Disassociation of muscle triglyceride content and insulin sensitivity after exercise training in patients with Type 2 diabetes.
OBJECTIVE
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).


CONCLUSIONS
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.
Bruce
C R
CR
Exercise Metabolism Group, School of Medical Sciences, RMIT University, PO Box 71, Bundoora, Victoria 3083, Australia.
Kriketos
A D
AD
Cooney
G J
GJ
Hawley
J A
JA
D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000378:metabolism; D000273:Adipose Tissue / Q000033:anatomy & histology; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D015992:Body Mass Index; D002950:Citrate (si)-Synthase / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism* / Q000503:physiopathology*; D015444:Exercise / Q000502:physiology*; D015309:Glucose Clamp Technique; D006801:Humans; D007328:Insulin / Q000494:pharmacology*; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism*; D010101:Oxygen Consumption; D010809:Physical Fitness; D012016:Reference Values; D014280:Triglycerides / Q000378:metabolism*
D001786:Blood Glucose; D007328:Insulin; D014280:Triglycerides; D015094:3-Hydroxyacyl CoA Dehydrogenases; D002950:Citrate (si)-Synthase