Effectiveness of a back care pillow as an adjuvant physical therapy for chronic non-specific low back pain treatment: a randomized controlled trial.

[Purpose] The aim of this study was to investigate the effect of a back care pillow (BCP) on pain, lumbar range of motion (LROM) and functional disability of patients with chronic non-specific low back pain (LBP). [Subjects and Methods] Fifty-two subjects who were aged between 20-69 years old, who presented with LBP of more than 3 months duration with a numerical rating scale (NRS) value of at least 4 were randomly assigned to treatment (BCP) and control (CON) groups. Participants in each group received six sessions of the 30 minutes treatment for two weeks. The BCP group was asked to wear the BCP during the daytime during the study period. Pain, lumbar ROM and functional disability were assessed before and after the 2-week treatment, and at the end of a 12-week follow up. [Results] After the 2-week treatment and 12-week follow up, all outcomes had improved in both groups; the BCP group had maintained the decrease in pain intensity and improved lumbar ROM in the extension position after the 12-week follow up, and showed better improvements in all outcomes at 2 weeks and after the 12-week follow up. [Conclusion] BCP combined with physical therapy had better pain, lumbar ROM and functional disability outcomes than physical therapy alone.

The development of diet-induced obesity and glucose intolerance in C57BL/6 mice on a high-fat diet consists of distinct phases.

High-fat (HF) diet-induced obesity and insulin insensitivity are associated with inflammation, particularly in white adipose tissue (WAT). However, insulin insensitivity is apparent within days of HF feeding when gains in adiposity and changes in markers of inflammation are relatively minor. To investigate further the effects of HF diet, C57Bl/6J mice were fed either a low (LF) or HF diet for 3 days to 16 weeks, or fed the HF-diet matched to the caloric intake of the LF diet (PF) for 3 days or 1 week, with the time course of glucose tolerance and inflammatory gene expression measured in liver, muscle and WAT. HF fed mice gained adiposity and liver lipid steadily over 16 weeks, but developed glucose intolerance, assessed by intraperitoneal glucose tolerance tests (IPGTT), in two phases. The first phase, after 3 days, resulted in a 50% increase in area under the curve (AUC) for HF and PF mice, which improved to 30% after 1 week and remained stable until 12 weeks. Between 12 and 16 weeks the difference in AUC increased to 60%, when gene markers of inflammation appeared in WAT and muscle but not in liver. Plasma proteomics were used to reveal an acute phase response at day 3. Data from PF mice reveals that glucose intolerance and the acute phase response are the result of the HF composition of the diet and increased caloric intake respectively. Thus, the initial increase in glucose intolerance due to a HF diet occurs concurrently with an acute phase response but these effects are caused by different properties of the diet. The second increase in glucose intolerance occurs between 12-16 weeks of HF diet and is correlated with WAT and muscle inflammation. Between these times glucose tolerance remains stable and markers of inflammation are undetectable.

The effect of eicosapentaenoic and docosahexaenoic acid on protein synthesis and breakdown in murine C2C12 myotubes.

Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have been found to stimulate protein synthesis with little information regarding their effects on protein breakdown. Furthermore whether there are distinct effects of EPA and DHA remains to be established. The aim of the current study was to determine the distinct effects of EPA and DHA on protein synthesis, protein breakdown and signalling pathways in C2C12 myotubes. Fully differentiated C2C12 cells were incubated for 24h with 0.1% ethanol (control), 50 µM EPA or 50 µM DHA prior to experimentation. After serum (4h) and amino acid (1h) starvation cells were stimulated with 2 mM L-leucine and protein synthesis measured using (3)H-labelled phenylalanine. Protein breakdown was measured using (3)H-labelled phenylalanine and signalling pathways (Akt, mTOR, p70S6k, 4EBP1, rps6 and FOXO3a) via Western blots. Data revealed that after incubation with EPA protein synthesis was 25% greater (P<0.05) compared to control cells, with no effect of DHA. Protein breakdown was 22% (P<0.05) lower, compared to control cells, after incubation with EPA, with no effect of DHA. Analysis of signalling pathways revealed that both EPA and DHA incubation increased (P<0.05) p70s6k phosphorylation, EPA increased (P<0.05) FOXO3a phosphorylation, with no alteration in other signalling proteins. The current study has demonstrated distinct effects of EPA and DHA on protein metabolism with EPA showing a greater ability to result in skeletal muscle protein accretion.

