Nitrogen economy in alcoholic patients without liver disease

Ethanol impairs post-prandial hepatic protein metabolism.

“…Plasma VLDL-apo-B100 were purified by ultracentrifugation, as previously described (23 During meal infusion, the rate of endogenous leucine appearance (tsmol kg-' min'), an index of whole body proteolysis, was calculated by subtracting the ig leucine infusion rate from the rate of total leucine appearance. This assumes that (a) the ig delivered leucine is completely absorbed and reaches the systemic pool in the form of leucine or KIC (24); and (b) acute ethanol administration does not affect the enteral absorption of amino acids (7). The rate of leucine oxidation (Omol kg-l mind) was calculated by dividing the expired rate of 14CO2 (dpm kg-' min') by the plasma [14C]KIC SA (dpm/pmol) (11), and assuming a 70 and an 82% C02 recovery in the post-absorptive and in the absorptive state (25), respectively.…”

“…Acute ethanol administration inhibits protein synthesis in vitro in isolated hepatocytes (2), in perfused livers (3), and in vivo in rat liver (4). In humans it is known that the intravenous infusion of ethanol reduces urinary nitrogen excretion (5); whereas the isocaloric replacement of glucose and lipids with ethanol in a 3-6-wk diet of normal (6) or alcoholic subjects (7,8) results in a negative nitrogen balance and weight loss. The presence of adequate amounts of amino acids in the diet of these subjects (6,8) rules out the possibility that protein malnutrition, commonly indicated as the cause of many complications of chronic alcoholism (9), was responsible for the negative nitrogen balance.…”

“…Thus a direct "toxic" effect of ethanol ingestion on protein metabolism must be considered. However, nitrogen balance studies (6)(7)(8) cannot provide any insight into the mechanism(s), i.e., increased protein breakdown and/or decreased protein synthesis, by which ethanol leads to net protein catabolism.…”

Glucose Turnover Rate and Peripheral Insulin Sensitivity in Alcoholic Patients without Liver Damage

“…An in creased gluconeogenesis could be one of the pathways responsible for this higher oxygen consumption. We have shown an enhanced protein catabolism during alcohol intake and early abstinence [23]; an increased rate of protein breakdown is associated frequently with simultaneous increases in gluconeogen esis [24], Finally, an increased glycogenolysis is another possible explanation, probably re lated to the withdrawal syndrome and the resultant increased catecholamine levels [25]: It was not possible to control glycoge nolysis in our design, because a full depletion of liver glycogen requires a complete fast of at least 72 h [26], which is dangerous and unacceptable to the patients.…”

Protein turnover in alcoholism: should it be considered as a whole body event or tissue specific phenomena?

“…Non-oxidative disposal was taken as being indicative of whole body protein synthesis [3]. Although the practical complexity of protein turnover measurements dictates that the data are clearly not of diagnostic signifi cance, the information must nevertheless be interpreted in terms of nonhepatic changes in protein synthesis and the nutritional consequences for the whole body [6,7]. Fur thermore, it is important to note that the study of Hirsch et al [3] emphasizes the fundamental need to screen for continued ethanol consumption, despite assurances by patients or clinical strategies to curb alcohol consumption.…”