Graduate Studies Faculty

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Daniel L. Marks, M.D., Ph.D.

Professor, Pediatric Endocrinology
Member, Knight Cancer Institute
Director, Oregon Child Health Research Center
Admin Unit: SOM-Pediatrics Department
Phone: 503-494-6218
Lab Phone: 503-494-5948
Fax: 503-494-1933
Office: BRB 315
Mail Code: L 481
Neuroscience Graduate Program
Research Interests:
melanocortin cachexia neuroendocrinology obesity diabetes weight regulation inflammation neuroscience pediatrics pediatric endocrinology medical » Click here for more about Dr. Marks's research » PubMed Listing
Preceptor Rotations
Dr. Marks has not indicated availability for preceptor rotations at this time.
Faculty Mentorship
Dr. Marks has not indicated availability as a mentor at this time.

Summary of Current Research

Cachexia, or disease-associated wasting, is a devastating metabolic disorder with relative anorexia, increased metabolic rate, and loss of lean body mass as its primary features. It is an important determinant of survival and quality of life in a number of disorders in children including cancer, AIDS, renal failure, cystic fibrosis, and Alzheimer's disease.

The central melanocortin system has been shown to be critical for the regulation of body weight, and appears to be the primary neural system involved in the tonic inhibition of feeding and maintenance of a normal metabolic rate. My studies have demonstrated that blockade of melanocortin signaling through the type 4 melanocortin receptor (MC4-R) dramatically attenuates the cachexia that is normally observed in animal models of acute and chronic disease including cancer, renal failure, and models of chronic infection. We have also shown that blocking the type 3 melanocortin receptor (MC3-R) enhances the susceptibility to cachexia in these disease states, probably due to the loss of the autoinhibitory feedback effect of the MC3-R on POMC neurons.

Our most recent work has provided a demonstration that POMC neurons are activated by cytokines  and that these neurons express receptors for several anorexigenic cytokines. Collectively, our work supports the hypothesis that cachexia is caused by the action of circulating factors (primarily cytokines) on the hypothalamic melanocortin system, with a resultant activation of this system leading to hypophagia, increased metabolic rate, and loss of lean body mass.

Recent Publications


  • M.D., University of Washington, Seattle, 1995
  • Ph.D., Physiology & Neurobiology, University of Washington, Seattle, 1993
  • B.S., Biology, University of Oregon, Eugene, 1988

Previous Positions

Non-Academic Interests