Fish oil positively regulates anabolic signalling alongside an increase in whole-body gluconeogenesis in ageing skeletal muscle.

PURPOSE: Fish oil, containing mainly long-chain n-3 polyunsaturated fatty acids (LCn-3PUFA), has been found to acutely stimulate protein synthesis and insulin-mediated glucose metabolism. However, the underlying mechanism and more prolonged effect of fish oil during ageing remain to be determined. METHODS: Fish oil (EPAX6000; 49.6 % eicosapentaenoic acid, 50.4 % docosahexaenoic acid) or control oil (60 % olive, 40 % soy) supplementation was delivered, via chocolate-derived sweets, to rats for 8 weeks. Throughout the study, food intake and body weight were recorded and body composition was investigated using EchoMRI. During the last 40 min of a 6 h infusion, with labelled dextrose ([U-(13)C]glucose) and amino acids ([1-(13)C]phenylalanine), blood samples were collected to assess glucose and phenylalanine kinetics. Soleus and longissimus dorsi muscles were extracted for protein and mRNA analyses. RESULTS: Fish oil had no effect on food intake or body composition. An increased whole-body glucose turnover, mainly accounted for via an increase in endogenous glucose production, was observed with fish oil feeding. No effects on whole-body phenylalanine turnover were observed. In longissimus dorsi, fish oil augmented the phosphorylation of phosphoinositide 3-kinase (PI3K)([Tyr458]) (P = 0.04) and 70 kDa ribosomal protein S6 kinase (p70s6k)([Thr389]) (P = 0.04). There were no differences in protein kinase B (Akt)([Ser473]), mammalian target of rapamycin (mTOR)([Ser2448]), protein phosphatase 2A (PP2A) 56 kDa regulatory B subunit γ (PP2A-B56-γ), forkhead box containing proteins O-subclass 3a (FOX03a)([Ser253]) or inflammatory markers (Interleukin-6, Interleukin-1 ß, tumour necrosis factor-α, and cyclooxygenase-2). CONCLUSIONS: Our data suggest that the fish oil may stimulate endogenous glucose production and increase anabolic signalling in ageing rats.

The effect of exercise induced cytokines on insulin stimulated glucose transport in C2C12 cells.

Skeletal muscle contractile activity increases the production of the myokines interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-15 (IL-15) and also skeletal muscle glucose transport. Previous work has revealed a role for IL-6 in mediating glucose uptake, while research on the physiological roles of IL-8 and IL-15 is not so abundant. In the present study we investigated the effects of different concentrations and combinations of IL-6, IL-8 and IL-15 on insulin stimulated glucose transport in C2C12 cells. Furthermore, we also measured AMPK Thr172 and Akt Ser473 phosphorylation via Western blotting. Exposure to 20 pg/ml of individual cytokines had no affect on glucose transport while 1 ng/ml enhanced (P<0.05) glucose uptake with IL-6, IL-8 and IL-15, respectively. Moreover, the combinations of IL-8+IL-6 and IL-15+IL-6 at both 20 pg/ml and 1 ng/ml stimulated (P<0.05) glucose transport with IL-8+IL-15 and IL-8+IL-6+IL-15 only increasing (P<0.05) glucose transport at 1 ng/ml, with no affect observed of these combinations at 20 pg/ml. The changes in glucose transport were all associated with an increase (P<0.05) in AMPK Thr172 phosphorylation with no changes in Akt Ser473 phosphorylation. These findings demonstrated that the exercise induced myokines IL-6, IL-8 and IL-15 enhance glucose transport at 1 ng/ml, with changes only seen at 20 pg/ml with certain myokine combinations. Furthermore these changes in insulin stimulated glucose transport were associated with increased AMPK phosphorylation.