The potential role of adenosine in the pathophysiology of the insulin resistance syndrome

被引:39
作者
Bakker, SJL
Gans, ROB
ter Maaten, JC
Teerlink, T
Westerhoff, HV
Heine, RJ
机构
[1] Univ Groningen Hosp, Dept Internal Med, NL-9700 RB Groningen, Netherlands
[2] Vrije Univ Amsterdam Hosp, Res Inst Endocrinol Reprod & Metab, Amsterdam, Netherlands
[3] Vrije Univ Amsterdam, Dept Mol Cell Physiol, Amsterdam, Netherlands
关键词
adenosine; insulin resistance; obesity; non-insulin-dependent diabetes mellitus; uric acid; hypertension; hematocrit; sympathetic nervous system;
D O I
10.1016/S0021-9150(00)00745-0
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
An increased intracellular availability of the co-enzyme A esters of long-chain fatty acids is thought to underlie many aspects of the insulin resistance syndrome. However, the cause of clustering of a hyperdynamic circulation, sympathetic activation. hypertension, hyperuricaemia, and a raised haematocrit in the insulin resistance syndrome remains to be elucidated. We propose a mechanism that expands the etiological role of long-chain fatty acids. By inhibiting adenine nucleotide translocators. elevated intracellular concentrations of the co-enzyme A esters of long-chain fatty acids impair mitochondrial oxidative phosphorylation. This is expected to result in a chronic systemic increase in extracellular adenosine concentrations. As adenosine stimulates the sympathetic nervous system, induces systemic vasodilatation, stimulates erythropoiesis. and induces renal vasoconstriction with renal sodium retention, increased extracellular ADO concentrations: may be the common denominator explaining the above-mentioned and still unexplained phenomena associated with the insulin resistance syndrome. Along the same lines, hyperuricaemia can be explained by the fact that adenosine is broken down to urate and because of increased renal urate retention. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:283 / 290
页数:8
相关论文
共 101 条
[1]  
Azevedo A, 1999, J CARDIOVASC RISK, V6, P321
[2]   Cytosolic triglycerides and oxidative stress in central obesity:: the missing link between excessive atherosclerosis, endothelial dysfunction, and β-cell failure? [J].
Bakker, SJL ;
IJzerman, RG ;
Teerlink, T ;
Westerhoff, HV ;
Gans, ROB ;
Heine, RJ .
ATHEROSCLEROSIS, 2000, 148 (01) :17-21
[3]   Effects of intravenous adenosine on renal function in healthy human subjects [J].
Balakrishnan, VS ;
Coles, GA ;
Williams, JD .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 1996, 271 (02) :F374-F381
[4]   A POTENTIAL ROLE FOR ENDOGENOUS ADENOSINE IN CONTROL OF HUMAN GLOMERULAR AND TUBULAR FUNCTION [J].
BALAKRISHNAN, VS ;
COLES, GA ;
WILLIAMS, JD .
AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 265 (04) :F504-F510
[5]  
Balis M E, 1976, Adv Clin Chem, V18, P213, DOI 10.1016/S0065-2423(08)60299-1
[6]   Fetal origins of cardiovascular disease [J].
Barker, DJP .
ANNALS OF MEDICINE, 1999, 31 :3-6
[7]  
Baron A D, 1994, Curr Opin Nephrol Hypertens, V3, P631, DOI 10.1097/00041552-199411000-00013
[8]   Insulin resistance syndrome in 8-year-old Indian children - Small at birth, big at 8 years, or both? [J].
Bavdekar, A ;
Yajnik, CS ;
Fall, CHD ;
Bapat, S ;
Pandit, AN ;
Deshpande, V ;
Bhave, S ;
Kellingray, SD ;
Joglekar, C .
DIABETES, 1999, 48 (12) :2422-2429
[9]   HIGH-ALTITUDE TRAINING - ASPECTS OF HEMATOLOGICAL ADAPTATION [J].
BERGLUND, B .
SPORTS MEDICINE, 1992, 14 (05) :289-303
[10]  
BERNE RM, 1983, FED PROC, V42, P3136