Lombardo Y B, Menahan L A
Horm Metab Res. 1979 Jan;11(1):9-14. doi: 10.1055/s-0028-1092672.
Hypertrophy of liver cells, as measured by decreased mg DNA per g wet liver, from obese mice (C57BL/6J ob/ob) was associated with a marked increase in triacylglycerol content per g wet liver when compared with control lean mice (C57BL/6J ?/+). The difference between the rates of net glucose production from lactate in isolated perfused livers from obese and lean mice was small when expressed per g wet liver. However, calculation of these rates either on a DNA or body weight basis indicated that the rate of gluconeogenesis in livers from obese mice was twice that of lean mice. Using perfused livers from lean mice, the ratio of net uptake of C3-substrate to gluconeogenesis indicated that a major proportion of lactate disappearing from the perfusion medium could not be accounted for in the appearance of glucose; but using the perfused livers of obese mice, almost all of the net lactate disappearance could be accounted for by a net increase in glucose production.
通过每克湿肝中DNA含量降低来衡量，肥胖小鼠（C57BL/6J ob/ob）的肝细胞肥大与每克湿肝中三酰甘油含量显著增加有关，与对照瘦小鼠（C57BL/6J?/+）相比。当以每克湿肝表示时，肥胖和瘦小鼠分离灌注肝脏中由乳酸产生的净葡萄糖生成速率差异很小。然而，以DNA或体重为基础计算这些速率表明，肥胖小鼠肝脏中糖异生速率是瘦小鼠的两倍。使用瘦小鼠的灌注肝脏，C3底物净摄取与糖异生的比率表明，灌注培养基中消失的大部分乳酸不能在葡萄糖出现中得到解释；但使用肥胖小鼠的灌注肝脏，几乎所有的乳酸净消失都可以由葡萄糖生成的净增加来解释。
