[Purpose] The purpose of this study was to investigate the effect of forward head posture (FHP) on proprioception by determining the cervical position-reposition error. [Subjects and Methods] A sample population was divided into two groups in accordance with the craniovertebral angle: the FHP group and the control group. We measured the craniovertebral angle, which is defined as the angle between a horizontal line passing through C7 and a line extending from the tragus of the ear to C7. The error value of the cervical position sense after cervical flexion, extension, and rotation was evaluated using the head repositioning accuracy test. [Results] There were significant differences in the error value of the joint position sense (cervical flexion, extension, and rotation) between the FHP and control groups. In addition, there was an inverse correlation between the craniovertebral angle and error value of the joint position sense. [Conclusion] FHP is associated with reduced proprioception. This result implies that the change in the muscle length caused by FHP decreases the joint position sense. Also, proprioception becomes worse as FHP becomes more severe.

No abstract

In the present study, we investigated the possibility that the WNT/β-catenin pathway plays a role in inflammatory responses both in an human inflammatory condition and in an in vitro inflammation model. First, we analyzed gene expression patterns of the peripheral blood cells from asthma patients compared with those from normal subjects using microarray analyses. We found that intracellular signaling molecules of the WNT/β-catenin pathway were significantly changed in asthma patients compared with the levels in the controls. Next, we determined whether major components of the WNT/β-catenin pathway were involved in the lipopolysaccharide (LPS)-induced inflammatory response of the RAW264.7 macrophage cell line. Among the members of WNT/β-catenin pathway, the protein levels of low-density lipoprotein receptor-related protein (LRP) 6, dishevelled (DVL) 2, and AXIN1, which were measured using western blotting, did not significantly change in the presence of LPS. In contrast, the LPS induced a rapid phosphorylation of glycogen synthase kinase (GSK) 3β and accumulation of β-catenin protein. It was found that β-catenin plays a significant role in the LPS-induced inflammatory response through the performance of small interfering RNA (siRNA) transfection experiments. The mRNA level of IL-6 was significantly elevated in β-catenin siRNA-transfected cells compared with that in control siRNA-transfected cells after LPS treatment. Furthermore, nuclear factor-κB (NF-κB) activity was also significantly increased in β-catenin siRNA-transfected cells compared with the level seen in control siRNA-transfected cells. Taken together, these results suggest that β-catenin plays a role as a negative regulator, preventing the overproduction of inflammatory cytokines such as IL-6 in LPS-induced inflammatory responses.

Shikonin, 5,6-dihydroxyfl avone-7-glucuronic acid, is the main ingredient of Lithospermum erythrorhizon Sieb. et Zucc, and was reported to have various biological activities including antiinfl ammatory, anticancer, antimicrobial and others. This study aimed to elucidate, for the fi rst time, the antiobesity activity of shikonin and its mechanism of action. Shikonin was found to inhibit fat droplet formation and triglyceride accumulation in 3T3-L1 adipocytes. The half inhibitory concentration, IC 50 , for the inhibition of triglyceride accumulation was found to be 1.1 mM. The expression of genes involved in lipid metabolism, such as FABP4 and LPL, were signifi cantly inhibited following shikonin treatment. Shikonin also inhibited the ability of PPARg and C/EBPa, the major transcription factors of adipogenesis, to bind to their target DNA sequences. The expressions of mRNA and protein of PPARg and C/EBPa were signifi cantly down-regulated following shikonin treatment. Among the upstream regulators of adipogenesis, only SREBP1C was found to be down-regulated by shikonin. The results of this study suggest that shikonin down-regulates the expression of SREBP1C and subsequently the expression of PPARg and C/EBPa. Together, these changes result in the down-regulation of lipid metabolizing enzymes and reduced fat accumulation.

1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the active metabolite of vitamin D, was found to have anti-adipogenic activity, however, its mechanism of action has not been fully elucidated. In this study, 3T3-L1 preadipocytes were differentiated in the presence and absence of 1,25(OH)2D3, and the expression of the genes and proteins of the wingless-type MMTV integration site (WNT)/β-catenin pathway were analyzed. While the expression of the members of the WNT/β-catenin pathway were significantly downregulated during the adipogenesis of untreated 3T3-L1 cells, 1,25(OH)2D3 treatment was found to maintain the WNT/β-catenin pathway. Among the members of the WNT/β-catenin pathway, the levels of WNT10B and disheveled (DVL)2 as well as the phosphorylation of glycogen synthase kinase (GSK)3β were maintained by 1,25(OH)2D3 treatment. The levels of nuclear β-catenin, which were downregulated during adipogenesis, were also maintained by 1,25(OH)2D3 treatment. The results of this study suggested that the anti-adipogenic effect of 1,25(OH)2D3 was mediated by the maintenance of the WNT/β-catenin pathway, which was normally downregulated during adipogenesis.

Abstract. AMP-activated protein kinase (AMPK) is known to sense the cellular energy state and regulates various cellular energy metabolism pathways through its activation by AMP, an indicator of a low-energy state. 5-Aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AIcAR), an activator of AMPK, efficiently inhibited the adipogenesis of 3T3-L1 cells. To elucidate its possible mechanism of action, the expression levels of β-catenin and other members of the WNT/β-catenin pathway were analyzed during the adipogenesis of 3T3-L1 cells in the presence or absence of AIcAR. It was found that AIcAR significantly enhanced β-catenin expression and its nuclear accumulation. Transfection of β-catenin small interfering RNA (siRNA) significantly prevented the effects of AIcAR on the expression of various genes. The expression of the major genes of adipogenesis including the peroxisome proliferator-activated receptor (PPAR)γ, the ccAAT/ enhancer binding protein (c/EPB)α, the fatty acid binding protein (FABP)4 and lipoprotein lipase (LPL), which were all reduced by AICAR treatment, were significantly recovered in β-catenin siRNA-transfected cells. Among the members of the WNT/β-catenin pathway, the expression of low density lipoprotein receptor-related protein (LRP)6, dishevelled (DVL)2 and DVL3 were significantly up-regulated by AICAR treatment, whereas the expression of AXIN was downregulated. The present study provides compelling evidence that AIcAR inhibits adipogenesis through the modulation of the WNT/β-catenin pathway.

No abstract

In this study, the antiobesity effects of baicalin, 5,6-dihydroxyflavone-7-glucuronic acid, were characterized using an in vitro system of adipogenesis, i.e. fat cell formation. Baicalin-treatment of 3T3-L1 preadipocytes was shown to inhibit triglyceride accumulation and lipid droplet formation during induced adipogenesis. Microarray analyses showed that baicalin modulated the expression of genes located in pathways such as adipogenesis, cholesterol biosynthesis, focal adhesion and others. In the adipogenesis pathway, treatment with baicalin significantly down-regulated terminal differentiation markers of adipocytes including fatty acid binding protein 4. The effects of baicalin on the core part of the adipogenesis pathway, however, were paradoxical; the expression levels of CCAAT/enhancer binding protein (C/EBP)beta and C/EBPdelta were up-regulated, while the expression levels of the peroxisome proliferator-activated receptor (PPAR)gamma and C/EBPalpha were down-regulated. The antiadipogenic mechanisms of baicalin can be explained by its effects on the upstream part of adipogenesis pathway; baicalin not only up-regulates the antiadipogenic regulators, C/EBPgamma, C/EBP homologous protein and Kruppel-like factor (KLF)2, but also down-regulates the proadipogenic regulator, KLF15. The overall effects of baicalin on these upstream regulators of adipogenesis were antiadipogenic, resulting in the down-regulation of downstream genes and the inhibition of cellular fat accumulation.