An intervention study to promote self-improvement of lifestyle in a Japanese community: a new health support program.

OBJECTIVE: To assess the effectiveness of two health support programs developed to improve the lifestyle of community residents through exercise, nutrition-based health education, and group dynamics. METHODS: A total of 171 subjects were selected from community residents showing an abnormal result in at least one metabolic syndrome-related laboratory test. The subjects were divided into two groups: a group participating only in the 5-month initiation program (i.e., the initial program; n = 83), and a group participating both the initiation program and the subsequent 6-month enhancing program (i.e., the total program; n = 88). Each group was followed up for 1 year after completing the intervention program. The effectiveness of the intervention was determined based on data from the Health Promoting Lifestyle Profile II and laboratory tests, which were collected four times during the 2-year follow-up. Thirty-nine individuals were selected as the control group, based on the same criteria, to confirm the effectiveness of completing the intervention program. RESULTS: The results demonstrate that completion of the initiation programe was an effective intervention in terms of individual improvements in lifestyle and laboratory test results. The improvements achieved by the end of the initiation program had been sustained at the end of the total program, and were similar in both groups. One year after the end of the total program, both groups showed similar findings, confirming the effectiveness of the intervention. CONCLUSION: The results of this study demonstrate the effectiveness of two health support programs for improving the lifestyle of community residents. It is worth noting that, at the end of the 2-year follow-up, the improvements in lifestyle due to the initiation program were similar to those of the total program.

TZDs reduce mitochondrial ROS production and enhance mitochondrial biogenesis.

Although it has been reported that thiazolidinediones (TZDs) may reduce cardiovascular events in type 2 diabetic patients, its precise mechanism is unclear. We previously demonstrated that hyperglycemia-induced production of reactive oxygen species from mitochondria (mtROS) contributed to the development of diabetic complications, and metformin normalized mt ROS production by induction of MnSOD and promotion of mitochondrial biogenesis by activating the PGC-1alpha pathway. In this study, we examined whether TZDs could inhibit hyperglycemia-induced mtROS production by activating the PGC-1alpha pathway. We revealed that pioglitazone and ciglitazone attenuated hyperglycemia-induced ROS production in human umbilical vein endothelial cells (HUVECs). Both TZDs increased the expression of NRF-1, TFAM and MnSOD mRNA. Moreover, pioglitazone increased mtDNA and mitochondrial density. These results suggest that TZDs normalize hyperglycemia-induced mtROS production by induction of MnSOD and promotion of mitochondrial biogenesis by activating PGC-1alpha. This phenomenon could contribute to the prevention of diabetic vascular complications.

Endothelial MnSOD overexpression prevents retinal VEGF expression in diabetic mice.

We previously proposed that hyperglycemia-induced mitochondrial ROS overproduction is a key event in the development of diabetic complications. In this study, we established a novel transgenic mouse (eMnSOD-Tg), which specifically expressed MnSOD in endothelial cells, by employing a Tie2 promoter/enhancer, and investigated the impact of mitochondrial ROS production on diabetic retinopathy in vivo. Using immunohistochemistry, overexpression of MnSOD in endothelial cells was confirmed in eMnSOD-Tg mice. By introduction of diabetes by streptozotocin, levels of urinary 8-hydroxydeoxyguanosine, a marker of mitochondrial oxidative stress, and expression of VEGF mRNA and protein and fibronectin mRNA in retinas were increased in wild-type littermates. However, these observations were ameliorated in eMnSOD-Tg mice, although control and eMnSOD-Tg mice showed a comparable level of hyperglycemia. In the present study, we newly developed a line of transgenic mice, which specifically express MnSOD in endothelium. In addition, overexpression of mitochondrial-specific SOD in endothelium could prevent diabetic retinopathy in vivo.

Chronic hepatitis B with flare due to co-infection of hepatitis delta virus during lamivudine therapy.

In 1997, a 27-year-old homosexual man contracted acute hepatitis B that developed into chronic hepatitis. Because of repeated flares, administration of lamivudine was started in March 2002. Hepatitis B virus (HBV) DNA immediately decreased, but the serum level of alanine aminotransferase gradually increased. Drug-induced hepatitis due to lamivudine was excluded. It was suspected that the progression of liver damage was caused by hepatitis delta virus (HDV), because the patient was positive for both anti-HDV antibody and HDV RNA. Co-infection of HDV should be considered a possibility if liver injury is not improved by lamivudine therapy.