Ralph Rabkin
Academic Appointments
- Emeritus Faculty, Acad Council, Medicine - Nephrology
Key Documents
Contact Information
- Academic Offices
Personal Information Email Tel (650) 858-3985
Professional Overview
Honors and Awards
- Fellow, American Heart Association (2003)
- Training Award, Juvenile Diabetes Foundation International (1989)
- Member, American Society of Clinical Investigators, American Society of Clinical Investigators (1982)
- Fellow, Royal College of Physicians and Surgeons, Royal College of Physicians and Surgeons, Glasgow (1982)
- Kidney Research Award, 1974 Charlotte Roberts Trust Fund (1974)
- Glaxo-Allenbury Award for Research in Endocrinology and Metabolism, Glaxo-Allenbury Award (1969)
Professional Education
| MB. MBCHB: | University Cape Town, Medicine (1960) |
| MD: | University Witwatersrand, Medicine (1975) |
Graduate & Fellowship Program Affiliations
Internet Links
Scientific Focus
Current Research Interests
I am an Active Emeritus Professor Medicine/ Nephrology at Stanford University. I began my long career in investigative medicine over 40 years ago. My first major contribution was one of the earliest randomized clinical trials evaluating beta-blockade for angina (Rabkin R et al. The prophylactic value of propranolol in angina pectoris. Am J Cardiol. 1966;18:370-83.). Moving from clinical investigation, (e.g. The effect of renal disease on the renal uptake and excretion of insulin in man. Rabkin R et al, NEJM, 1970, 282:182-187), my research became more basic orientated and focused on the renal metabolism of peptide hormones (Factors influencing the handling of insulin by the isolated rat kidney. Rabkin, R. and A.E. Kitabchi. J. Clin. Invest. 1978, 161:169-175. The handling of immunoreactive vasopressin by the isolated perfused rat kidney. Rabkin, R et al. J. Clin. Invest. 1979. 63:6-13). More recently I have focused on the mechanisms accounting for the resistance to growth hormone, insulin-like growth factor-1 and amino acids in uremia to explain their role in the impaired body growth and muscle wasting that is common in chronic kidney disease (CKD) (Schaefer F, Chen Y, Tsao T, Nouri P, and Rabkin R. (2001). Impaired JAK-STAT signal transduction contributes to growth hormone resistance in chronic uremia. J Clin Invest 108: 467-475) Chen Y, Sood S, McIntire K, Roth R, Rabkin R. Leucine stimulated mTOR signaling is partly attenuated in skeletal muscle of chronically uremic rats especially when work overloaded. American Journal of Physiology. Endocrinology and metabolism. (2011) 301, E873-871. Intrigued by my findings in rats with CKD, that exercise can correct some of the skeletal muscle abnormalities in signal transduction and IGF-1 and myostatin gene expression, I have been motivated to go from the bench to the bedside, and have brought together an outstanding group of clinical investigators with expertise in exercise rehabilitation as well as clinical trials in CKD patients and together we are embarking on a 4 year VA Merit Review Funded study “Exercise to Prevent Muscle Mass and Functional Loss in Elderly Dialysis Patients”.
Publications
- A marked deficiency in circulating and renal IGF-I peptide does not inhibit compensatory renal enlargement in uninephrectomized mice. Growth Horm IGF Res. 2011; (5): 279-84
- Leucine-stimulated mTOR signaling is partly attenuated in skeletal muscle of chronically uremic rats. Am J Physiol Endocrinol Metab. 2011; (5): E873-81
- The effects of type 1 IGF receptor inhibition in a mouse model of diabetic kidney disease. Growth Horm IGF Res. 2011; (5): 285-91
- Uremia attenuates growth hormone-stimulated insulin-like growth factor-1 expression, a process worsened by inflammation. Kidney Int. 2010; (1): 89-95
- Endotoxin-induced growth hormone resistance in skeletal muscle. Endocrinology. 2009; (8): 3620-6
- Increased renal Akt/mTOR and MAPK signaling in type I diabetes in the absence of IGF type 1 receptor activation. Endocrine. 2009; (1): 126-34
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