Infection impairs insulin-dependent hepatic glucose uptake during total parenteral nutrition

被引:12
作者
Donmoyer, CM [1 ]
Chen, SS [1 ]
Lacy, DB [1 ]
Pearson, DA [1 ]
Poole, A [1 ]
Zhang, YQ [1 ]
McGuinness, OP [1 ]
机构
[1] Vanderbilt Univ, Dept Mol Physiol & Biophys, Sch Med, Nashville, TN 37232 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM | 2003年 / 284卷 / 03期
关键词
liver; insulin; dog; glycogen; nutritional support;
D O I
10.1152/ajpendo.00035.2002
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Total parenteral nutrition (TPN) markedly augments net hepatic glucose uptake (NHGU) and hepatic glycolysis in the presence of mild hyperglycemia and hyperinsulinemia. This increase is impaired by an infection. We determined whether the adaptation to TPN alters the responsiveness of the liver to insulin and whether infection impairs that response. Chronically catheterized dogs received TPN for 5 days. On day 3 of TPN, either a nonlethal hypermetabolic infection was induced (INF, n = 5) or a sham surgery was performed (SHAM, n = 5). Forty-two hours after clot implantation, somatostatin and glucagon (34 +/- 3 vs. 84 +/- 11 pg/ml in artery, SHAM vs. INF) were infused, and a three-step (120 min each) isoglycemic (similar to120 mg/dl) hypermsulinernic (similar to12, 25, and 50 muU/ml) clamp was performed to simulate levels seen in normal, infected, and exogenous insulin treatment states. In SHAM, NHGU (3.5 +/- 0.2 to 4.2 +/- 0.4 to 4.6 +/- 0.5 mg(.)kg(-1).min(-1)) modestly increased. In INF, NHGU was consistently lower at each insulin step (1.1 +/- 0.5 to 2.6 +/- 0.5 to 2.8 +/- 0.7 mg(.)kg(-1.)min(-1)). Although NHGU increased from the first to the second step in INF, it did not increase further with the highest dose of insulin. Despite increases in NHGU, net hepatic lactate release did not increase in SHAM and fell in INK In summary, in the TPN-adapted state, liver glucose uptake is unresponsive to increases in insulin above the basal level. Although the infection-induced increase in insulin sustains NHGU, further increments in insulin enhance neither NHGU nor glycolysis.
引用
收藏
页码:E574 / E582
页数:9
相关论文
共 26 条
[1]  
BERNT E, 1984, METHOD ENZYMAT AN, P1704
[2]   RAPID METHOD FOR DETERMINATION OF GLYCOGEN CONTENT AND RADIOACTIVITY IN SMALL QUANTITIES OF TISSUE OR ISOLATED HEPATOCYTES [J].
CHAN, TM ;
EXTON, JH .
ANALYTICAL BIOCHEMISTRY, 1976, 71 (01) :96-105
[3]   Hyperinsulinemia compensates for infection-induced impairment in net hepatic glucose uptake during TPN [J].
Donmoyer, CM ;
Chen, SS ;
Hande, SA ;
Lacy, DB ;
Ejiofor, J ;
McGuinness, OP .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2000, 279 (02) :E235-E243
[4]   Fructose augments infection-impaired net hepatic glucose uptake during TPN administration [J].
Donmoyer, CM ;
Ejiofor, J ;
Lacy, DB ;
Chen, SS ;
McGuinness, OP .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2001, 280 (05) :E703-E711
[5]   Small increases in insulin inhibit hepatic glucose production solely caused by an effect on glycogen metabolism [J].
Edgerton, DS ;
Cardin, S ;
Emshwiller, M ;
Neal, D ;
Chandramouli, V ;
Schumann, WC ;
Landau, BR ;
Rossetti, L ;
Cherrington, AD .
DIABETES, 2001, 50 (08) :1872-1882
[6]  
FOSTER LB, 1974, CLIN CHEM, V20, P365
[7]   VALIDITY AND RELIABILITY OF LIQUID-CHROMATOGRAPHY WITH ELECTROCHEMICAL DETECTION FOR MEASURING PLASMA-LEVELS OF NOREPINEPHRINE AND EPINEPHRINE IN MAN [J].
GOLDSTEIN, DS ;
FEUERSTEIN, G ;
IZZO, JL ;
KOPIN, IJ ;
KEISER, HR .
LIFE SCIENCES, 1981, 28 (05) :467-475
[8]   DOSE-RESPONSE RELATIONSHIPS FOR THE EFFECTS OF INSULIN ON GLUCOSE AND FAT-METABOLISM IN INJURED PATIENTS AND CONTROL SUBJECTS [J].
HENDERSON, AA ;
FRAYN, KN ;
GALASKO, CSB ;
LITTLE, RA .
CLINICAL SCIENCE, 1991, 80 (01) :25-32
[9]  
LANG CH, 1989, CIRC SHOCK, V28, P165
[10]   INSULIN-MEDIATED GLUCOSE-UPTAKE BY INDIVIDUAL TISSUES DURING SEPSIS [J].
LANG, CH ;
DOBRESCU, C ;
MESZAROS, K .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1990, 39 (10) :1096-1107