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The Journal of Nutrition Vol. 128 No. 12 December 1998,
pp. 2529-2529
LETTER TO THE EDITOR:
Dear Editor:
In your recent report of the symposia on dietary protein's influence on bone metabolism (Barzel et al. 1998, Heaney 1998 Both arginase and nitric oxide synthase (NOS) use as a substrate the amino acid L-arginine. Arginase produces urea and L-ornithine, and NOS produces nitric oxide (NO) and L-citrulline. Increasing dietary protein upregulates urea synthesis (Briggs et al. 1977). This may competitively decrease the available substrate for NOS and decrease the production of NO (Cook et al. 1994 NO has also been shown to be important in the regulation of bone formation. It is expressed in both osteoblasts and osteoclasts, and it inhibits osteoclastic resorption of bone and modulates bone mineral metabolism (Ralston 1997 Elderly adults have several areas of altered physiology that lead to a decrease in NO production. Postmenopausal women have decreased estrogen. Celermajer et al. (1994) Singh (1995) Much research still needs to be done to determine the specific influences of these enzymatic pathways and their involvement with dietary protein and bone metabolism. It may be found that their influence is more or less potent than that of pH on bone physiology. But there is ample evidence that they also play a part in this important controversy.
LETTER
, Massey 1998), the emphasis was put on the influence of pH and dietary calcium. An alternate mechanism that also needs to be considered, but was not addressed, is the influence of increased dietary protein on the urea cycle and its resulting sequelae that may also effect bone homeostasis.
). The competitive nature of these enzymes has been shown in other studies (Jansen et al. 1992). NO has diverse and important functions in virtually every human system. In the kidney inhibition of NO synthesis by N omega-nitro-L-arginine (L-NAME) causes renal hypertrophy in rats (Vaskonen et al. 1997). Rats fed a high protein diet for 1 mo also develop renal hypertrophy which can be reversed by supplementing them with L-arginine (Reyes et al. 1994). This can be explained if during times of increased amino acid load arginase is the favored pathway at the expense of NO production.
). In vitro and animal studies have verified that a decrease in the NO concentrations increase the number of osteoclasts and osteoclastic resorption of bone (Holliday et al. 1997) Estrogen has been shown to increase the production of NO in cultured osteoblasts (Armour et al. 1998). NO donors prevent bone loss in ovariectomized rats, and inhibition of NOS attenuates the protective effect of estrogen replacement therapy in ovariectomized rats (Wimalawansa et al. 1996).
found a steep decline in endothelial function occurred around the time of menopause. Decreases in potassium, common in the elderly, also decrease NO availability (Yang et al. 1998). There may be a normal decrease in endogenous L-arginine production associated with aging (Reckelhoff et al. 1994). Prior et al. (1996) found a decrease in blood L-arginine levels after a protein meal in elderly adults. This is further evidence of the possible effect of dietary protein on L-arginine availability in the elderly population.
found that intravenous L-arginine caused calciuria in rats. Whether this is an acute response to an i.v. load of L-arginine, or whether it is also found in humans taking oral L-arginine is unknown. Oral L-arginine has been shown stimulate NO production (Kharitonov et al. 1995, Wheeler et al. 1997).
Duane T. Lowe
375th Medical Group
Scott AFB, IL 62225
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FOOTNOTES |
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Manuscript received 20 July 1998. Initial reviews completed . Revision accepted 31 August 1998.
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LITERATURE CITED |
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