一氧化氮在全胃肠外营养大鼠肝脂肪变性中的作用

目的 探讨一氧化氮（nitric oxide,NO)在全胃肠外营养（total parenteral nutrition,TPN)引起的肝脂肪变性中的作用。方法 30只正常Wistar大鼠随机分为5组：A组,自由进食和水;B组,TPN;C组,TPN＋精氨酸;D组,TPN＋N^G-硝基－L－精氨酸甲酯（N^G-nitrio-L-arginine methyl ester,L-NAME);E组,TPN＋精氨酸＋L－NAME。实验7d后测肝功能,肝内脂肪,肝脏NO含量及一氧化氮合酶（nitric oxide synthase,NOS)活性和肝脏组织学检查。结果 B组肝内脂肪较A组显增加（P＜0.05),D组肝内脂肪增加较B组更显（P＜0.05),C组肝内脂肪较B组明显减少（P＜0.05),E组肝内脂肪与B组相似（P＞0.05),肝内NOS活性及分布与肝内脂肪含量及分布相平行。结论 一氧化氮可减轻TPN引起的肝脂肪变性。     

胃癌手术后早期肠内营养对T淋巴细胞亚群的影响

目的 探讨胃癌病人手术后早期肠内营养对T淋巴细胞免疫功能的影响。方法 30例胃癌根治术病人随机分成3组：对照组、肠外营养组（TPN组）、肠内营养组（TEN组）,分别给予普通静脉输液、全肠外营养及全肠内营养8d。术前、术后第1、3、6、9天以碱性磷酸酶－抗碱性磷酸酶（APAAP）法测定T淋巴细胞亚群（CD3、CD4、CD8）变化。结果 对照组和TPN组术后CD3、CD4阳性细胞数及CD4／CD8比值明显降低,CD8阳性细胞数明显升高。TNE组术后第1天CD3、CD4阳性细胞数及CD4／CD8比值明显降低,但自术后第3天起即开始上升,并逐渐恢复至术前水平。术后第3、6、9天CD3、CD4阳性细胞数及CD4／CD8比值明显高于对照组和TPN组（P＜0.05),而CD8阳性细胞数明显低于对照组和TPN（P＜0.05),术后第9天时CD4／CD8比值明显高于术前水平。结论 早期肠内营养可纠正胃癌手术后病人的T淋巴细胞免疫抑制状态,促进T淋巴细胞免疫功能的恢复。     

门冬氨酸鸟氨酸对肝硬化肝癌术后肝功能的影响

目的：观察门冬氨酸鸟氨酸（LOLA）对肝癌合并肝硬化半肝切除术后肝功能的影响。方法：通过随机、对照的方法,将66例肝癌合并肝硬化行半肝切除患者分为2组,仅治疗组于术后1～7 d静脉应用LOLA。全部患者分别在术前及术后1、3、5、7、10、14 d抽外周静脉血检查谷丙转氨酶（ALT）、谷草转氨酶（AST）、总胆红素（TB）、直接胆红素（DB）。结果：治疗组术后1、3、5 d ALT明显低于对照组（P〈0.05）,术后3、5 d AST明显低于对照组（P〈0.05）。治疗组术后7 d ALT恢复正常的比率高于对照组。LOLA对术后TB、DB无影响。两组术后肝功能不全的发生率无差异（P=0.557）。结论：LOLA能促进肝癌肝硬化半肝切除术后肝脏功能的早期恢复。     

生长激素强化肠外营养对胃肠道恶性肿瘤患者蛋白代谢及免疫功能的影响

目的 探讨重组人生长激素（rhGH)强化肠外营养对胃肠道恶性肿瘤患者术后蛋白分解代谢及免疫功能的影响。方法 随机选择38例行胃肠道癌根治性手术的病人分为对照级(n=20)和rhGH治疗组（n=18)。两组均术后早期行TPN支持,rhGH组术后第1－6d于上午9点皮下注射rhGH(Saizen 8 U)。结果 对照组术后第5,10d的血清白蛋白、前白 蛋白、转铁蛋白、CD4^ 、CD4^ /CD8^ 及白细胞介素2浓度均较术前明显下降（P＜0．01）,CD8^ 较术前明显上升（P＜0．01）;rhGH治疗组上述指标在术后第10d明显恢复,与对照组比较差异显著（P＜0．01）。结论 生长激素强化肠外营养可以促进胃肠道癌病人术后的蛋白合成,改善其免疫功能。     

