Disassociation of muscle triglyceride content and insulin sensitivity after exercise training in patients with Type 2 diabetes
AIM/HYPOTHESIS: We determined the effect of exercise training on insulin sensitivity and muscle lipids (triglyceride [TG(m)] and long-chain fatty acyl CoA [LCACoA] concentration) in patients with Type 2 diabetes. METHODS: Seven patients with Type 2 diabetes and six healthy control subjects who were matched for age, BMI, % body fat and VO(2)peak participated in a 3 days per week training program for 8 weeks. Insulin sensitivity was determined pre- and post-training during a 120 min euglycaemic-hyperinsulinaemic clamp and muscle biopsies were obtained before and after each clamp. Oxidative enzyme activities [citrate synthase (CS), beta-hydroxy-acyl-CoA (beta-HAD)] and TG(m) were determined from basal muscle samples pre- and post training, while total LCACoA content was measured in samples obtained before and after insulin-stimulation, pre- and post training. RESULTS: The training-induced increase in VO(2)peak (approximately 20%, p<0.01) was similar in both groups. Compared with control subjects, insulin sensitivity was lower in the diabetic patients before and after training (approximately 60%; p<0.05), but was increased to the same extent in both groups with training (approximately 30%; p<0.01). TG(m) was increased in patients with Type 2 diabetes (170%; p<0.05) before, but was normalized to levels observed in control subjects after training. Basal LCACoA content was similar between groups and was unaltered by training. Insulin-stimulation had no detectable effect on LCACoA content. CS and beta-HAD activity were increased to the same extent in both groups in response to training ( p<0.001). CONCLUSION/INTERPRETATION: We conclude that the enhanced insulin sensitivity observed after short-term exercise training was associated with a marked decrease in TG(m) content in patients with Type 2 diabetes. However, despite the normalization of TG(m )to levels observed in healthy individuals, insulin resistance was not completely reversed in the diabetic patients.
|Authors||Bruce, C. R.;Kriketos, A. D.;Cooney, G. J.;Hawley, J. A. :|
|Responsible Garvan Author|
|URL link to publisher's version||http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=14673522|
|OpenAccess link to author's accepted manuscript version||https://publications.gimr.garvan.org.au/open-access/1758|