Wolfe B M, Havel J R, Marliss E B, Kane J P, Seymour J, Ahuja S P
J Clin Invest. 1976 Feb;57(2):329-40. doi: 10.1172/JCI108284.
Splanchnic metabolism was studied to quantify changes underlying the fatty liver, hyperlipemia, and hypoglycemia produced by ethanol. Four subjects fasted for 15 h were compared with five subjects fasted for 69 h under basal conditions and during continuous intravenous infusion of sufficient ethanol to give a concentration of 3-5 mM in arterial blood plasma. Splanchnic storage of fatty acids was estimated from the difference between uptake of FFA and secretion of derived products. Basal values for splanchnic uptake of FFA were twofold higher after the 69-h fast while splanchnic storage of fatty acids and production of ketone bodies increased threefold. Values for basal secreation into the blood of triglycerides derived from FFA were similar in the two groups. In both nutritional states, the fraction of FFA taken up in the splanchnic region oxidized to ketone bodies and to CO2 fell when ethanol was given because of preferential oxidation of ethanol to acetate, and the fraction esterified rose. However, systemic transport and splanchnic uptake of FFA fell with ethanol in subjects fasted 15 h, so that neither storage of triglycerides in splanchnic tissues nor secretion into the blood increased. In subjects fasted 69 h, ethanol increased transport of FFA and splanchnic storage of fat. In all but one subject it also increased secretion of triglycerides into the blood. The concentration of glucose in blood fell during ethanol infusion in all five subjects undergoing the 69-h fast. Mean splanchnic glucose production was maintained at about one-half of the pre-ethanol value, despite virtual cessation of splanchnic uptake of lactate and of those amino acids that are metabolized via malate. Quantitative estimates of extrasplanchnic metabolism suggest that enhanced formation of alpha-glycerophosphate from glucose, in addition to impaired hepatic gluconeogenesis, may contribute to ethanol-induced hypoglycemia in man.
研究了内脏代谢，以量化乙醇所致脂肪肝、高脂血症和低血糖背后的变化。将4名禁食15小时的受试者与5名禁食69小时的受试者在基础状态下以及在持续静脉输注足够乙醇以使动脉血浆浓度达到3 - 5 mM期间进行比较。通过游离脂肪酸（FFA）摄取与衍生产物分泌之间的差异来估计内脏脂肪酸储存。禁食69小时后，内脏对FFA的摄取基础值高出两倍，而内脏脂肪酸储存和酮体生成增加了三倍。两组中源自FFA的甘油三酯向血液中的基础分泌值相似。在两种营养状态下，给予乙醇后，在内脏区域摄取的FFA中氧化为酮体和CO2的部分减少，因为乙醇优先氧化为乙酸盐，而酯化部分增加。然而，在禁食15小时的受试者中，乙醇使FFA的全身转运和内脏摄取下降，因此内脏组织中甘油三酯的储存和向血液中的分泌均未增加。在禁食69小时的受试者中，乙醇增加了FFA的转运和脂肪的内脏储存。除一名受试者外，在所有受试者中乙醇还增加了甘油三酯向血液中的分泌。在所有5名进行69小时禁食的受试者中，乙醇输注期间血液中葡萄糖浓度下降。尽管内脏对乳酸和那些通过苹果酸代谢的氨基酸的摄取实际上停止，但平均内脏葡萄糖生成维持在乙醇给药前值的约一半左右。对内脏外代谢的定量估计表明，除了肝糖异生受损外，由葡萄糖增强生成α-磷酸甘油可能导致人类乙醇诱导的低血糖。
