Amelioration of insulin resistance and hypertension in a fructose-fed rat model with fish oil supplementation

被引:56
作者
Huang, YJ
Fang, VS
Juan, CC
Chou, YC
Kwok, CF
Ho, LT
机构
[1] VET GEN HOSP, DEPT MED RES & EDUC, TAIPEI, TAIWAN
[2] VET GEN HOSP, DEPT INTERNAL MED, TAIPEI, TAIWAN
[3] NATL YANG MING UNIV, DEPT PHYSIOL, TAIPEI 112, TAIWAN
[4] MIL 803 GEN HOSP, DEPT CLIN PATHOL, TAIPEI, TAIWAN
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 1997年 / 46卷 / 11期
关键词
D O I
10.1016/S0026-0495(97)90226-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
In type II diabetic patients, one can detect several pathologic changes including insulin resistance and hypertension. Sprague-Dawley rats fed a fructose-rich diet (group F) exhibited these characteristic abnormalities within 2 weeks and were an excellent laboratory animal model for research on insulin action and development of hypertension. Since fish oils containing omega-3 fatty acids have a beneficial effect in preventing atherosclerotic diseases, we performed repeated experiments to test the effects of fish oil supplementation in group F rats. Compared with control rats on a normal diet (group C), group F consistently developed hypertriglyceridemia without elevated plasma free fatty acid (FFA), fasting hyperinsulinemia together with fasting hyperglycemia (insulin resistance syndrome), and systolic hypertension within 3 weeks, Insulin-stimulated glucose uptake and insulin binding of adipocytes were significantly reduced, Rats fed the same high fructose diet but supplemented with fish oil (group O) had alleviation of al of these metabolic defects and a normalized insulin sensitivity and blood pressure. beta-Cell function as shown by plasma glucose and insulin responses to oral glucose remained intact in group F and group O. The plasma endothelin-1 (ET-1) level and ET-1 binding to adipocytes were not different among the three groups. Based on these results, we suggest that dietary high fructose induced hypertriglyceridemia and insulin resistance with normal islet function, and-that the induced hypertension was not associated with plasma ET-1 abnormalities and was probably caused by other undefined pathologic changes that can be prevented by dietary omega-a fatty acids. Copyright (C) 1997 by W.B. Saunders Company.
引用
收藏
页码:1252 / 1258
页数:7
相关论文
共 41 条
[1]   DOES SUPPLEMENTATION OF DIET WITH FISH-OIL REDUCE BLOOD-PRESSURE - A METAANALYSIS OF CONTROLLED CLINICAL-TRIALS [J].
APPEL, LJ ;
MILLER, ER ;
SEIDLER, AJ ;
WHELTON, PK .
ARCHIVES OF INTERNAL MEDICINE, 1993, 153 (12) :1429-1438
[2]  
BANG HO, 1976, ACTA MED SCAND, V200, P69
[3]   PROTECTIVE EFFECTS OF DIETARY FISH OIL ON FOCAL CEREBRAL INFARCTION [J].
BLACK, KL ;
CULP, B ;
MADISON, D ;
RANDALL, OS .
PROSTAGLANDINS AND MEDICINE, 1979, 3 (05) :257-268
[4]   CHRONIC EXPOSURE OF CULTURED ENDOTHELIAL-CELLS TO EICOSAPENTAENOIC ACID POTENTIATES THE RELEASE OF ENDOTHELIUM-DERIVED RELAXING FACTOR(S) [J].
BOULANGER, C ;
SCHINI, VB ;
HENDRICKSON, H ;
VANHOUTTE, PM .
BRITISH JOURNAL OF PHARMACOLOGY, 1990, 99 (01) :176-180
[5]   VALIDATION IN AWAKE RATS OF A TAIL-CUFF METHOD FOR MEASURING SYSTOLIC PRESSURE [J].
BUNAG, RD .
JOURNAL OF APPLIED PHYSIOLOGY, 1973, 34 (02) :279-282
[6]  
BURR ML, 1989, LANCET, V2, P757
[7]   ENDOTHELIN-1 INHIBITS INSULIN-STIMULATION GLUCOSE-UPTAKE IN ISOLATED RAT ADIPOCYTES [J].
CHOU, YC ;
PERNG, JC ;
JUAN, CC ;
JANG, SY ;
KWOK, CF ;
CHEN, WL ;
FONG, JC ;
HO, LT .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1994, 202 (02) :688-693
[8]  
CONNOR WE, 1993, ANN NY ACAD SCI, V683, P337
[9]  
DYERBERG J, 1986, NUTR REV, V44, P125, DOI 10.1111/j.1753-4887.1986.tb07603.x
[10]   ELEVATED PLASMA-GLUCOSE AND LOWERED TRIGLYCERIDE LEVELS FROM OMEGA-3 FATTY-ACID SUPPLEMENTATION IN TYPE-II DIABETES [J].
FRIDAY, KE ;
CHILDS, MT ;
TSUNEHARA, CH ;
FUJIMOTO, WY ;
BIERMAN, EL ;
ENSINCK, JW .
DIABETES CARE, 1989, 12 (04) :276-281