is essential for scientists to not merely identify the individual physiological mechanisms that control food intake, energy homeostasis, and reward, but to also view these processes as inextricably integrated. No organ or signaling pathway is in a physiological vacuum.

Endocannabinoids and the Gut-Brain Axis

A research emphasis in the DiPatrizio laboratory is on the lipid messengers, the endocannabinoids, which are “thrifty lipids” that naturally drive the seeking and sensing of calorie-dense foods, and the storage of their energy content for future use. Growing evidence suggests that gustatory signals from dietary fat drive its intake in mammals, and a portion of our work suggests a critical role for gut-brain endocannabinoid signaling in controlling this attraction to fatty foods. For example, tasting dietary fat stimulates endocannabinoid signaling in the rodent small intestine through vagal cholinergic neurotransmission, and this local signaling event in the gut is thought to provide positive feedback to the brain to promote intake and preference for high-energy palatable foods. Thus, the endocannabinoid system is proposed to be selected by evolution due to its ability to maximize the probability of survival in natural environments where feast is commonly followed by famine. In modern environments where food is plentiful, however, excessive endocannabinoid signaling in the brain and periphery may contribute to the “addiction-like” phenotype inherent to compulsive eating, and promote obesity.

The DiPatrizio laboratory is funded by grants from the National Institutes of Health.

Awards, Honors, & Fellowships

  • NIH K99/R00 Pathway to Independence grant award from the National Institute on Drug Abuse, 2013.
  • Society for the Study of Ingestive Behavior Test Diet® Award for achievements in, and contributions to, the field of ingestive behavior, 2011.
  • Society for Neuroscience Postdoctoral Trainee Award, 2010.
  • National Institute on Drug Abuse Early Career Investigator Award, 2009.
  • Society for the Study of Ingestive Behavior New Investigator Award, Paris, France, 2008.
  • National Institute on Aging Postdoctoral Fellowship, University of California, Irvine, School of Medicine, 2008.
  • American Society for Pharmacology and Experimental Therapeutics award for Systems and Integrative Pharmacology, 2006.

Selected Publications

  • Price C, Argueta  DA, Medici V, Bremer AA, Lee V, Nunez MV, Chen GX, Keim NL, Havel PJ, Stanhope KL,  DiPatrizio  N.V. Plasma fatty acid ethanolamides are associated with postprandial triglycerides, ApoCIII and ApoE in humans consuming high fructose corn syrup (HFCS)-sweetened beverage.  American Journal of Physiology, Endocrinology and Metabolism, 2018; ePub ahead of print.

  • Angelini R, Argueta DA, Piomelli D, DiPatrizio NV. (2017) Identification of a widespread palmitoylethanolamide contamination in standard laboratory glassware. Cannabis and Cannabinoid Research. 2(1) 123-132.
  • Argueta DA and DiPatrizio NV. (2017) Peripheral endocannabinoid signaling controls hyperphagia in western diet-induced obesity. Physiology and Behavior. 171: 32-39.

  • Thompson Z, Argueta D, Garland Jr. T, DiPatrizio NV.  (2017) Circulating levels of endocannabinoids respond acutely to voluntary exercise, are altered in mice selectively bred for high voluntary wheel running, and differ between the sexes. Physiology and Behavior.

  • DiPatrizio NV. (2016) Endocannabinoids in the gut. Cannabis and Cannabinoid Research. 1(1) 67-77.

  • DiPatrizio NV, Igarashi M, Narayanaswami V, Murray C, Gancayco J, Russell A, Jung KM, Piomelli D. (2015) Fasting stimulates 2-AG biosynthesis in the small intestine: role for cholinergic pathways. American Journal of Physiology.

  • DiPatrizio NV and Piomelli D. (2015) Intestinal lipid-derived signals that sense dietary fat. Journal of Clinical Investigation. 125(3) 891-8.

  • DiPatrizio NV. (2014) Is fat taste ready for primetime? Physiology and Behavior. 136:145-54.
  • DiPatrizio NV, Joslin A, Jung KM, and Piomelli D (2013) Endocannabinoid signaling in the gut mediates preference for dietary unsaturated fats. FASEB Journal. 27(6)2313-20.

  • DiPatrizio NV and Piomelli D. (2012) The thrifty lipids: endocannabinoids and the neural control of energy conservation. Trends in Neurosciences. 35(7) 403-11.

  • Jung KM, Clapper J, Fu J, D’Agostino, G, Guijarro A, Thongkham D, Avanesian A, Astarita G, DiPatrizio NV, Frontini A, Cinti S, Diano S, and Piomelli D. (2012) 2-arachidonoylglycerol signaling in forebrain regulates systemic energy metabolism. Cell Metabolism. 15:299-310. 

  • Jung, KM, Sepers M, Henstridge CM, Lassalle O, Neuhofer D, Martin H, Ginger M, Frick A, DiPatrizio NV, Mackie K, Katona I, Piomelli D, and Manzoni OJ. (2012) Uncoupling of the endocannabinoid signaling complex in a mouse model of fragile X syndrome. Nature Communications. (3)1080.                                                

  • DiPatrizio NV, Astarita G, Schwartz GJ, Li X, and Piomelli D. (2011) From the cover: Endocannabinoid signal in the gut controls dietary fat intake. Proceedings of the National Academy of Sciences, USA. 108(31) 12904-8. *Featured in the New York Times, Science Times, “When Fatty Feasts are Driven by Overdrive”; July 12, 2011.

  • *Fu J, *DiPatrizio NV, Guijarro A, Schwartz GJ, Li X, Gaetani S, Astarita G, and Piomelli D. (2011) Sympathetic activity regulates fat-induced OEA signaling in the small intestine. Journal of Neuroscience. 31(15):5730-36. *Authors contributed equally.

  • DiPatrizio NV and Simansky KJ. (2008) Activating parabrachial cannabinoid CB1Rs selectively stimulates intake of palatable foods in rats. Journal of Neuroscience. 28(39):9702-9.

  • DiPatrizio NV and Simansky KJ. (2008) Inhibiting parabrachial fatty acid amide hydrolase activity selectively increases the intake of palatable foods via cannabinoid CB1 receptors. Am J Physiol Regul Integr Comp Physiol. 295(5):R1409-14.

  • Jarbe T and DiPatrizio NV. (2005) Delta9-tetrahydrocannabinol induced hyperphagia and tolerance assessment: Interactions between the CB1 receptor agonist delta9-THC and the CB1 receptor antagonist SR-141716 (rimonabant) in rat. Behav Pharmacol. 16:373-380.

  • Jarbe T, Andrzejewski M and DiPatrizio NV. (2002) Interactions between the CB1 receptor agonist Delta 9-THC and the CB1 receptor antagonist SR-141716 in rats: open-field revisited. Pharmacol Biochem Behav. 73(4);911-9.

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