There is reason to believe that both of these occur as results of hepatic disorder. The generation of sugar in connection with rapid cell growth in germinating seeds and growing plants, and also in rapidly growing animal tissues as in the body of the fœtus and fœtal membranes, and finally in the inflammatory products of pneumonia and in leucocytes, seems to imply that it is essential to such cell growth (Murchison). In keeping with this is the fact that the liver is of relatively much greater size in the fœtus and in the young and rapidly growing animal, and also in meat producing animals which have been selected and bred through many generations for early maturity and rapid fattening. The enormous development of adipose tissue and of lipomata in such animals is essentially abnormal, though it is a deviation from the natural that is esteemed as evidence of excellence, and a necessary condition of success in the meat producing industry. While other conditions are necessary to the production of such obesity, such as abundance of rest, slow, shallow breathing, a genial climate, and a generous hydro-carbonaceous food, yet all of these would prove ineffective without a large liver, working under high pressure in producing a large output of sugar. The mere obesity in the meat producing animal is not considered as disease and it is only when the tendency to fat production culminates in an adipose degeneration of the muscles and other tissues that actual disease is conceded.
Emaciation in certain cases is traceable to the opposite condition. A small or inactive liver with a diminished production of sugar and fat will ensure loss of weight, which is still further aggravated by decreased secretion of bile and insufficient absorption of peptones. Experimentally this condition has been repeatedly brought about by making a biliary fistula, and cutting off all bile from the intestine. Death preceded by extreme emaciation ensues in 12 months (Murchison). This being the case with the escape of all the bile secreted, a slower but no less certain emaciation must follow on a structural or functional disorder of the liver which is attended with a greatly lessened production of bile. This, indeed, is the condition met with in advanced glycosuria, when the liver is the seat of general fatty degeneration.
From the experiment of the removal of the pancreas we may infer that diseases of this organ which pervert or destroy its normal functions, will check glycogenesis in the liver by withholding the supposed pancreatic ferment, and by so doing will conduce to emaciation and marasmus.
So far as obesity and emaciation are dependent on diet they may be checked by subjecting the patient to the dietary which will favor a more healthy liver function. For excessive obesity a strictly nitrogenous food in restricted amount will tend to lessen the glycolytic action of the liver and secure the formation of muscle rather than fat. An outdoor life, and an active though not exhaustive use of the muscles will greatly favor this result. For the carnivora or omnivora a diet of lean meat or skim milk might be employed, while for the herbivora, wheat bran, cotton seed hulls, beans, peas, vetches, or cotton seed would measureably meet the demand. Cholagogues and saline laxatives, by eliminating from the liver and intestine, will contribute to the same end.
If emaciation depends on a deficiency of sugar, that may be freely fed along with richly amylaceous food, and the liver may be stimulated to increased glycogenesis, by stimulants such as chloroform, ammonia, or ether, and by a moderate use of carbonate of soda or other alkalies. Ether has in addition a stimulating effect on the pancreas and will tend to increase that ferment which stimulates the liver to its glycogenic work. Mild laxatives and cholagogues will second this, such as small doses of podophyllin, taraxacum, nitro-muriatic acid, chloride or bromide of ammonium, plenty of pure air, abundance of green or aqueous food, and plenty of pure drinking water. Finally moderate exercise, by increasing the aspiratory action of the chest and thereby accelerating the hepatic circulation is a material stimulant of the glycolytic function. Bitter and other tonics are contributions to the same object and should not be neglected.
SECONDARY OR REMOTE RESULTS OF LIVER DISEASE.
In gout: Arrest of oxidation of proteids into urea. Deposits of biurate of lime on joints, and other disorders. Urinary calculi containing urates, cystine, xanthine, etc., also from imperfect oxidation of albuminoids. Oxalic acid represents a similar arrest. Kidney degenerations from irritating urates and oxalates. Fatty kidney from excessive glycogenesis. Digestive disorders from excess or deficiency of bile or torpid liver. Nervous disorders, dullness, lameness, vertigo, spasms, irritability from hepatic inactivity and resulting poisons. Sore throat and bronchitis from hepatic derangement. Skin eruptions in tardy or imperfect action of the liver. Treatment: Abundant water, succulent vegetables, ensilage, fresh grains, balanced ration, in carnivora and omnivora oat meal, buttermilk, clear meat juice, avoid sweets, gravies, spiced animal food. Dangers for pampered horses, dogs, and old improved meat producing animals. Open air exercise. Laxatives with alkalies, salines, mercurous and mercuric chloride, pilocarpin, chlorides, iodides, bromides, nitro-muriatic acid, ipecacuan, euonymus, bitters.
Among the many secondary results of hepatic disorder, and which are habitually described as affections of other organs a few may be mentioned as indicating the wide range of influence exercised by the liver in disease as well as in health.
Gout as it appears in fowls and omnivora is directly due to the arrest of the transformation of the albuminoids into urea. Circulating in the system in the form of the less perfectly oxidized and less soluble uric acid, it determines deposits of biurate of lime around the joints, with local inflammations, and disorders of circulation and innervation, and altered spirit, temper, etc.
Urinary calculi in the same animals, are composed largely of urate of lime, cystine, xanthine and other nitrogenous products representing various stages of oxidation short of the final transition into urea and ammonia. Recognizing the active rôle which the urinary bacteria fill in this respect we must still acknowledge the great importance, as causative agents, of an excess in the urine of these comparatively insoluble products.