精氨酸对梗阻性黄疸病人肾脏损害的保护作用

目的 观察精氨酸对梗阻性黄疸（梗黄）病人肾功能的保护效应。方法34例梗黄病人,随机分为两组,分别在术前给予一般治疗（梗黄组）和精氨酸治疗（治疗组）,连续治疗7d,观察手术前后血ET（内毒素）及Ccr（内生肌酥清除率）变化,并与20例无黄疸的慢性胆囊炎、胆囊结石病人（对照组）比较。结果（1）入院时梗黄组与治疗组外周血ET及Ccr水平比较,差别无显著意义（P>0.05）,但上述两组ET均显著高于对照组（P<0.01）,Ccr显著低于对照组（P<0.01）;（2）梗黄组术后第1天血ET较术前升高（P<0.05）,Ccr更趋下降（P<0.05）,7d后随血ET水平下降,Ccr逐渐升高,第14天ET和Ccr两项指标接近正常水平;ET与Ccr呈显著负相关（P<0.05）;（3）治疗组用药后血ET水平下降,术后保持较低水平,而Ccr用药后升高,第7天ET、Ccr两项指标已接近正常水平。结论 术前使用精氨酸可显著降低梗黄病人内毒素血症,提高内生肌酥清除率,对肾功能具有良好的保护作用。     

添加谷氨酰胺的营养支持对肝功能不全患者术后的影响

目的评价手术后使用添加谷氨酰胺的营养支持对肝功能不全患者胃肠黏膜功能、免疫功能及肝脏功能的影响。方法（1）10例健康志愿者取血行PCR检测细菌DNA作为空白对照;（2）40例符合入选标准的大手术患者．随机分为使用不含谷胺酰胺的全肠外营养组（TPN）与使用含谷氨酰胺的全肠外营养组（GTPN）．每组20例。两组在外科手术后以等氮等热卡营养摄入行全胃肠外营养10d。分别于手术后第5天和第10天观察比较患者血生化指标、胃肠道通透性指标及免疫学指标。结果（1）健康志愿者外周血行PCR检测细菌DNA结果均为阴性。（2）TPN组和GTPN组患者术后5d血浆转氨酶水平与术前相比升高,术后10d GTPN组血浆转氨酶水平明显高于TPN组（P〈0．05）。（3）GTPN组术后第10天血浆总蛋白（TP）水平与白蛋白（ALB）水平与术前相比无明显降低（P〉0．05）,TPN组则明显降低（P〈0．001）。（4）GTPN组手术后第10天肠黏膜通透性无明显升高（P〉0．05）,TPN组则升高明显（P〈0．05）。（5）术后第10天GTPN组外周血淋巴细胞亚群CD4／CD8比值明显高于TPN组（P〈0．01）,GTPN组术后10d IL-6浓度未见明显变化,TPN组IL-6浓度明显升高（P〈0．01）。结论肝功能不全患者手术后使用添加谷氨酰胺的营养支持可以较好地维护术后血浆蛋白水平,保护肠黏膜屏障,提高患者的免疫功能,但有可能影响患者的肝功能。     

原发性小肝癌微波消融治疗前后外周血播散癌细胞及免疫功能变化

目的研究微波消融治疗原发性小肝癌（≤5cm）对外周血播散癌细胞及细胞免疫功能影响。方法微波消融治疗19例小肝癌病人，手术切除治疗21例。于术前、术后30min、1d及7d采外周静脉血，巢式RT—PCR检测AFP mRNA，监测CD3、CD4、CD8及CD4／CD8。结果巢式RT—PCR检测外周血AFP mRNA，两组40例病人术前阳性率为40％（16／40）；微波组和手术组均有3例病人治疗前AFP mRNA阴性，术后30min转为阳性，两组之间比较无差异；微波组术后7d内外周血细胞免疫功能无明显变化，手术组降低。随访1～16个月，4例肝内复发或远处转移病人治疗前后AFP mRNA均阳性。结论与手术切除相比，微波消融治疗原发性小肝癌也可同样程度地造成癌细胞脱落人血，对外周血细胞免疫功能（7d内）无明显影响，有其自身特点；治疗前后外周血AFP mRNA均呈阳性表达（7d内）者，复发／转移的可能性增大。     

