Endothelial function and biochemical vascular markers in first-degree relatives of type 2 diabetic patients: the effect of exercise training

Metabolism ◽  
2006 ◽  
Vol 55 (11) ◽  
pp. 1508-1515 ◽  
Author(s):  
Torben Østergård ◽  
Birgit Nyholm ◽  
Troels K. Hansen ◽  
Lars M. Rasmussen ◽  
Jørgen Ingerslev ◽  
...  
2006 ◽  
Vol 290 (5) ◽  
pp. E998-E1005 ◽  
Author(s):  
Torben Østergård ◽  
Jesper L. Andersen ◽  
Birgit Nyholm ◽  
Sten Lund ◽  
K.Sreekumaran Nair ◽  
...  

First-degree relatives of type 2 diabetic patients (offspring) are often characterized by insulin resistance and reduced physical fitness (V̇o2 max). We determined the response of healthy first-degree relatives to a standardized 10-wk exercise program compared with an age-, sex-, and body mass index-matched control group. Improvements in V̇o2 max(14.1 ± 11.3 and 16.1 ± 14.2%; both P < 0.001) and insulin sensitivity (0.6 ± 1.4 and 1.0 ± 2.1 mg·kg−1·min−1; both P < 0.05) were comparable in offspring and control subjects. However, V̇o2 maxand insulin sensitivity in offspring were not related at baseline as in the controls ( r = 0.009, P = 0.96 vs. r = 0.67, P = 0.002). Likewise, in offspring, exercise-induced changes in V̇o2 maxdid not correlate with changes in insulin sensitivity as opposed to controls ( r = 0.06, P = 0.76 vs. r = 0.57, P = 0.01). Skeletal muscle oxidative capacity tended to be lower in offspring at baseline but improved equally in both offspring and controls in response to exercise training (Δcitrate synthase enzyme activity 26 vs. 20%, and Δcyclooxygenase enzyme activity 25 vs. 23%. Skeletal muscle fiber morphology and capillary density were comparable between groups at baseline and did not change significantly with exercise training. In conclusion, this study shows that first-degree relatives of type 2 diabetic patients respond normally to endurance exercise in terms of changes in V̇o2 maxand insulin sensitivity. However, the lack of a correlation between the V̇o2 maxand insulin sensitivity in the first-degree relatives of type 2 diabetic patients indicates that skeletal muscle adaptations are dissociated from the improvement in V̇o2 max. This could indicate that, in first-degree relatives, improvement of insulin sensitivity is dissociated from muscle mitochondrial functions.


2006 ◽  
Vol 291 (5) ◽  
pp. E906-E912 ◽  
Author(s):  
Pietro Lucotti ◽  
Emanuela Setola ◽  
Lucilla D. Monti ◽  
Elena Galluccio ◽  
Sabrina Costa ◽  
...  

Because chronic l-arginine supplementation improves insulin sensitivity and endothelial function in nonobese type 2 diabetic patients, the aim of this study was to evaluate the effects of a long-term oral l-arginine therapy on adipose fat mass (FM) and muscle free-fat mass (FFM) distribution, daily glucose levels, insulin sensitivity, endothelial function, oxidative stress, and adipokine release in obese type 2 diabetic patients with insulin resistance who were treated with a combined period of hypocaloric diet and exercise training. Thirty-three type 2 diabetic patients participated in a hypocaloric diet plus an exercise training program for 21 days. Furthermore, they were divided into two groups in randomized order: the first group was also treated with l-arginine (8.3 g/day), and the second group was treated with placebo. Although in the placebo group body weight, waist circumference, daily glucose profiles, fructosamine, insulin, and homeostasis model assessment index significantly decreased, l-arginine supplementation further decreased FM ( P < 0.05) and waist circumference ( P < 0.0001), preserving FFM ( P < 0.03), and improved mean daily glucose profiles ( P < 0.0001) and fructosamine ( P < 0.03). Moreover, change in area under the curve of cGMP (second messenger of nitric oxide; P < 0.001), superoxide dismutase (index of antioxidant capacity; P < 0.01), and adiponectin levels ( P < 0.02) increased, whereas basal endothelin-1 levels ( P < 0.01) and leptin-to-adiponectin ratio ( P < 0.05) decreased in the l-arginine group. Long-term oral l-arginine treatment resulted in an additive effect compared with a diet and exercise training program alone on glucose metabolism and insulin sensitivity. Furthermore, it improved endothelial function, oxidative stress, and adipokine release in obese type 2 diabetic patients with insulin resistance.


Diabetes Care ◽  
2007 ◽  
Vol 30 (10) ◽  
pp. 2511-2513 ◽  
Author(s):  
H. M. De Feyter ◽  
S. F. Praet ◽  
N. M. van den Broek ◽  
H. Kuipers ◽  
C. D. Stehouwer ◽  
...  

2010 ◽  
Vol 118 (10) ◽  
pp. 607-615 ◽  
Author(s):  
Sandra J. Hamilton ◽  
Gerard T. Chew ◽  
Timothy M.E. Davis ◽  
Gerald F. Watts

Dyslipidaemia contributes to endothelial dysfunction and CVD (cardiovascular disease) in Type 2 diabetes mellitus. While statin therapy reduces CVD in these patients, residual risk remains high. Fenofibrate corrects atherogenic dyslipidaemia, but it is unclear whether adding fenofibrate to statin therapy lowers CVD risk. We investigated whether fenofibrate improves endothelial dysfunction in statin-treated Type 2 diabetic patients. In a cross-over study, 15 statin-treated Type 2 diabetic patients, with LDL (low-density lipoprotein)-cholesterol <2.6 mmol/l and endothelial dysfunction [brachial artery FMD (flow-mediated dilatation) <6.0%] were randomized, double-blind, to fenofibrate 145 mg/day or matching placebo for 12 weeks, with 4 weeks washout between treatment periods. Brachial artery FMD and endothelium-independent NMD (nitrate-mediated dilatation) were measured by ultrasonography at the start and end of each treatment period. PIFBF (post-ischaemic forearm blood flow), a measure of microcirculatory endothelial function, and serum lipids, lipoproteins and apo (apolipoprotein) concentrations were also measured. Compared with placebo, fenofibrate increased FMD (mean absolute 2.1±0.6 compared with −0.3±0.6%, P=0.04), but did not alter NMD (P=0.75). Fenofibrate also increased maximal PIFBF {median 3.5 [IQR (interquartile range) 5.8] compared with 0.3 (2.1) ml/100 ml/min, P=0.001} and flow debt repayment [median 1.0 (IQR 3.5) compared with −1.5 (3.0) ml/100 ml, P=0.01]. Fenofibrate lowered serum cholesterol, triacylgycerols (triglycerides), LDL-cholesterol, apoB-100 and apoC-III (P≤0.03), but did not alter HDL (high-density lipoprotein)-cholesterol or apoA-I. Improvement in FMD was inversely associated with on-treatment LDL-cholesterol (r=−0.61, P=0.02) and apoB-100 (r=−0.54, P=0.04) concentrations. Fenofibrate improves endothelial dysfunction in statin-treated Type 2 diabetic patients. This may relate partly to enhanced reduction in LDL-cholesterol and apoB-100 concentrations.


2014 ◽  
Vol 60 (06/2014) ◽  
Author(s):  
Xh. Zhuang ◽  
Fd. Sun ◽  
Sh. Chen ◽  
Yt. Liu ◽  
W. Liu ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document