BackgroundThis study aimed to analyze the effect of exercise and/or dietary change on improvement of non-alcoholic fatty liver disease (NAFLD) in chronic high-fat diet (HFD)-induced obese mice.MethodsForty male C57BL/6 (8 weeks old) mice were divided into normal diet (CO, n = 8) and high-fat diet (HF, n = 32) groups. The HF group was fed with 60% fat chow for 16 weeks to induce obesity. After the obesity induction period, the HF group was subdivided into HFD + sedentary (n = 8), HFD + training (HFT, n = 8), dietary change to normal-diet + sedentary (HFND, n = 8), and dietary change to normal-diet + training (HFNDT, n = 8) groups, and the mice in the training groups underwent treadmill training for 8 weeks, 5 times per week, 40 min per day.ResultsA 24-week HFD induced increase of cannabinoid-1 receptor (CB1), fatty acid synthase (FAS), and AMP-activated protein kinase (AMPK) protein expressions (p < 0.05) and decrease of p-AMPK and carnitine palmitoyltransferase1 (CPT1) protein expressions (P < 0.05), resulting in increased liver fat accumulation. Treatment of exercise with dietary change and dietary change alone decreased CB1 and AMPK protein expressions with increased p-AMPK and CPT1 protein expressions (P < 0.05), leading to decreased body weight and liver fat (P < 0.05). The CB1 and FAS protein expressions in the HFT group were still higher than those in the CO group (P < 0.05), but the p-AMPK and CPT1 protein expressions were higher than those in the HF group (P < 0.05). Moreover, improved glucose tolerance and decreased liver fat were confirmed, although treatment of exercise alone had no effect on weight loss compared to pre-exercise.ConclusionsEven in the case of obesity induced by chronic HFD, exercise and/or dietary interventions have preventive and therapeutic effects on fat accumulation in the liver, resulting from upregulations of lipolytic factors. Therefore, the results of this study suggested that treatment of exercise alone without dietary change also leads to improvement of NAFLD and glucose tolerance without weight loss benefits.
We investigated whether alterations in autonomic nervous system (ANS) activity were associated with metabolic. Ten type 1 diabetic children (11.8 ± 0.8 yr) and ten healthy children (10.7 ± very low-frequency (VLF) reflecting thermogenic sympathetic function; low-frequency (LF), an indicator of sympatho-vagal activity; high-frequency (HF) reflecting parasympathetic activity exclusively; and total power (TOTAL) representing overall ANS activity. All ANS activities including thermogenic sympathetic activity were significantly decreased in children with type 1 diabetes mellitus (T1DM) in comparison to control children (Total power, p < 0.01; LF, p < 0.01; HF, p < 0.05 and VLF, p < 0.01). Triglyceride (TG) and TG/HDL-C levels of atherogenic risk profiles were also significantly increased in T1DM children (p < 0.01 and p < 0.05, respectively). However, Fourier pulsatility index (PI) and blood flow velocity (FLOW) did not show any significant difference between groups. It was concluded that T1DM children might possess significantly lower ANS activities with elevated atherogenic risk factors in comparison with normal children even at the early stage of life. Therefore, it should consider therapies that can reduce these risk factors causing diabetic complications in childhood.
SummaryBackgroundPrehypertension has been associated with target-organ damage. This study sought to determine the impact of prehypertension (PHT) on QT dispersion and left ventricular hypertrophy (LVH) in adult black Nigerians.MethodsOne hundred and one subjects with office blood pressure (BP) < 140/90 mmHg were categorised according to their office BP into normotensive (BP < 120/80 mmHg, n = 57) and prehypertensive (BP 120–139/80–89 mmHg, n = 44) groups. Echocardiography and electrocardiography (ECG) were performed on the subjects.ResultsThirty-four males aged 53.65 ± 16.33 years and 67 females aged 52.42 ± 12.00 years were studied. The mean QT interval dispersion (QTd) of the normotensive (38.96 ± 11.06 ms) and prehypertensive (38.41 ± 11.81 ms) groups were similar (p = 0.81). Prehypertensive subjects had higher left ventricular mass (LVM) (165.75 ± 33.21 vs 144.54 ± 35.55 g, p = 0.024), left ventricular mass index 1 (LVMI-1) (91.65 ± 16.84 vs 80.45 ± 18.65 g/m2, p = 0.021) and left ventricular mass index 2 (LVMI-2) (54.96 ± 10.84 vs 47.51 ± 12.00 g/m2.7, p = 0.017). QTd was independent of echocardiographic and electrocardiographic LVH (p > 0.05).ConclusionCompared with normotension, prehypertension is associated with higher LVM but similar QTd. This suggests that structural remodelling precedes electrical remodelling in prehypertension.
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