Insulin resistance induced in dairy steers by tumor necrosis factor alpha is partially reversed by 2,4-thiazolidinedione

被引:37
作者
Kushibiki, S [1 ]
Hodate, K
Shingu, H
Ueda, Y
Shinoda, M
Mori, Y
Itoh, T
Yokomizo, Y
机构
[1] Tohoku Natl Agr Exptl Stn, Dept Anim Prod, Morioka, Iwate 0200198, Japan
[2] Natl Inst Anim Ind, Dept Anim Physiol, Tsukuba, Ibaraki 3050901, Japan
[3] Natl Inst Anim Hlth, Dept Biol Prod, Tsukuba, Ibaraki 3050856, Japan
关键词
D O I
10.1016/S0739-7240(01)00102-3
中图分类号
S8 [畜牧、 动物医学、狩猎、蚕、蜂];
学科分类号
0905 ;
摘要
The aim of this study was to determine whether 2,4-thiazolidinedione (2,4-TZD) influences the effects of peripheral insulin action in steers given recombinant bovine tumor necrosis factor (TNF) alpha (rbTNF). Steers were treated once daily for 9 d (d0 - d8) with either s.c. injection of rbTNF (2.5 mug/kg), rbTNF + i.v. injection of 2,4-TZD (2.0 mg/kg), or s.c. injection of saline (control). The plasma glucose, NEFA, and insulin concentrations in the rbTNF-treated group increased compared to those in the control and rbTNF + 2,4-TZD groups, whereas glucagon concentration decreased. A single i.v. injection of insulin (0.2 U/kg), glucose (112.5 mg/kg), or growth hormone (GH)-releasing hormone (GHRH) (0.25 mug/kg) was performed on d4, d6, and d8, respectively. In the insulin challenge, the net area under the glucose curve (AUC) was smaller in the rbTNF group than in the control and rbTNF + 2,4-TZD groups. In the glucose challenge, the net insulin AUC was smaller in rbTNF + 2,4-TZD group than in rbTNF group. In the GHRH challenge, there was no difference in GH responses to GHRH between the rbTNF and rbTNF + 2,4-TZD groups, respectively. We conclude that 2,4-TZD treatment partially reverses the impairment of peripheral insulin action caused by rbTNF injection in steers. (C) 2001 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:25 / 37
页数:13
相关论文
共 45 条
[1]   Tumor necrosis factor-α alters glucose metabolism in suckling rats [J].
Battelino, T ;
Goto, M ;
Krzisnik, C ;
Zeller, WP .
JOURNAL OF LABORATORY AND CLINICAL MEDICINE, 1999, 133 (06) :583-589
[2]   Effect of tumor necrosis factor-alpha on insulin action in cultured rat skeletal muscle cells [J].
Begum, N ;
Ragolia, L .
ENDOCRINOLOGY, 1996, 137 (06) :2441-2446
[3]   CACHECTIN (TUMOR NECROSIS FACTOR) - A MACROPHAGE HORMONE GOVERNING CELLULAR-METABOLISM AND INFLAMMATORY RESPONSE [J].
BEUTLER, B ;
CERAMI, A .
ENDOCRINE REVIEWS, 1988, 9 (01) :57-66
[4]  
ELSASSER TH, 1991, P SOC EXP BIOL MED, V198, P547
[5]  
EXTON JH, 1972, METABOLISM, V21, P550
[6]   15-DEOXY-DELTA(12,14)-PROSTAGLANDIN J(2) IS A LIGAND FOR THE ADIPOCYTE DETERMINATION FACTOR PPAR-GAMMA [J].
FORMAN, BM ;
TONTONOZ, P ;
CHEN, J ;
BRUN, RP ;
SPIEGELMAN, BM ;
EVANS, RM .
CELL, 1995, 83 (05) :803-812
[7]   Acute and chronic exposure to tumor necrosis factor-alpha fails to affect insulin-stimulated glucose metabolism of isolated rat soleus muscle [J].
Furnsinn, C ;
Neschen, S ;
Wagner, O ;
Roden, M ;
Bisschop, M ;
Waldhausl, W .
ENDOCRINOLOGY, 1997, 138 (07) :2674-2679
[8]   Pioglitazone induces in vivo adipocyte differentiation in the obese Zucker fa/fa rat [J].
Hallakou, S ;
Doare, L ;
Foufelle, F ;
Kergoat, M ;
GuerreMillo, M ;
Berthault, MF ;
Dugail, I ;
Morin, J ;
Auwerx, J ;
Ferre, P .
DIABETES, 1997, 46 (09) :1393-1399
[9]  
HARRIS PKW, 1994, MOL PHARMACOL, V45, P439
[10]   Thiazolidinediones [J].
Henry, RR .
ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA, 1997, 26 (03) :553-&