A long-term sucrose-rich diet increases diacylglycerol content and membrane nPKCθ expression and alters glucose metabolism in skeletal muscle of rats

被引:15
作者
D'Alessandro, Maria E. [1 ]
Chicco, Adriana G. [1 ]
Lombardo, Yolanda B. [1 ]
机构
[1] Univ Litoral, Dept Biochem, Sch Biochem, RA-3000 Santa Fe, Argentina
关键词
muscle lipid metabolism; sucrose-rich diet; dyslipidemia; insulin resistance;
D O I
10.1016/j.nutres.2006.06.001
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
This study was designed to examine the possible metabolic pathways that could be involved in the increase of lipid storage in the gastrocnemius muscle and insulin resistance in rats fed a sucrose-rich diet (sucrose 63%, wt/wt) for 30 weeks. In the gastrocnemius muscle, malonyl-CoA, diacylglycerol (DAG), and long-chain acyl-CoA (LC ACoA) contents; novel protein kinase C 0 (nPKC theta) and Glut4 protein mass; and hexokinase, GSa, and pyruvate dehydrogenase (PDH) and PDH kinase activities were analyzed. The results were compared with age-matched rats fed a control diet (starch 63%, wt/wt) during the same period. In the sucrose-rich-fed rats, 2 major findings are reported: (1) a significant increase of DAG levels and nPKC theta protein mass in the membrane fraction, accompanied by a high increase of both triglycerides and LC ACoA contents in the gastrocnemius muscle; and (2) a significant decrease of hexokinase activity without changes of Glut4 protein mass and an altered glucose oxidation (low PDH complex and high PDH kinase activities). These findings suggest that different metabolic pathways could contribute to the development of insulin resistance in the skeletal muscle of long-term sucrose-fed rats: (1) a high level of LC ACoA by their esterification to DAG could stimulate the increase and translocation of the nPKC theta isozyme to the cell membrane, which might interfere with insulin signaling pathways; (2) a decrease in the hexokinase activity alters glucose phosphorylation and could impair insulin-mediated glucose disposal; (3) a significant reduction of flux through PDH complex may limit glucose oxidation via the glucose-fatty acid cycle. (c) 2006 Published by Elsevier Inc.
引用
收藏
页码:289 / 296
页数:8
相关论文
共 45 条
[1]  
BERGMEYER HU, 1974, METHOD ENZYMAT AN, P1100
[2]   Triacylglycerol accumulation in human obesity and type 2 diabetes is associated with increased rates of skeletal muscle fatty acid transport and increased sarcolemmal FAT/CD36 [J].
Bonen, A ;
Parolin, ML ;
Steinberg, GR ;
Calles-Escandon, J ;
Tandon, NN ;
Glatz, JFC ;
Luiken, JJFP ;
Heigenhauser, GJF ;
Dyck, DJ .
FASEB JOURNAL, 2004, 18 (07) :1144-+
[3]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[4]  
Bray GA, 2004, AM J CLIN NUTR, V79, P537
[5]   Relationship to insulin resistance of the Adult Treatment Panel III diagnostic criteria for identification of the metabolic syndrome [J].
Cheal, KL ;
Abbasi, F ;
Lamendola, C ;
McLaughlin, T ;
Reaven, GM ;
Ford, ES .
DIABETES, 2004, 53 (05) :1195-1200
[6]   Muscle lipid metabolism and insulin secretion are altered in insulin-resistant rats fed a high sucrose diet [J].
Chicco, A ;
D'Alessandro, ME ;
Karabatas, L ;
Pastorale, C ;
Basabe, JC ;
Lombardo, YB .
JOURNAL OF NUTRITION, 2003, 133 (01) :127-133
[7]  
CHICCO AG, 1994, J BIOL CHEM, V269, P19427
[8]   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
[9]   EXPRESSION OF THE MAJOR ISOENZYME OF PROTEIN-KINASE-C IN SKELETAL-MUSCLE, NPKC-THETA, VARIES WITH MUSCLE-TYPE AND IN RESPONSE TO FRUCTOSE-INDUCED INSULIN-RESISTANCE [J].
DONNELLY, R ;
REED, MJ ;
AZHAR, S ;
REAVEN, GM .
ENDOCRINOLOGY, 1994, 135 (06) :2369-2374
[10]   Long-chain acyl-CoA esters as indicators of lipid metabolism and insulin sensitivity in rat and human muscle [J].
Ellis, BA ;
Poynten, A ;
Lowy, AJ ;
Furler, SM ;
Chisholm, DJ ;
Kraegen, EW ;
Cooney, GJ .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2000, 279 (03) :E554-E560