Mares (and subsequently many other observers), having noted that, following the ingestion of _purin-free_ protein food, a marked increase in endogenous uric acid excretion ensued, suggested that the said augmentation was the outcome of the “wear and tear” entailed upon the nuclear material of the _secretory glands of the gastro-intestinal tract_, following such intake. The effects yielded on uric acid excretion by those antithetic drugs, atropine and pilocarpine, certainly seem to lend colour to Mares’ hypothesis. Following the injection of _atropine_, the rise in uric acid output, that normally follows the ingestion of protein, was inhibited. But in sequence to _pilocarpine_, an _excitant_ and not like _atropine_, a depressor of secretory activity, a marked increase in uric acid excretion followed. The contrast in response was naturally translated as striking evidence of the important _rôle_ played by the _digestive glands_ on uric acid excretion; in other words, it was held that the major portion of the endogenous uric acid was the reflex of such intensified glandular action. In opposition, however, Burian, as the outcome of his experimental studies, maintained that a _fractional_ portion only of the endogenous uric acid could be derived from the _nucleo-protein of the body cells_. This, inasmuch as it would entail a far too extensive katabolism of nuclear substance. Accordingly he propounded the view that the endogenous uric acid in the main was derived from the _hypoxanthine_ of the _inosinic_ acid present in _muscular_ tissue. In this connection it may be noted that, on a diet approximating to Voit’s standard, 0·5 gram of purin is excreted daily. This, it is calculated, is equivalent to nearly 100 grams of thymus or allied tissue, which probably far exceeds the amount that could be gleaned from cellular katabolism. PROTEINS AND THEIR DERIVATIVES A comparison of the influence of _proteins_ as contrasted with that of their digested products, the _amino-acids_, it was thought, might furnish a clue as to the extent of which the alleged activity of the _digestive glands_ was responsible for the increased uric acid output that followed the intake of non-purin protein food. Such was the supposition entertained by H. B. Lewis, M. S. Dunn, and E. A. Doisy. Alive, moreover, to the deficiency of the older procedure in use for the determination of small amounts of uric acid, Lewis and his collaborators invoked the more accurate colorimetric method of Folin and Denis (as modified by Benedict and Hitchcock).