Newer Methods of Nutritional Biochemistry, Volume 5: With by Anthony A. Albanese

By Anthony A. Albanese

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W . Mace, and R. W . Gottin, Life Sci. 8 , 1299-1307 (1969). 41. S. J. Goldsmith and S. M . Glick, Mount Sinai J. Med. 3 7 , 501-509 (1970). 42. S. M . Glick, J. Roth, R. S. Yalow, and S. A. Berson, Res. Prog. Hormone Res. 2 1 , 241 (1965). 43. K. Takebe, H. Kuncta, S. Sawano, Y . Horinchi, and K. Mashimo, J. Clin. Endoc. Metab. 2 9 , 1630-1633 (1969). 44. F. C. Greenwood and J. Landon, Nature (London) 2 1 0 , 540 (1966). 45. D. Rabinowitz, T. J. Merimea, J. A. Burgess, and L. Riggs, J. Clin. Endoc.

Sharp et al. (149), in an extension of the Arctic studies mentioned previously, assessed urinary sodium, potassium, creatinine, oxogenic steroids, and oxosteroids in 4 subjects studied every second day for 8 days after a 12-hour phase shift and, after 14 days on the new schedule, for a similar period after reversion to the previous sched- 24 GEORGE A. CHRISTIE ule. Obvious dissociation of the rhythms occurred, with oxosteroids adapting on the second day, sodium and water excretion by the fourth, and potassium and oxogenic steroids taking 6 to 8 days to adapt fully.

Unfortunately, no nocturnal samples were obtained, and it is not possible to say whether an abnormality in HGH circadian rhythm was present. However, Hansen and Johansen (48) report a steady hypersecretion in such patients. High levels are also seen, but with a superimposed circadian rhythm which is essentially normal in phase in conditions with primordial short stature (53). 005). Basal levels were also elevated, suggesting that this need not necessarily present a block to the stimulation of HGH release, contrary to the suggestion of Takebe et al.

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