The modifying effect of nutritional intake of the posttraumatic depletion in hepatic glycogen in rats.

Hepatic glycogen levels were measured in rats both on oral food ad libitum and where intravenous nutrition was supplied at 0.1, 0.2, and 0.35 Kcal/gm of body weigh/day at 24 and 72 hours after injury. While on oral food rats with a closed femoral fracture had a lower level (25 +/- 6.5 mg/gm of liver) than normal (66 +/- 9.1 mg/gm of liver, P less than 0.005), 24 hours after injury. There was a corresponding rise in blood sugar (161 +/- 20 leads to 240 +/- 23 mg/100 ml, P less than 0.005) at 24 hours. However the food intake fell (23.8 +/- 1.5 leads to 16.6 +/- 2.4 gm/day, P less than 0.01) during the first 24 hours after the injury. When intravenous nutrition was given at a caloric level of 0.35 Kcal/gm/day, hepatic glycogen levels were above normal and there was no difference between injured and noninjured animals. At 0.2 Kcal/gm/day there was also no difference between injured and noninjured animals, but glycogen levels fell from norman levels (78 +/- 12.9 mg/gm) to lower levels (33 +/- 11.9 mg/gm, P less than 0.01) over the 24-hour to 72-hour period. Low levels of caloric intake (0.1 Kcal/gm/day) resulted in a fall in glycogen level in both injured and noninjured animals, with the decrease being significantly greater in the injured animals. It is concluded that maintenance of the caloric intake of rats at normal or high levels via the intravenous route can prevent the depletion of hepatic glycogen produced by a femoral fracture.