Funaki N, Tanaka Y, Mak K M, Lieber C S
Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center, NY 10468.
J Hepatol. 1992 Jul;15(3):367-71. doi: 10.1016/0168-8278(92)90070-6.
The effect of continuous intraperitoneal infusion of uridine diphosphoglucose on ethanol-induced suppression of lipocyte proliferation was studied in regenerating rat livers from 1-4 days after hepatectomy. Proliferating lipocytes were positively identified using a two-sequence immunohistochemical staining for cytoplasmic desmin and bromodeoxyuridine-labelled nuclei. Hepatectomy rapidly stimulated lipocyte proliferation which peaked 2 days after hepatectomy (labelling index, 17.9 +/- 0.81%). uridine diphosphoglucose or glucose infusion did not modify the time course of lipocyte proliferation. Ethanol feeding to hepatectomized rats receiving saline or glucose infusion resulted in a 71% (p less than 0.005) and 61% (p less than 0.005) inhibition of lipocyte proliferation, respectively, 2 days after hepatectomy, thereby abolishing the characteristic proliferative peak observed in rats not treated with ethanol. In contrast, uridine diphosphoglucose infusion doubled the labelling index (13.1 +/- 2.34%) in ethanol-fed rats compared to that in corresponding rats treated with saline (5.28 +/- 1.29%; p less than 0.005) or glucose (6.51 +/- 0.64%; p less than 0.005). This resulted in the appearance of a proliferative peak, albeit smaller than normal, 2 days after hepatectomy. In sham-operated rats, lipocyte proliferation was low with a labelling index of 1.88 +/- 0.13% at the time of operation and of 1.69 +/- 0.23% 2 days thereafter. Uridine diphosphoglucose infusion to sham-operated rats for 2 days did not significantly affect lipocyte proliferation (labelling index 1.79 +/- 0.06%). The present study demonstrated that uridine diphosphoglucose does not affect lipocyte proliferation in the regenerating or sham-operated livers, but that it partially reverses the ethanol-induced suppression of lipocyte proliferation after hepatectomy.
在肝切除术后1至4天的再生大鼠肝脏中，研究了持续腹腔内输注尿苷二磷酸葡萄糖对乙醇诱导的脂肪细胞增殖抑制的影响。使用针对细胞质结蛋白和溴脱氧尿苷标记细胞核的双序列免疫组织化学染色来阳性鉴定增殖的脂肪细胞。肝切除术迅速刺激脂肪细胞增殖，在肝切除术后2天达到峰值（标记指数，17.9±0.81%）。尿苷二磷酸葡萄糖或葡萄糖输注并未改变脂肪细胞增殖的时间进程。对接受盐水或葡萄糖输注的肝切除大鼠喂食乙醇，在肝切除术后2天分别导致脂肪细胞增殖抑制71%（p<0.005）和61%（p<0.005），从而消除了未用乙醇处理的大鼠中观察到的特征性增殖峰值。相比之下，与相应的接受盐水（5.28±1.29%；p<0.005）或葡萄糖（6.51±0.64%；p<0.005）处理的大鼠相比，尿苷二磷酸葡萄糖输注使乙醇喂养大鼠的标记指数加倍（13.1±2.34%）。这导致在肝切除术后2天出现一个增殖峰值，尽管比正常情况小。在假手术大鼠中，脂肪细胞增殖较低，手术时标记指数为1.88±0.13%，术后2天为1.69±0.23%。对假手术大鼠输注尿苷二磷酸葡萄糖2天并未显著影响脂肪细胞增殖（标记指数1.79±0.06%）。本研究表明，尿苷二磷酸葡萄糖不影响再生或假手术肝脏中的脂肪细胞增殖，但它部分逆转了肝切除术后乙醇诱导的脂肪细胞增殖抑制。
