title: Hyperglycemic diet and training alter insulin sensitivity, intramyocellular lipid content but not UCP3 protein expression in rat skeletal muscles.
abstract: Intramyocellular lipids (IMCL) and mitochondrial uncoupling protein-3 (UCP3) have been implicated in the development of muscular insulin resistance. This study aimed to investigate the role of IMCL and UCP3 in the development of glucose intolerance and muscular insulin resistance during 12 weeks of an obesity-inducing 'cafeteria-style' diet alone (CAF), or in conjunction with exercise training from weeks 8-12 (CAFTR), in rats. At the end of the intervention period, gain in body weight was 20% higher in CAF (305+/-10 g) than controls (CON) (255+/-14 g; p<0.001) and CAFTR (253+/-7 g; p<0.001). Furthermore, compared with CON, the Matsuda insulin sensitivity index (ISI), assessed during a 2-h intravenous glucose tolerance test, was markedly lower in CAF (6.7+/-0.4) than in either CON (15.6+/-1.4; p<0.001) or CAFTR (11.2+/-1.1; p<0.001). Moreover, in CAF glucose transport at a submaximal insulin concentration (200 microU/ml) was reduced by approximately 60% (p<0.05) in both red and white gastrocnemius muscles, but not in m. soleus. However, glucose transport in CAFTR was similar to CON in red gastrocnemius. In CAF fiber-specific IMCL content determined in m. soleus and extensor digitorum longus (EDL), was higher than in CON (p<0.01) and CAFTR (p<0.001). Muscle UCP3 protein content was not changed by any of the interventions. Interestingly, within CAF and CAFTR, ISI closely negatively correlated with IMCL content in both type I (soleus, r=-0.93; EDL, r=-0.90; p<0.05) and IIa (EDL, r=-0.52, p<0.05) muscle fibers. These findings indicate that changes in IMCL content but not UCP3 content are implicated in short-term effects of cafeteria-style diet and exercise training on muscular insulin sensitivity in rats.
authors.affiliation: Department of Biomedical Kinesiology, Faculty of Kinesiology and Rehabilitation Sciences, Research Centre for Exercise and Health, K.U. Leuven, B-3001 Leuven, Belgium.
authors.forename: Morad
authors.initials: M
authors.lastname: Vaisy
authors.forename: Karolina
authors.initials: K
authors.lastname: Szlufcik
authors.forename: Michael
authors.initials: M
authors.lastname: Maris
authors.forename: Katrien
authors.initials: K
authors.lastname: De Bock
authors.forename: Matthijs K C
authors.initials: MK
authors.lastname: Hesselink
authors.forename: Bert O
authors.initials: BO
authors.lastname: Eijnde
authors.forename: Patrick
authors.initials: P
authors.lastname: Schrauwen
authors.forename: Peter
authors.initials: P
authors.lastname: Hespel
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D004032:Diet; D005227:Fatty Acids / Q000378:metabolism; D005247:Feeding Behavior / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects; D018149:Glucose Intolerance / Q000150:complications / Q000378:metabolism; D006943:Hyperglycemia / Q000150:complications / Q000378:metabolism*; D007328:Insulin / Q000097:blood / Q000494:pharmacology*; D007333:Insulin Resistance; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism*; D050356:Lipid Metabolism / Q000187:drug effects*; D008297:Male; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D010805:Physical Conditioning, Animal; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D000071247:Uncoupling Protein 3
chemical_list: D001786:Blood Glucose; D005227:Fatty Acids; D007328:Insulin; D007473:Ion Channels; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; C000604394:Ucp3 protein, rat; D000071247:Uncoupling Protein 3