The effects of insulin on transport and metabolism of glucose in skeletal muscle from hyperthyroid and hypothyroid rats

被引:84
作者
Dimitriadis, G
ParryBillings, M
Bevan, S
Leighton, B
Krause, U
Piva, T
Tegos, K
Challiss, RAJ
Wegener, G
Newsholme, EA
机构
[1] UNIV OXFORD, DEPT BIOCHEM, OXFORD OX1 2JD, ENGLAND
[2] UNIV MAINZ, INST ZOOL, MAINZ, GERMANY
[3] 401 MIL GEN HOSP, CLIN RES UNIT, ATHENS, GREECE
[4] UNIV LEICESTER, DEPT CELL PHYSIOL & PHARMACOL, LEICESTER LE1 7RH, LEICS, ENGLAND
关键词
fructose 2,6-bisphosphate; glucose transport/utilization; hexokinase; muscle; prostaglandins; thyroid hormones;
D O I
10.1046/j.1365-2362.1997.1380688.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The effects of insulin on the rates of glucose disposal were studied in soleus muscles isolated from hyper- or hypothyroid rats. Treatment with triiodothyronine for 5 or 10 days decreased the sensitivity of glycogen synthesis but increased the sensitivity of lactate formation to insulin. The sensitivity of 3-O methylglucose to insulin was increased only after 10 days of treatment and was accompanied by an increase in the sensitivity of 2-deoxyglucose phosphorylation; however, 2-deoxyglucose and glucose 6-phosphate in response to insulin remained unaltered. In hypothyroidism, insulin-stimulated rates of 3-O-methylglucose transport and 2-deoxyglucose phosphorylation were decreased; however, at basal levels of insulin, 3-O-methylglucose transport was increased, while 2-deoxyglucose phosphorylation was normal. In these muscles, the sensitivity of lactate formation to insulin was decreased; this defect was improved after incubation of the muscles with prostaglandin E-2. The results suggest: (a) in hyperthyroidism, insulin-stimulated rates of glucose utilization in muscle to form lactate are increased mainly because of a decrease in glycogen synthesis; when hypethyroidism progresses in severity, increases in the sensitivity of glucose transport to insulin and in the activity of hexokinase may also be involved; (b) in hypothyroidism, the decrease in insulin-stimulated rates of glucose utilization is caused by decreased rates of glycolysis; (c) prostaglandins may be involved in the changes in sensitivity of glucose utilization to insulin observed in muscle in altered thyroid states.
引用
收藏
页码:475 / 483
页数:9
相关论文
共 43 条
[1]  
Beutler E., 1975, A manuel of biochemical methods, V2nded
[2]  
BRATUSCHMARRAIN PR, 1984, AM J PHYSIOL, V247, pE681, DOI 10.1152/ajpendo.1984.247.5.E681
[3]   INCREASED GLUCOSE TRANSPORTER (GLUT4) PROTEIN EXPRESSION IN HYPERTHYROIDISM [J].
CASLA, A ;
ROVIRA, A ;
WELLS, JA ;
DOHM, GL .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1990, 171 (01) :182-188
[4]   INSULIN RESISTANCE IN GRAVES-DISEASE - A QUANTITATIVE INVIVO EVALUATION [J].
CAVALLOPERIN, P ;
BRUNO, A ;
BOINE, L ;
CASSADER, M ;
LENTI, G ;
PAGANO, G .
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 1988, 18 (06) :607-613
[5]   INFLUENCE OF HYPOTHYROIDISM ON GROWTH-HORMONE BINDING BY RAT-LIVER [J].
CHERNAUSEK, SD ;
UNDERWOOD, LE ;
VANWYK, JJ .
ENDOCRINOLOGY, 1982, 111 (05) :1534-1538
[6]  
CHU DTW, 1985, J BIOL CHEM, V260, P9994
[7]   EFFECT OF THYROID STATUS ON INSULIN ACTION IN RAT ADIPOCYTES AND SKELETAL-MUSCLE [J].
CZECH, MP ;
MALBON, CC ;
KERMAN, K ;
GITOMER, W ;
PILCH, PF .
JOURNAL OF CLINICAL INVESTIGATION, 1980, 66 (03) :574-582
[8]   EFFECTS OF INSULIN-LIKE GROWTH FACTOR-I ON THE RATES OF GLUCOSE-TRANSPORT AND UTILIZATION IN RAT SKELETAL-MUSCLE INVITRO [J].
DIMITRIADIS, G ;
PARRYBILLINGS, M ;
BEVAN, S ;
DUNGER, D ;
PIVA, T ;
KRAUSE, U ;
WEGENER, G ;
NEWSHOLME, EA .
BIOCHEMICAL JOURNAL, 1992, 285 :269-274
[9]   EFFECTS OF INVIVO ADMINISTRATION OF INSULIN-LIKE GROWTH FACTOR-I ON THE RATE OF GLUCOSE-UTILIZATION IN THE SOLEUS MUSCLE OF THE RAT [J].
DIMITRIADIS, G ;
PARRYBILLINGS, M ;
DUNGER, D ;
BEVAN, S ;
COLQUHOUN, A ;
TAYLOR, A ;
CALDER, P ;
KRAUSE, U ;
WEGENER, G ;
NEWSHOLME, EA .
JOURNAL OF ENDOCRINOLOGY, 1992, 133 (01) :37-43
[10]   STUDIES ON THE EFFECTS OF GROWTH-HORMONE ADMINISTRATION IN-VIVO ON THE RATES OF GLUCOSE-TRANSPORT AND UTILIZATION IN RAT SKELETAL-MUSCLE [J].
DIMITRIADIS, G ;
PARRYBILLINGS, M ;
LEIGHTON, B ;
PIVA, T ;
DUNGER, D ;
CALDER, P ;
BOND, J ;
NEWSHOLME, E .
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 1994, 24 (03) :161-165