精氨酸对恶性梗阻性黄疸患者肿瘤坏死因子-ɑ和可溶性白细胞介素2受体的影响

目的探讨精氨酸(Arginine,Arg)对恶性梗阻性黄疸患者围手术期肿瘤坏死因了浕(TNF-浕)和可溶性白细胞介素2受体(sIL-2R)的影响。方法选择经手术治疗的恶性梗阻性黄疸患者60例,随机分成常规治治疗组(R组)和加用精氨酸组(A组),每组30例。另取单纯性胆囊炎患者30例做对照组(C组)。R组术后给予常规营养支持,B组于术前1 d至术后7 d每日加用精氨酸20 g/d。分别于术前1 d、术后3 d、7 d、14 d取静脉血检测肝功能指标总胆红素(TB)、直接胆红素(DB)、丙氨酸氨基转移酶(ALT)、碱性磷酸酶(ALP)和TNF-浕及sIL-2R。结果A组病人术后7d及14d的肝功能TB、DB、ALT、ALP水平均较R组好转(P<0.01或P<0.05);A组病人TNF-浕和sIL-2R水平较R组明显下降,7 d时二组比较P<0.05,14 d时二组比较P<0.01。结论精氨酸能够减轻梗阻性黄疸对病人肝功能的损害,降低TNF-浕和sIL-2R的水平,改善梗阻性黄疸病人机体的免疫状态。     

ω-3不饱和脂肪酸促进胃肠道恶性肿瘤患者术后康复的疗效研究

目的研究ω-3不饱和脂肪酸促进胃肠道恶性肿瘤患者术后康复及减少术后并发症的作用。方法将华西医院胃肠外科2009年2月1日至6月1日收治的40例胃肠道恶性肿瘤患者按随机数字表法分为对照组和实验组各20例。术后2组连续行7d肠外营养支持治疗,实验组每天加用ω-3不饱和脂肪酸10g。术前、术后第2天及第8天早晨分别抽血检测患者肝、肾功能及机体免疫指标,并记录2组患者的术前及术后7d平均体温、术后肛门排气时间、术后住院时间及并发症发生情况。结果2组患者的一般情况具有可比性（P〉0.05）。术后第2天,实验组总胆红素水平低于对照组,NK细胞及B细胞水平高于对照组,差异均有统计学意义（P〈0.05）;术后第8天,实验组谷丙转氨酶、谷草转氨酶及血尿素氮水平低于对照组,CD4^＋细胞及NK细胞水平高于对照组,差异亦有统计学意义（P〈0.05）。实验组术后肛门排气时间及术后住院时间明显短于对照组,差异有统计学意义（P〈0.05）;2组间术后平均体温及术后并发症发生率相比较,差异均无统计学意义（P〉0.05）。结论ω-3不饱和脂肪酸能够促进患者术后肝、肾功能和机体免疫功能恢复,促进术后肠道功能恢复及缩短术后住院时间,但是对术后并发症发生率无明显影响。     

精氨酸对恶性梗阻性黄疸患者肿瘤坏死因子-α和可溶性白细胞介素2受体的影响

目的 探讨精氨酸(Arginine,Arg)对恶性梗阻性黄疸患者围手术期肿瘤坏死因了α(TNF-α)和可溶性白细胞介素2受体(sIL-2R)的影响.方法 选择经手术治疗的恶性梗阻性黄疸患者60例,随机分成常规治治疗组(R组)和加用精氨酸组(A组),每组30例.另取单纯性胆囊炎患者30例做对照组(C组).R组术后给予常规营养支持,B组于术前1 d至术后7 d每日加用精氨酸20 g/d.分别于术前1 d、术后3 d、7 d、14 d取静脉血检测肝功能指标总胆红素(TB)、直接胆红素(DB)、丙氨酸氨基转移酶(ALT)、碱性磷酸酶(ALP)和TNF-α及sIL-2R.结果 A组病人术后7d及14d的肝功能TB、DB、ALT、ALP水平均较R组好转(P＜0.01或P＜0.05);A组病人TNF-α和sIL-2R水平较R组明显下降,7 d时二组比较P＜0.05,14 d时二组比较P＜0.01.结论 精氨酸能够减轻梗阻性黄疸对病人肝功能的损害,降低TNF-α和sIL-2R的水平,改善梗阻性黄疸病人机体的免疫状态.     

