Muscle atrophy results from a variety of conditions such as disease states, neuromuscular injuries, disuse, and aging. Absence of gravitational loading during spaceflight or long-term bed rest predisposes humans to undergo substantial loss of muscle mass and, consequently, become unfit and/or unhealthy. Disuse- or inactivity-induced skeletal muscle protein loss takes place by differential modulation of proteolytic and synthetic systems. Transcriptional, translational, and posttranslational events are involved in the regulation of protein synthesis and degradation in myofibers, and these regulatory events are known to be responsive to contractile activity. However, regardless of the numerous studies which have been performed, the intracellular signals that mediate skeletal muscle wasting due to muscular disuse are not completely comprehended. Understanding the triggers of atrophy and the mechanisms that regulate protein loss in unloaded muscles may lead to the development of effective countermeasures such as exercise and dietary intervention. The objective of the present review is to provide a window into the molecular processes that underlie skeletal muscle remodeling and to examine what we know about exercise and nutrition countermeasures designed to minimize muscle atrophy.
Influence of oxidative stress on fusion of pre-synaptic plasma membranes with phosphatidylcholine (PC) liposomes as a model of synaptic vesicle was investigated. The inhibitory effect of vitamin E on the decline in the fusion caused by oxidative stress was also assessed. Rats subjected to hyperoxia as oxidative stress showed significant increases in the levels of lipid hydroperoxides and protein carbonyl moieties in pre-synaptic plasma membranes in the brain. The ζ potential of pre-synaptic membrane surface was decreased markedly. When synaptosomes were incubated with PC liposomes labeled by either rhodamine B or calcein as a fluorescence probe, or 12-doxyl stearic acid as an ESR spin trapping agent, translocation of each probe into oxidatively damaged pre-synaptic membranes was decreased significantly. Fatty acid composition analysis in pre-synaptic membranes obtained from normal rats revealed a marked increase in linoleic acid and a moderate decrease in docosahexaenoic content after the incubation with liposomes. However, rats subjected to hyperoxia did not show marked changes in these fatty acid contents in their pre-synaptic membranes after the incubation. Such changes caused by hyperoxia were inhibited by vitamin E treatment of rats. These results suggest that oxidative damage of pre-synaptic membranes caused by oxidative stress lowers the lipid-mixing for the membrane fusion. The results of this study imply that vitamin E prevents the deficit in neurotransmission at nerve terminals due to the decline in fusion between pre-synaptic membrane and synaptic vesicles caused by oxidative membrane damage.
It is well known that some amino acids inhibit bacterial growth. L-Serine is known to inhibit the growth of Escherichia coli by inhibition of homoserine dehydrogenase (EC 188.8.131.52). It has been reported that this L-serine inhibition may be prevented by the addition of L-isoleucine or L-threonine to the medium. In our study, however, recovery of the growth inhibition of Escherichia coli by L-serine occurred in the presence of several amino acids, especially L-phenylalanine. In an attempt to further elucidate this inhibition mechanism, different intermediates of aromatic amino acid biosynthesis were added to the growth medium. Recovery from the inhibition did not occur in the presence of prephenate but did occur when phenylpyruvate was added to the medium. The specific activity of prephenate dehydratase decreased in cells grown in the presence of L-serine. However, L-serine did not inhibit in vitro prephenate dehydratase activity, and the expression of pheA, which encodes the prephenate dehydratase, was not depressed by L-serine. We suggest that L-serine acts via another inhibition mechanism. Although this inhibition mechanism has not been fully elucidated, our results suggest that the addition of L-serine to the growth medium inhibits prephenate dehydratase synthesis and thus affects L-phenylalanine biosynthesis.
Epidemiological studies showed that habitual fish intakes were associated with lower blood inflammatory markers. In the present study the effects of a fish oil-containing food on inflammatory markers were investigated in healthy, mostly middle-aged subjects (59 men and 82 women) with normal to mildly elevated triglyceride levels. Study subjects were randomly allocated to two groups in a double-blind manner; one group ingested an eicosapentaenoic acid (EPA)-rich fish oil-fortified drink (0.60 g EPA+0.26 g docosahexaenoic acid/d, EPA group, n=68) for 12 wk. The rest of the subjects took a placebo (control group, n=73). Plasma levels of high sensitivity C-reactive protein (hs-CRP) and soluble tumor necrosis factor-receptors 1 and 2 (sTNF-Rs 1 and 2) were measured at the start and end of intervention. EPA concentrations in the total RBC phospholipid fraction significantly increased by 79% in the EPA group at the end of the study, and they changed very little in the control group (+0.68%). The inflammatory markers did not change in either group. It is likely that fish oil does not change hs-CRP or sTNF-Rs 1 or 2 in subjects without active inflammation.
