IntroductionLutein is a carotenoid whose protective effects in the retina have been reported in various studies. The effect of lutein has not been reported in the retina of the Ins2Akita/+ mouse, a well-characterized genetic model for diabetic retinopathy (DR) in which the etiology of diabetes is better defined than the chemically induced diabetes. The objective of the present study is to investigate the effect of long-term administration of lutein in early stages of DR using the Ins2Akita/+ mouse.Research design and methodsHeterozygous male Ins2Akita/+ and age-matched wild-type mice were used. Lutein was administered to the mice in drinking water starting 6 weeks old daily until analysis at 4.5, 6.5 or 9 months of age. Plain water served as non-treatment control. Microglia were immunostained with ionized calcium-binding adapter molecule 1 (Iba-1) and cluster of differentiation 68 (CD68) in retinal flat-mounts. Vascular endothelial growth factor (VEGF) level in the retina was assessed by enzyme-linked immunosorbent assay (ELISA). Vascular permeability was analyzed in retinal flat-mounts after fluorescein isothiocyanate (FITC)-dextran perfusion. Retinal occludin expression was assessed via Western blots. Retinal function was examined by electroretinography (ERG).ResultsIncreased microglial reactivity was detected in the Ins2Akita/+ mouse retina and was suppressed by lutein. Lutein administration also reduced the upregulation of VEGF in the Ins2Akita/+ mouse retina. Increased vascular leakage and decreased occludin expression were observed in the Ins2Akita/+ mouse retina, and these alterations were attenuated by lutein treatment. ERG recordings showed reduced a-wave and b-wave amplitudes in the Ins2Akita/+ mice. With lutein treatment, the ERG deficits were significantly alleviated.ConclusionsWe showed beneficial effects of long-term lutein administration in the Ins2Akita/+ mouse retina, including suppression of retinal inflammation, protection of retinal vasculature and preservation of retinal function. These results point to lutein’s potential as a long-term therapeutic intervention for prevention of inflammation and retinal degeneration in patients with early DR.

Aims/IntroductionThe aim of the present study was to determine the effect of moderate aerobic exercise on cardiac autonomic function in type 2 diabetic patients.Materials and MethodsHeart rate variability of 20 patients with type 2 diabetes was assessed. Resting electrocardiogram for the heart rate variability analysis at spontaneous respiration was recorded for 5 min in the supine position before and after 6 months of supervised aerobic training given three times per week.ResultsIn time domain measures, the square root of the mean of the sum of the squares of differences between adjacent R-R intervals (RMSSD; 29.7 [26–34.5] vs 46.4 [29.8–52.2] ms, P = 0.023) and the percentage of consecutive RR intervals that differ by more than 50 ms (pNN50; 10.7 [5.5–12.7] vs 26.1 [6.6–37.2]%, P = 0.025] were significantly increased after exercise. In frequency domain measures, low frequency (62.4 [59.1–79.2] vs 37 [31.3–43.3] nu, P = 0.003) and low frequency/high frequency (1.67 [1.44–3.8] vs 0.58 [0.46–0.59]%, P = 0.009) were significantly decreased, whereas high frequency (95 [67–149] vs 229 [98–427] ms2, P = 0.006) and high frequency (37.6 [20.8–40.9] vs 63 [56.7–68.7] normalized units, P = 0.003) were significantly increased after exercise. In a Poincaré plot, standard deviation perpendicular to the line of the Poincaré plot (SD1; 21.3 [18.5–24.8]–33.1 [21.5–37.2] ms, P = 0.027) was significantly increased after exercise.ConclusionsThese data suggest that three times per week moderate intensity aerobic exercise for 6 months improves cardiac rhythm regulation as measured by heart rate variability in type 2 diabetic patients.

This study suggests that thrice-a-week moderate intensity aerobic exercise for six months improves cardiac rhythm regulation as measured by HRV in obese adults with type 2 diabetes.

The aim of the study was to determine if heart rate variability (HRV) showed any changes in patients with newly diagnosed epilepsy in comparison with controls. Sixty‐five patients with epilepsy (38 males and 27 females), aged 30–50 years, who had never previously received treatment with antiepileptic drugs were eligible for inclusion in this study. Resting electrocardiogram (ECG) at spontaneous respiration was recorded for 5 min in supine position. Time‐domain analysis, frequency‐domain analysis, and Poincare plot of HRV were recorded from ECG. In time‐domain measures, the square root of the mean of the sum of the squares of differences between adjacent RR intervals (RMSSD) and percentage of consecutive RR intervals that differ by more than 50 msec (pNN50) were significantly less in patients with epilepsy. In frequency‐domain measures, high frequency [(HF) msec2], HF (nu), and low frequency [LF (msec2)] were significantly less in patients with epilepsy while LF (nu) and LF/HF were significantly high in patients with epilepsy. In Poincare plot, standard deviation perpendicular to line of Poincare plot (SD1) and standard deviation along the line of entity in Poincare plot (SD2) were significantly less in patients with epilepsy. Our results suggest that epileptic patients have an impact on the cardiac autonomic function as measured by HRV.