Effect of Web-based lifestyle modification on weight control: a meta-analysis.

OBJECTIVE: Web-based treatment programs are attractive in primary care because of their ability to reach numerous individuals at low cost. Our aim of this meta-analysis is to systematically review the weight loss or maintenance effect of the Internet component in obesity treatment programs. METHODS: MEDLINE and EMBASE literature searches were conducted to identify studies investigating the effect of Web-based individualized advice on lifestyle modification on weight loss. Randomized controlled trials that consisted of a Web-user experimental and non-Web user control group were included. Weight changes in the experimental group in comparison with the control group were pooled with a random-effects model. RESULTS: A total of 23 studies comprising 8697 participants were included. Overall, using the Internet had a modest but significant additional weight-loss effect compared with non-Web user control groups (-0.68 kg, P=0.03). In comparison with the control group, stratified analysis indicated that using the Internet as an adjunct to obesity care was effective (-1.00 kg, P<0.001), but that using it as a substitute for face-to-face support was unfavorable (+1.27 kg, P=0.01). An additional effect on weight control was observed when the aim of using the Internet was initial weight loss (-1.01 kg; P=0.03), but was not observed when the aim was weight maintenance (+0.68 kg; P=0.26). The relative effect was diminished with longer educational periods (P-trend=0.04) and was insignificant (-0.20 kg; P=0.75) in studies with educational periods of 12 months or more. CONCLUSION: The current meta-analysis indicates that the Internet component in obesity treatment programs has a modest effect on weight control. However, the effect was inconsistent, largely depending on the type of usage of the Internet or the period of its use.

The regulation of adiponectin receptors expression by acute exercise in mice.

Adiponectin is an adipocyte-derived factor that plays a pivotal role in lipid and glucose metabolism. Recently, two types of adiponectin receptors (AdipoR1 and AdipoR2) were identified. While, although physical exercise is useful for improving insulin sensitivity, the effect of physical exercise on adiponectin and adiponectin receptors are still unclear. In present study, we investigated whether acute exercise affects the plasma adiponectin concentration and expression of adiponectin receptor in skeletal muscle and liver in healthy mice C57BL/6. Following an acute exercise, plasma glucose, insulin, FFA, and adiponectin were measured. The mRNA levels of AdipR1 and AdipoR2 were also analyzed. Although acute exercise did not significantly change plasma adiponectin concentration at 2 hours or 18 hours after the exercise compared with control group, the expression levels of AdipoR1 significantly increased in both skeletal muscle (2H: 1.2-fold, p=0.0423, 18H: 1.4-fold, p=0.0006) and liver (2H: 1.3-fold, p=0.0448) compared with control group. In contrast, the level of AdipoR2 mRNA was decreased in skeletal muscle (18H: 0.8-fold, p=0.027) and liver (2H: 0.9-fold, p=0.1551) compared with control group. Additionally, the transcription factor Foxo1 mRNA expression level was also significantly increased in skeletal muscle (2H: 10-fold, p=0.0001, 18H: 3-fold, p=0.0424) and liver (2H: 2-fold, p=0.002, 18H: 2-fold, p=0.0014) compared with control group by the acute exercise. These findings suggest that acute exercise affects the expression level of adiponectin receptors, and an increase of Foxo1 expression might be relative to regulate adiponectin receptors.

Insulin up-regulates tumor necrosis factor-alpha production in macrophages through an extracellular-regulated kinase-dependent pathway.

Hyperinsulinemia has recently been reported as a risk factor for atherosclerotic diseases such as coronary heart disease; however, the effect of insulin on the development of atherosclerosis is not well understood. Here we have investigated the direct effect of insulin on macrophages, which are known to be important in the atherosclerotic process. We treated THP-1 macrophages with insulin (10(-7) m) and examined the gene expression using nucleic acid array systems. The results of array analysis showed that insulin stimulated gene expression of tumor necrosis factor-alpha (TNF-alpha) the most among all genes in the analysis. In addition, insulin administration to macrophages enhanced both mRNA expression and protein secretion of TNF-alpha in a dose-dependent manner. To determine the signaling pathway involved in this TNF-alpha response to insulin, we pretreated the cells with three distinct protein kinase inhibitors: wortmannin, PD98059, and SB203580. Only PD98059, which inhibits extracellular signal-regulated kinases, suppressed insulin-induced production of TNF-alpha mRNA and protein in THP-1 macrophages. These observations indicate that insulin stimulates TNF-alpha production in macrophages by regulating the expression of TNF-alpha mRNA and that the extracellular signal-regulated kinase signaling pathway may have a critical role in stimulating the production of TNF-alpha in response to insulin in macrophages.