CARBOHYDRATES AND FATS. 911 



entering the splanchnic nerves, proceed to the hver by way of the 

 hepatic plexus and nerves. On this view the center in the medulla 

 constitues a "sugar-regulating center," which may be acted on 

 reflexly and thus control the process of the conversion of glycogen 

 to sugar. Others have held the view that the effect is exercised 

 indirectly through the adrenal glands. They believe that the 

 sugar puncture results in a reflex stimulation of the adrenal 

 glands, whereby more epinephrin is thrown into the circulation, 

 and that the increase in glycogenolysis is due to the action of the 

 epinephrin on the liver cells. Later experiments do not support 

 wholly either one of these views, but indicate rather that while the 

 nerve-fibers involved act directly upon the liver cells the presence 

 of the adrenal glands is in some way necessary for the reaction.* 

 Just how this mechanism acts under normal conditions cannot, 

 therefore, be determined. It is known, however, that under condi- 

 tions of emotional excitement or nervous stress glycosuria is apt to 

 occur, and the explanation usually offered is that the secretion of 

 the adrenals is increased by reflex stimulation with a resulting in- 

 crease in sugar output from the liver. In both of these possibilities,, 

 a reflex stimulation of the hepatic nerves or of the adrenal glands, 

 there is a break down in the completeness of the regulation which 

 affects chiefly the process of glycogenolysis. There is an acceler- 

 ated conversion of glycogen to sugar, or, as it is sometimes fig- 

 uratively expressed, a mobilization of the sugar reserves. Within 

 certain limits this reaction may be regarded as a provision or 

 adaptation for increasing the supph^ of energy-yielding material to 

 the muscles under conditions which usually demand great muscular 

 activity. But when the stimulus is excessive the output of sugar 

 may be sufficiently great to bring about an approach to a patho- 

 logical condition since it leads to hyperglycemia and glycosuria. 

 In this connection we may recall also the severe form of glycosuria 

 following upon removal of the pancreas, the so-called 'pancreatic 

 diabetes (p. 885) . Here also the trouble is referable to a change in 

 one of the internal secretions, but in this instance it is a defective 

 rather than an excessive secretion which induces the glycosuria. 

 Whether the loss of the internal secretion of the pancreas affects 

 the stage of glycogenolysis or the stage of glycolysis is perhaps an 

 open question. The usual view has been that this secretion is con- 

 cerned somehow with the metabolism of sugar in the tissues in 

 some such way as is suggested in the preceding paragraph upon 

 the intermediary metabolism of the carbohydrates. 



In mankind defective sugar metabohsm manifests itself chiefly 

 in the disease known as diabetes meUiius. In this severe and often 



* For review and literature consult Macleod, Harvey Lecture, "Journal of 

 the American Medical Association," April 18, 1914. 