Reversal of hepatic steatosis in rats by addition of glucagon to total parenteral nutrition (TPN)

Infusion of total parenteral nutrition (TPN) with excess carbohydrate calories leads to hepatic steatosis in rats that is associated with an elevated portal insulin/glucagon molar ratio. Previously we have shown that adding glucagon to TPN prevents hepatic steatosis in rats. In this study we attempted to reverse the steatosis by adding glucagon to TPN after 1 week of TPN alone. Adult rats (n = 28) received internal jugular catheters: Group 1 (n = 7), saline (3 cc/h) and chow ad libitum; Group 2 (n = 7), 25% dextrose base TPN solution for 1 week; Group 3 (n = 7), 25% dextrose base TPN for 2 weeks; Group 4 (n = 7), 25% dextrose base TPN for 1 week and then glucagon (15 micrograms/100 g/day) added to TPN for the second week. The infusion rate of TPN was 1.2 ml/100 g/hr (40% kcal greater than control). At 7 days (Group 2) and 14 days (Groups 1, 3, and 4) portal and peripheral venous blood levels were drawn for insulin and glucagon radioimmunoassay, blood glucose determination, and liver function tests; livers were removed for histology and lipid content determination. Blood glucose was equivalent among all groups. Liver function tests were within normal limits. Panlobular vacuolization of the hepatocytes was noted on histology in Groups 2 and 3. Hepatic lipid content was significantly elevated in Group 3. The portal insulin/glucagon molar ratio was increased because of excessive portal venous insulin in Groups 2 and 3 (P less than 0.05 by ANOVA). In contrast, portal venous insulin and the insulin/glucagon molar ratio did not increase in Group 4 and hepatic lipid infiltration was absent when glucagon was added to the TPN solution after 1 week of TPN solution alone. The results suggest that the addition of glucagon to hypertonic dextrose TPN is not only protective in preventing hepatic steatosis, but may reverse steatosis, possibly by increasing hepatic lipid export.     

一氧化氮对全胃肠外营养肝脂肪变性的保护作用

目的探讨一氧化氮(NitricOxide,NO)对全胃肠外营养(TotalParenteralNutrition,TPN)引起的肝脂肪变性的作用。方法30只Wistar大鼠随机分为5组A组，正常对照；B组，TPN；C组，TPN+精氨酸；D组，TPN+N     

���ڳ��ڳ���Ӫ��֧�ֶԸ�Ӳ�����г�����Ӱ����о�

??Early postoperative enteral nutrition compared with parenteral nutrition in patients with liver cirrhosis after hepatectomy LAI Jia-ming*, LIANG Li-jian,HUA Yu-peng, et al. *Department of Hepatobiliar Surgery, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510080, China Corresponding author: LIANG Li-jian, E-mail??LiangLJ@medmail.com.cn Abstract Objective To evaluate the impact of early enteral nutrition over parenteral nutrition in patients with liver cirrhosis after hepatectomy. Methods Thrity -five patients with liver cirrhosis undergoing liver resection were study: EEN group, received early enteral nutrition (n=16); PN group, received parenteral nutrition (n=19). The two groups were received nutritional formulas with isocaloric and isonitrogenous 24 hours after operation, and they were ended at postoperative day 7. The general conditions, liver function tests, clinic complications, clinic nutritional variables on three time point that included preoperative phase, postoperative day 1 (POD 1) and postoperative day 8 (POD8) were observed respectively. Results No significant difference was found in length of hospital stay, liver function,and clinic nutritional variables between the two groups. In the EEN group, the serum prealbumin and albumin level neared the preoperative level on POD8. Nutritional complication rate of EEN group was increased signiflcanly ??but mild than the PN group respectively .The time of gut function recover was shorter than PN group.The costs of nutritional drugs showed a signiflcant decrease in the EEN group. Conclusion Early enteral nutrition is safe, rational and effective in patients with liver cirrhosis after hepatectomy.     

一氧化氮对正常及肝硬化大鼠全胃肠外营养肝损害的影响

目的　探讨一氧化氮（Nitricoxide,NO）在全胃肠外营养(Total Parenteral Nutrition,TPN)导致正常肝脏及肝硬化大鼠肝损害中的影响。　方法　30只正常Wistar大鼠和30只肝硬化Wistar大鼠各自分别随机分为5组A组,自由进食和水;B组,TPN;C组,TPN+精氨酸;D组TPN+N     

