HEPATIC AND MUSCLE GLUCOSE-METABOLISM DURING TOTAL PARENTERAL-NUTRITION - IMPACT OF INFECTION

We examined the impact of infection on hepatic and muscle glucose meta bolism in dogs adapted to chronic total parenteral nutrition (TPN). St udies were done in five conscious chronically catheterized dogs, in wh ich sampling (artery, portal and hepatic vein, and iliac vein), infusi on catheters (inferior vena cava), and Transonic flow probes (hepatic artery, portal vein, and iliac artery) were implanted. Fourteen days a fter surgery, dogs were placed on TPN. After 5 days of TPN, an infecti on was induced, and the TPN was continued. The balance of substrates a cross the liver and limb was assessed on the day before infection (day 0) and 18 (day I) and 42 h (day 2) after infection. On day 0, the liv er was a marked net consumer of glucose (4.3 +/- 0.6 mg.kg(-1).min(-1) ) despite near normoglycemia (117 +/- 5 mg/dl) and only mild hyperinsu linemia (16 +/- 2 mu U/ml). In addition, the majority (79 +/- 13%) of the glucose taken up by the liver was released as lactate (34 +/- 6 mu mol.kg(-1).min(-1)). After infection, net hepatic glucose uptake decr eased markedly on day 1 (1.6 +/-. 0.9 mg.kg(-1).min(-1)) and remained suppressed on clay 2 (2.4 +/- 0.5 mg.kg(-1).min(-1)). Net hepatic lact ate output also decreased on days 1 and 2 (15 +/- 5 and 12 +/- 3 mu mo l.kg(-1).min(-1), respectively). This occurred despite increases in ar terial plasma glucose on days 1 and 2 (135 +/- 9 and 144 +/- 9 mg/dl, respectively) and insulin levels on days 1 and 2 (57 +/- 14 and 34 +/- 9 mu U/ml, respectively). In summary, the liver undergoes a profound adaptation to TPN, making it a major site of glucose disposal and conv ersion to lactate. Infection impairs hepatic glucose uptake, forcing T PN-derived glucose to be removed by peripheral tissues.