About

Douglas Elmendorf is a professor of public policy at Harvard University's Kennedy School of Government, holding the title of Lucius N. Littauer Professor of Public Policy and Harvard University Distinguished Service Professor. He was named dean of the Kennedy School in June 2015 and stepped down from that role in June 2024. Elmendorf has a distinguished background working on budget policy, monetary policy, macroeconomic analysis and forecasting, health care, Social Security, income security programs, and financial markets. His previous roles include serving as director of the US Congressional Budget Office from January 2009 through March 2015, as well as being a senior fellow at the Brookings Institution, assistant director of the Division of Research and Statistics at the Federal Reserve Board, deputy assistant secretary for economic policy at the US Treasury Department, senior economist at the White House’s Council of Economic Advisers, and assistant professor at Harvard University. He earned his PhD and AM in economics from Harvard University and his AB summa cum laude from Princeton University.

Research topics

• Biology
• Endocrinology
• Neuroscience
• Immunology
• Cell biology
• Medicine
• Internal medicine
• Genetics

Selected publications

• Enteroendocrine cell lineages that differentially control feeding and gut motility

  eLife · 2023 · 58 citations

  • Biology
  • Cell biology
  • Endocrinology

  knock-in mice) to restrict reporter expression to intestinal epithelium. Combined use of Cre and Flp alleles effectively targeted major transcriptome-defined enteroendocrine cell lineages that produce serotonin, glucagon-like peptide 1, cholecystokinin, somatostatin, or glucose-dependent insulinotropic polypeptide. Chemogenetic activation of different enteroendocrine cell types variably impacted feeding behavior and gut motility. Defining the physiological roles of different enteroendocrine cell types provides an essential framework for understanding sensory biology of the intestine.

  PublisherDOI

• Author response: Enteroendocrine cell lineages that differentially control feeding and gut motility

  2023-02-08 · 2 citations

  peer-reviewOpen access
  PublisherDOI

• Prefrontal cortex melanocortin 4 receptors (MC4R) mediate food intake behavior in male mice

  Physiology & Behavior · 2023 · 8 citations

  • Neuroscience
  • Biology
  • Endocrinology

  BACKGROUND: Melanocortin 4 receptor (MC4R) activity in the hypothalamus is crucial for regulation of metabolism and food intake. The peptide ligands for the MC4R are associated with feeding, energy expenditure, and also with complex behaviors that orchestrate energy intake and expenditure, but the downstream neuroanatomical and neurochemical targets associated with these behaviors are elusive. In addition to strong expression in the hypothalamus, the MC4R is highly expressed in the medial prefrontal cortex, a region involved in executive function and decision-making. METHODS: Using viral techniques in genetically modified male mice combined with molecular techniques, we identify and define the effects on feeding behavior of a novel population of MC4R expressing neurons in the infralimbic (IL) region of the cortex. RESULTS: Here, we describe a novel population of MC4R-expressing neurons in the IL of the mouse prefrontal cortex that are glutamatergic, receive input from melanocortinergic neurons, and project to multiple regions that coordinate appetitive responses to food-related stimuli. The neurons are stimulated by application of MC4R-specific peptidergic agonist, THIQ. Deletion of MC4R from the IL neurons causes increased food intake and body weight gain and impaired executive function in simple food-related behavior tasks. CONCLUSION: Together, these data suggest that MC4R neurons of the IL play a critical role in the regulation of food intake in male mice.

  PublisherDOI

• Prefrontal cortex melanocortin 4 receptors (MC4R) mediate food intake behavior in mice

  bioRxiv (Cold Spring Harbor Laboratory) · 2022-06-02

  preprintOpen access

  Abstract Background Melanocortin 4 receptor (MC4R) activity in the hypothalamus is crucial for regulation of metabolism and food intake. The peptide ligands for the MC4R are associated with feeding, energy expenditure, and also with complex behaviors that orchestrate energy intake and expenditure, but the downstream neuroanatomical and neurochemical targets associated with these behaviors are elusive. In addition to strong expression in the hypothalamus, the MC4R is highly expressed in the medial prefrontal cortex, a region involved in executive function and decision-making. Methods Using viral techniques in genetically modified mice combined with molecular techniques, we identify and describe the neuronal dynamics, and define the effects on feeding behavior of a novel population of MC4R expressing neurons in the infralimbic region of the cortex. Results Here, we describe a novel population of MC4R-expressing neurons in the infralimbic (IL) region of the mouse prefrontal cortex that are glutamatergic, receive input from melanocortinergic neurons of the arcuate hypothalamus, and project to multiple regions that coordinate appetitive responses to food-related stimuli. The neurons are depolarized by application of MC4R-specific peptidergic agonist, THIQ. Deletion of MC4R from the IL neurons causes increased food intake and body weight gain and impaired executive function in simple food-related behavior tasks. Conclusion Together, these data suggest that MC4R neurons of the IL play a critical role in the regulation of food intake.

  PublisherOA PDFDOI

• Enteroendocrine cell lineages that differentially control feeding and gut motility

  bioRxiv (Cold Spring Harbor Laboratory) · 2022-03-20 · 2 citations

  preprintOpen access

  SUMMARY Enteroendocrine cells are specialized sensory cells of the gut-brain axis that are sparsely distributed along the intestinal epithelium. The functions of enteroendocrine cells have classically been inferred by the gut hormones they release. However, individual enteroendocrine cells typically produce multiple, sometimes apparently opposing, gut hormones in combination, and some gut hormones are also produced elsewhere in the body. Here, we developed approaches involving intersectional genetics to enable selective access to enteroendocrine cells in vivo . We constructed Villin1-p2a-FlpO knock-in mice to restrict reporter expression to intestinal epithelium and through combined use of Cre and Flp alleles, effectively targeted major transcriptome-defined enteroendocrine cell lineages that produce serotonin, glucagon-like peptide 1, cholecystokinin, somatostatin, or glucose insulinotropic peptide. Chemogenetic activation of different enteroendocrine cell types variably impacted feeding behavior, nausea-associated behaviors (conditioned flavor avoidance), and gut motility. Defining the physiological roles of different enteroendocrine cell types provides an essential framework for understanding sensory biology of the intestine.

  PublisherDOI

• Finance company failure in New Zealand during 2006–2009: Predictable failures?

  Journal of Contemporary Accounting & Economics · 2014-10-31 · 16 citations

  article1st author
  PublisherDOI

Frequent coauthors

• Fiona M. Gribble

  University of Cambridge

  12 shared

• Frank Reimann

  University of Cambridge

  12 shared

• Stephen D. Liberles

  Harvard University

  8 shared

• Judith A. Kaye

  8 shared

• Narendra R. Joshi

  Howard Hughes Medical Institute

  8 shared

• Marito Hayashi

  Howard Hughes Medical Institute

  8 shared

• Vadim Y. Bolshakov

  Harvard University

  4 shared

• Angela Kim

  Beth Israel Deaconess Medical Center

  4 shared