Sugar essential to growth. Ratio of liver to active increase in
weight. Obesity and fatty degeneration. Small inactive liver and
stunted growth, or loss of weight. Biliary fistula, death in 12
months. Influence of pancreas. Nitrogenous food for obesity, outdoor
life, exercise, cholagogues, salines. Saccharine and starchy food for
emaciation, hepatic, and pancreatic stimulants. Mild laxatives and
cholagogues, pure air, green, succulent food, pure water, bitters,
tonics, moderate exercise.
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.