Increasing dextrose concentrations in total parenteral nutrition (TPN) causes alterations in hepatic morphology and plasma levels of insulin and glucagon in rats.
Hepatic steatosis is an ongoing problem in total parenteral nutrition (TPN). The etiology of this deranged hepatic morphology is unclear, but lack of enteral stimulation and excess carbohydrate calories have been suggested as altering the intestinal hormone profile. In this study, adult male Sprague-Dawley rats (n = 28) received internal jugular catheters: group 1 (n = 7) received saline (3 cc/hr) and chow ad libitum; groups 2, 3, and 4 (n = 7) received 15, 20, and 25% dextrose-base TPN solutions, respectively, in quantities matching the caloric intake of paired ad libitum animals. At 7 days portal and peripheral venous blood samples were drawn for insulin and glucagon radioimmunoassay, and livers were removed for histologic examination and determination of total hepatic lipid content. Portal and peripheral insulin levels rose in a linear fashion with increasing dextrose concentration. Lipid content increased with elevated portal venous insulin/glucagon ratio in groups 3 and 4. Periportal fatty infiltration increased with increasing dextrose concentrations. The results suggest that the liver's response to altered portal insulin/glucagon ratio may play an important role in changes of hepatic morphology associated with TPN.
D000818:Animals; D005934:Glucagon / Q000097:blood*; D005947:Glucose / Q000494:pharmacology*; D007328:Insulin / Q000097:blood*; D008099:Liver / Q000473:pathology*; D008111:Liver Function Tests; D008297:Male; D009994:Osmolar Concentration; D010289:Parenteral Nutrition, Total; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D005934:Glucagon; D005947:Glucose