Desaturase activities in rat model of insulin resistance induced by a sucrose-rich diet

被引:49
作者
Brenner, RR
Rimoldi, OJ
Lombardo, YB
González, MS
Bernasconi, AM
Chicco, A
Basabe, JC
机构
[1] Natl Univ La Plata, Fac Ciencias Med, CONICET, INIBIOLP, RA-1900 La Plata, Argentina
[2] Univ Litoral, Fac Bioquim & Ciencias Biol, Dept Ciencias Biol, RA-3000 Santa Fe, Argentina
[3] Hosp Ninos Dr Ricardo Gutierrez, CEDIE, Buenos Aires, DF, Argentina
关键词
D O I
10.1007/s11745-003-1121-x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
A sucrose-rich diet, as compared with a similar starch diet, induces a time-dependent typical noninsulin-dependent diabetes syndrome characterized by insulin resistance in rats. Within the first 3 wk, there was glucose intolerance associated with hyperinsulinemia, hypertriglyceridemia; and high plasma FFA. In this study, we examined the effect of the sucrose-rich diet vs. the starch diet during short- (3 wk) and long-term treatment (6 mon) on hepatic Delta9, Delta6, and Delta5 desaturases. These enzymes modulate monounsaturated FA and PUFA biosynthesis, respectively. Sucrose feeding (3 wk) caused an initial hyperinsulinemia that was normalized within 6 mon. In the early period (3 wk), stearoyl-CoA desaturase-1 (SCD-1) mRNA and activity were decreased, whereas Delta6 desaturase mRNA abundance and Delta6 and Delta5 desaturase activities remained unchanged. After 6 mon of sucrose feeding, activities of the Delta9, Delta6, and Delta5 desaturases were each increased. The SCD-1 and A6 desaturase mRNA were also correspondingly higher. These increases were consistent with an increase in oleic acid, the 20:4/18:2 ratio, and 22:4n-6 and 22:5n-6 acids in liver and muscle lipids. On the other hand, the percentage of 22:6n-3 acid was decreased. In conclusion, a sucrose-rich diet after 6 mon induces an increase in rat liver SCD-1 and A6 desaturase mRNA and enzymatic activities that are opposite to the changes reported in insulin-dependent diabetes mellitus. It appears that neither blood insulin levels nor insulin resistance is a factor affecting the Delta9, Delta6, and Delta5 desaturase changes in mRNA and activity found with the sucrose-rich diet.
引用
收藏
页码:733 / 742
页数:10
相关论文
共 42 条
[1]  
Bergmeyer HI., 1974, METHODS ENZYMATIC AN
[2]   Effect of experimental diabetes on the fatty acid composition, molecular species of phosphatidyl-choline and physical properties of hepatic microsomal membranes [J].
Brenner, RR ;
Bernasconi, AM ;
Garda, HA .
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS, 2000, 63 (03) :167-176
[3]   EFFECT OF ARACHIDONIC ACID IN ALLOXAN-DIABETIC RAT [J].
BRENNER, RR ;
PELUFFO, RO ;
MERCURI, O ;
RESTELLI, MA .
AMERICAN JOURNAL OF PHYSIOLOGY, 1968, 215 (01) :63-+
[4]   Hormonal modulation of Δ6 and Δ5 desaturases:: case of diabetes [J].
Brenner, RR .
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS, 2003, 68 (02) :151-162
[5]   Effect of dexamethasone on the fatty acid composition of total liver microsomal lipids and phosphatidylcholine molecular species [J].
Brenner, RR ;
Ayala, S ;
Garda, HA .
LIPIDS, 2001, 36 (12) :1337-1345
[6]  
CATALA A, 1975, J BIOL CHEM, V250, P7481
[7]   MICRODETERMINATION OF PHOSPHORUS [J].
CHEN, PS ;
TORIBARA, TY ;
WARNER, H .
ANALYTICAL CHEMISTRY, 1956, 28 (11) :1756-1758
[8]   Troglitazone (CS-045) normalizes hypertriglyceridemia and restores the altered patterns of glucose-stimulated insulin secretion in dyslipidemic rats [J].
Chicco, A ;
Basabe, JC ;
Karabatas, L ;
Ferraris, N ;
Fortino, A ;
Lombardo, YB .
METABOLISM-CLINICAL AND EXPERIMENTAL, 2000, 49 (10) :1346-1351
[9]   Role of skeletal muscle on impaired insulin sensitivity in rats fed a sucrose-rich diet: Effect of moderate levels of dietary fish oil [J].
D'Alessandro, ME ;
Chicco, A ;
Karabatas, L ;
Lombardo, YB .
JOURNAL OF NUTRITIONAL BIOCHEMISTRY, 2000, 11 (05) :273-280
[10]   Unique ability of troglitazone to up-regulate peroxisome proliferator-activated receptor-γ expression in hepatocytes [J].
Davies, GF ;
McFie, PJ ;
Khandelwal, RL ;
Roesler, WJ .
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2002, 300 (01) :72-77