Because of a lapse in government funding, the information on this website may not be up to date, transactions submitted via the website may not be processed, and the agency may not be able to respond to inquiries until appropriations are enacted.
The NIH Clinical Center (the research hospital of NIH) is open. For more details about its operating status, please visit
Updates regarding government operating status and resumption of normal operations can be found at

U.S. Department of Health and Human Services
Lee Weinstein

 Contact Info

Tel: 301-402-2923

 Select Experience

  • ChiefMetabolic Diseases Branch, NIDDK2016-present
  • Acting ChiefMetabolic Diseases Branch, NIDDK2011-2016
  • Senior InvestigatorMetabolic Diseases Branch, NIDDK2000-present
  • M.D.Columbia University College of Physicians and Surgeons1983
  • B.S.Massachusetts Institute of Technology1979

 Related Links

  • Cell Biology/Cell Signaling
  • Clinical Research
  • Endocrinology
  • Genetics/Genomics
  • Molecular Biology/Biochemistry
  • Neuroscience/Neurophysiology/Neurodevelopment
Research Summary/In Plain Language

Research in Plain Language

Our lab studies the genetic regulation, chemical processes, and functional role of the Gsα protein, which is required for accumulation of the chemical messenger cyclic adenosine monophosphate (cAMP) inside cells.  Our lab studied both a human disease (Albright hereditary osteodystrophy, or AHO) that is associated with mutations in the Gsα-subunit gene and a mouse model with an intentionally inactivated Gsα-subunit gene.  Through these studies our lab demonstrated that, in some tissue, the copy of the Gsα-subunit gene inherited from the father is inactive due to a process called genomic imprinting.  This explains why maternal inheritance leads to a form of AHO that is associated with obesity and resistance to multiple hormones (pseudohypoparathyroidism type 1a, or PHP1a), while paternal inheritance is not.  We are continuing to study these patients in great detail and are developing various genetically engineered mouse models with deletion of the gene in order to understand its role in the development of obesity and diabetes.