The present study was carried out to explore the effects of oolong and green teas on improving the memory deficits and brain pathological changes in senescence accelerated-prone mice P8 (SAMP8). Six-month-old mice were supplied with oolong tea, green tea or water as the sole drinking fluid for 16 wk. The memory ability of mice was evaluated by passive and active avoidance tests, while the extent of the brain degeneration was measured by the spongiosis grades and the lipofuscin percentage in the hippocampus. The total grading score and serum biochemical levels were also measured. The results indicated that the mice supplemented with the oolong and green tea drinks reversed the cognitive impairment, lessened the spongy degeneration and lipofuscin, and increased the serum Trolox equivalent antioxidant capacity more than the control group. The total grading score of the oolong tea group was lower than that of the control group in male mice, whereas it did not differ among female groups. No differentiations in the concentrations of total cholesterol, triglyceride, glucose, iron or hemoglobin were observed among three drink groups. In conclusion, oolong and green teas could reduce the deteriorations of cognitive ability, brain degenerative changes and aging process in SAMP8, probably through the potent antioxidative activity of the tea.
The present study investigated the effect of the soybean polyphenol genistein on the stomach using a water immersion restraint (WIR) stress model. Male Wistar rats were administered 50 or 100 mg/kg/d of genistein for 2 wk or were not given any drug. Rats were subjected to WIR stress for 4 h. At the end of the WIR period, rats were sacrificed. Subsequently, rats underwent measurement of the ratio of the mucosal hemorrhagic erosion area to the whole stomach body area, myeloperoxidase (MPO) activity, superoxide dismutase (SOD) activity, thiobarbituric acid reactive substances (TBARS) level, and proinflammatory cytokines (tumor necrosis factor (TNF)-α and cytokine-induced neutrophil chemoattractant (CINC)-1) levels in the gastric tissue. Furthermore, an isolated rat stomach infusion model was employed for the endocrinological investigation of the effect of genistein. The extracted stomach canal and the vascular system, which comprised the experimental model, were subjected to perfusion. After 20 min of perfusion, the perfusate from the portal vein was collected, and the concentrations of histamine, gastrin, and somatostatin in the perfusate were measured. Experiments demonstrated that genistein administration resulted in significant suppression of WIR stress-induced gastric mucosal injury and MPO activity. Further, genistein significantly elevated SOD activity and significantly suppressed the TBARS level, production of TNF-α and CINC-1, and secretion of gastrin, histamine, and somatostatin. These data suggest that genistein protected against gastric mucosal injury, likely via its ability to inhibit oxidation, inflammation, and secretion of gastrin and histamine.
The aim of this study was to determine whether there was an association between body fat distribution, blood lipid profiles, and β3-adrenergic receptor gene polymorphism in Korean middle-aged women. Subjects were grouped according to BMI as obese (≥25 BMI, n=95) or non-obese (BMI<25, n=93). The Trp64Arg mutation of the β3-adrenergic receptor gene was detected by PCR-RFLP. Skinfold thickness, body circumference, intra-abdominal fat area by CT, and blood lipid profiles were also measured. Data were compared using ANOVA, Bonferroni t-test, and Chi-square. Significance for statistical analyses were set at p<0.05. In the obese group, 63.16% were Trp64Trp homozygotes and 36.84% were Trp64Arg heterozygotes, compared to 80.65% who were Trp64Trp homozygotes and 19.35% who were Trp64Arg heterozygotes in the non-obese group. These results indicated a significant (x2=4.943, p<0.05) difference between the two groups. Frequency of the Arg64 allele in the obese group (16.84%) showed a significant (x2=4.185, p<0.05) difference as compared to the non-obese group (9.68%). Skinfold thickness and body circumference of the Trp64Arg heterozygote group showed a consistent increase as compared to the Trp64Trp homozygote group. Visceral fat area and VSR of Trp64Arg heterozygote group showed a higher tendency than Trp64Trp homozygotes in the obese group, but these differences were not statistically significant. In conclusion, the Trp64Arg polymorphism of the β3-adrenergic receptor gene is associated with obesity in middle-aged Korean women, but it is difficult to suggest the prominent association of the Trp64Arg polymorphism of the β3-adrenergic receptor gene with prevalence of abdominal obesity or dyslipidemia in Korean middle-aged women.
The present study was designed to determine the effect of fenugreek seed extract (FG) on endurance capacity in male mice aged 4 wk. Mice were given orally either vehicle or FG (150, 300 mg/kg body weight) by stomach intubation for 4 wk. The 300 mg/kg FG group showed a significant increase in swimming time to exhaustion as compared to the control group. In the FG groups, blood lactate concentration was significantly lower than in the control group. In the control group, plasma non-esterified fatty acid (NEFA) and plasma glucose were decreased by swimming exercise. But in the FG group, NEFA and plasma glucose were significantly increased by swimming. FG treatment also significantly decreased fat accumulation. These results suggest that improvement in swimming endurance by the administration of FG is caused by the increase in utilization of fatty acids as an energy source.
In this study, we examined the effect of genistein on the severity of dermatitis and level of serum IgE in NC/Nga (NC) mice. NC mice housed in conventional conditions develop spontaneous atopic-like dermatitis; however, oral administration of 20 mg/kg genistein suppresses the development of dermatitis. We also investigated the levels of serum IgE in genistein-treated NC mice and found that the levels were the same as those in control NC mice. We further investigated in vitro IFN-γ and IL-4 production from spleen cells upon stimulation with anti-CD3 and anti-CD28 mAbs. IFN-γ production level in NC mice that received 20 mg/kg genistein was significantly lower than that in control NC mice. In contrast, the production level of IL-4 in genistein-treated mice was not significantly different from that in control mice but tended to increase in a dose-dependent manner.