The passive coping Roman Low Avoidance rat, a non-obese rat model for insulin resistance

被引:16
作者
Boersma, G. J. [1 ]
Scheurink, A. J. W. [1 ]
Wielinga, P. Y. [1 ]
Steimer, T. J. [2 ]
Benthem, L. [3 ]
机构
[1] Univ Groningen, Dept Neuroendocrinol, NL-9750 AA Haren, Netherlands
[2] Univ Hosp Geneva, APSI, Clin Psychopharmacol Unit, Geneva, Switzerland
[3] AstraZeneca, Biosci Diabet Obes, Molndal, Sweden
关键词
Coping style; Visceral adiposity; Intravenous glucose tolerance test; INTRAMYOCELLULAR LIPID-CONTENT; SKELETAL-MUSCLE; UNANESTHETIZED RAT; GENE-EXPRESSION; GLUCOSE; LINES; STRESS; NEUROENDOCRINE; HEPATOCYTES; ASSOCIATION;
D O I
10.1016/j.physbeh.2009.03.005
中图分类号
B84 [心理学];
学科分类号
04 ; 0402 ;
摘要
The aim of the study was develop to an animal model that links coping style to insulin resistance. We hypothesized that the psychogenetically selected Roman Low Avoidance (RLA) rats may serve as such a model. To test this hypothesis, we submitted both RLA and Roman High avoidance (RHA) rats to a series of intravenous glucose tolerance tests (IVGTT). These IVGTT were followed by post mortem metabolic characterization of the selection lines. It was found that plasma insulin levels are markedly elevated in the passively coping RLA rat. both in baseline conditions and during the intravenous glucose tolerance tests. The elevation in plasma insulin was accompanied with increased levels of plasma corticosterone, FFA, leptin and triglycerides but not by changes in body weight. We conclude that the passive, highly emotional RLA rat is metabolically different from both the RHA rat and the standard control Wistar rat and may serve as a non-obese animal model for insulin resistance. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:353 / 358
页数:6
相关论文
共 39 条
[1]  
Andrews RC, 1999, CLIN SCI, V96, P513, DOI 10.1042/cs0960513
[2]   OVERFEEDING-INDUCED OBESITY IN RATS - INSULIN SENSITIVITY AND AUTONOMIC REGULATION OF METABOLISM [J].
BALKAN, B ;
STRUBBE, JH ;
BRUGGINK, JE ;
STEFFENS, AB .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1993, 42 (12) :1509-1518
[3]   Surgical removal of visceral fat reverses hepatic insulin resistance [J].
Barzilai, N ;
She, L ;
Liu, BQ ;
Vuguin, P ;
Cohen, P ;
Wang, JL ;
Rossetti, L .
DIABETES, 1999, 48 (01) :94-98
[4]   Excess portal venous long-chain fatty acids induce syndrome X via HPA axis and sympathetic activation [J].
Benthem, L ;
Keizer, K ;
Wiegman, CH ;
De Boer, SF ;
Strubbe, JH ;
Steffens, AB ;
Kuipers, F ;
Scheurink, AJW .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2000, 279 (06) :E1286-E1293
[5]   SELECTION FOR HIGH RATES AND LOW RATES OF AVOIDANCE CONDITIONING IN RAT [J].
BIGNAMI, G .
ANIMAL BEHAVIOUR, 1965, 13 (2-3) :221-&
[6]  
BJORNTORP P, 1993, ADV EXP MED BIOL, V334, P279
[7]   Is insulin resistance caused by defects in insulin's target cells or by a stressed mind? [J].
Burén, J ;
Eriksson, JW .
DIABETES-METABOLISM RESEARCH AND REVIEWS, 2005, 21 (06) :487-494
[9]   Increased OB gene expression leads to elevated plasma leptin concentrations in patients with chronic primary hyperinsulinemia [J].
D'Adamo, M ;
Buongiorno, A ;
Maroccia, E ;
Leonetti, F ;
Barbetti, F ;
Giaccari, A ;
Zorretta, D ;
Tamburrano, G ;
Sbraccia, P .
DIABETES, 1998, 47 (10) :1625-1629
[10]   EFFECT OF ADRENALECTOMY ON INVIVO GLUCOSE-METABOLISM IN INSULIN RESISTANT ZUCKER OBESE RATS [J].
FREEDMAN, MR ;
STERN, JS ;
REAVEN, GM ;
MONDON, CE .
HORMONE AND METABOLIC RESEARCH, 1986, 18 (05) :296-298