Use of steatotic graft in living-donor liver transplantation

BACKGROUND: The degree of fatty infiltration in hepatic grafts is known to be an important risk factor for primary graft nonfunction in cadaveric liver transplantation. However, the effect of hepatic steatosis in living-donor liver transplantation (LDLT) has not yet been well defined. In this study, we evaluated the impact that the degree of hepatic graft steatosis has on the outcome of LDLT. METHODS: Sixty consecutive donors and recipients who underwent LDLT between October 1996 and August 2001 at Kyushu University Hospital were the subjects of this study. The pathologic findings of the prereperfusion biopsy of the graft were classified into the following three groups according to the degree of macrovesicular steatosis: None (n=23), 0% steatosis; Mild (n=23), 0% to 20% steatosis; and Moderate (n=6), 20% to 50% steatosis. Liver function tests including total bilirubin (at postoperative day [POD] 7), the peak alanine aminotransferase (ALT) and prothrombin time (at POD 3), and both patient and graft survival were compared among the groups. Furthermore, we also compared the donor parameters including the peak ALT and total bilirubin (at POD 3) and the operative time, blood loss, and length of hospital stay after surgery. RESULTS: The 1-year patient and graft survival were comparable among the groups. The peak ALT was significantly higher in the Moderate group (606+/-641 IU/L) than in the None (290+/-190 IU/L) and Mild (376+/-296 IU/L) groups. Total bilirubin (POD 7) and prothrombin time (POD 3) were comparable among the groups. The donor parameters were comparable among the groups except for the fact that the donor body weight of the Mild and Moderate groups were significantly heavier (P<0.0001) than that of the None group. CONCLUSIONS: In conclusion, the use of a fatty liver graft up to the moderate level can be justified in LDLT, even though ischemia-reperfusion injury tends to be severe in such grafts.     

肉毒碱治疗TPN大鼠肝脂肪变性的研究

目的 探讨在全胃肠外营养（ＴＰＮ）中补充肉毒碱减轻肝脂肪变性的作用。方法 １８只正常Ｗｉｓｔａｒ大鼠和１９只肝硬化Ｗｉｓｔａｒ大鼠分别随机分为６组,Ａ１组、Ａ２组,自由进食和进水（各６只）;Ｂ１组、Ｂ２组,ＴＰＮ（分别６只、７只）;Ｃ１组、 ,ＴＰＮ加肉毒碱（各６只）。各组实验结束后测肝功能,肝脂肪及行肝脏的组织学检查。结果 ＴＰＮ组肝内脂肪显著２,ＴＰＮ＋肉毒碱组肝内脂肪明显减少。结论 在ＴＰＮ     

Addition of glucagon to total parenteral nutrition (TPN) prevents hepatic steatosis in rats

Hepatic steatosis is one of the two principal hepatic complications of total parenteral nutrition (TPN), the other being cholestasis. While the cause is uncertain, an excess of carbohydrate calories in rats leads to an elevated portal insulin/glucagon (I/G) molar ratio, periportal fatty infiltration, and increased total hepatic lipid content. Insulin causes fatty acid biosynthesis, whereas glucagon causes hepatic release and inhibition of fatty acid synthesis. Thus we attempted to add glucagon to lower the I/G to see if this would affect the degree of hepatic fatty infiltration by encouraging hepatic fat mobilization. Adult rats (n = 21) received internal jugular catheters; Group 1 (n = 7) was given saline solution (3 ml/h) and chow ad libitum; Group 2 (n = 7), 25% dextrose-base (D25W) TPN solution; Group 3 (n = 7), D25W TPN + 33 micrograms/100 gm/day glucagon. At 7 days portal and peripheral venous blood samples were drawn for insulin and glucagon radioimmunoassay and blood glucose determination; livers were removed for histologic study and lipid determination. Blood glucose did not differ in any group. Hepatic lipid and peripheral and portal venous I/G were increased and periportal fatty infiltration was extensive in Group 2, whereas hepatic lipid and I/G were decreased and periportal fatty infiltration was absent in glucagon-infused rats (Group 3). An abnormally high I/G ratio in portal blood elicited by high-glucose TPN may be responsible, at least in part, for hepatic steatosis. By increasing hepatic lipid export, addition of glucagon to TPN may play a major role in decreasing hepatic steatosis.     

Effect of graft steatosis on liver function and organ survival after liver transplantation

BACKGROUND: It was the aim to determine the effect of graft steatosis on intraoperative organ blood flow, postoperative liver function, and organ survival. METHODS: A total of 225 consecutive liver transplants were reviewed. Liver blood flow, hepatic function (AST, ALT, prothrombin time), and organ survival were determined. Donor liver grafts were categorized into 2 subgroups: mild (<30%) (n = 175) and moderate to severe (>/=30%) (n = 50) macrovesicular steatosis. RESULTS: Moderate to severe steatosis was associated with significantly increased AST and ALT levels and significantly diminished prothrombin time on the first and second postoperative day. By day 7 differences in liver function were no longer evident. Organ blood flow was not affected by steatosis. After adjustment for potential confounders, organ survival did not depend on the degree of donor steatosis (5-year-survival rates: 68% and 58% with steatosis <30%, or >/= 30%, respectively) (hazard ratio .754, confidence interval .458-1.242, P = .268). CONCLUSION: Steatotic livers can be transplanted safely with good results for long-term organ survival if other contraindications are absent.     

胰岛素门静脉灌注促进活体肝移植术后肝再生的临床研究

目的 探讨成人活体肝移植(LDLT)术后胰岛素门静脉灌注对移植肝再生的促进作用.方法 2005年7月至2007年9月间接受右肝LDLT并自愿接受术后门静脉胰岛素灌注、有完整临床资料并存活超过30 d的15例成人受者作为研究对象(胰岛素组),同期未接受门静脉胰岛素灌注治疗、有完整临床资料并存活超过30 d的连续15例成人受者作为对照组研究对象(对照组).胰岛素组受者LDLT术中从胃网膜右静脉插入一根18 G硅胶管至门静脉系统,另一端固定于腹壁,术后以2 U/h速度静脉微泵持续均匀门静脉灌注胰岛素7 d.对照组无门静脉插管及胰岛素灌注.LDLT术前1d、术后7 d及30 d检测肝功能与外周血胰岛素水平,术中、术后7 d及术后30 d测量移植肝体积(GV).以GV比例(术后移植肝体积/术中移植肝体积之百分比)和供肝受者体重比(GRWB)比例(术后GRWR/术中GRWR之百分比例)作为移植肝再生检测指标.结果 LDLT术后7d胰岛素组与对照组受者移植肝GV比例分别为(186.1±35.4)%和(160.6±22.1)%,胰岛素组移植肝再生率高于对照组(P<0.05);胰岛素组与对照组受者GRWR比例分别为(179.0±35.8)%和(156.6±18.5)%,胰岛素组移植肝再生率亦高于对照组(P<0.05).LDLT术后30 d胰岛素组与对照组受者移植肝再生率的差异无统计学意义(P>0.05).LDLT术后7 d胰岛素组患者血清总胆红素、丙氨酸转氨酶和天冬氨酸转氨酶水平低于对照组.术后两组患者外周血胰岛素水平及外周胰岛素用量的差异均无统计学意义.结论 LDLT术后胰岛素门静脉灌注可能促进术后第1周移植肝再生.     

Addition of L-glutamine to total parenteral nutrition and its effects on portal insulin and glucagon and the development of hepatic steatosis in rats

Infusion of total parenteral nutrition (TPN) with excess carbohydrate calories leads to hepatic steatosis in rats and is associated with an elevated portal insulin/glucagon molar ratio. Previously we have shown that adding glucagon to TPN prevents and reverses hepatic steatosis in rats, possibly by increasing hepatic lipid export. It has been reported that steatosis is eliminated in rats by the addition of L-glutamine to TPN. In this study, we examined the effect of glutamine on portal insulin and glucagon levels and the development of hepatic steatosis. Adult rats (n = 19) received internal jugular catheters: Group 1 (n = 6), saline (3 cc/hr) and chow ad libitum; Group 2 (n = 7), 25% dextrose base TPN; Group 3 (n = 6), 25% dextrose base TPN with 2% glutamine. The infusion rate of TPN was 1.2 cc/100 g body wt/hr. Daily nitrogen balance was determined and at 7 days, portal venous blood was drawn for insulin and glucagon radioimmunoassay, livers were removed for histology and lipid content determination, and the small intestines were removed for mucosal protein and DNA content determination. Panlobular vacuolization of the hepatocytes was noted on histology in Group 2 (TPN) while Group 1 (chow) and Group 3 (TPN + glutamine) showed normal liver morphology. Hepatic lipid content was significantly elevated in Group 2 (P less than 0.05). The portal insulin/glucagon molar ratio was increased because of excessive portal venous insulin in Group 2 (TPN). In contrast, portal glucagon was significantly elevated while the insulin/glucagon ratio and hepatic lipid content did not increase above control levels in the glutamine-supplemented Group 3 rats.(ABSTRACT TRUNCATED AT 250 WORDS)