Rapid weight gain during infancy and early childhood is related to higher anthropometric measurements in preadolescence.

BACKGROUND: This study examined the relationship between rapid weight gain during infancy and/or early childhood and anthropometric measurements [body mass index (BMI), percent body fat (%BF), waist circumference (WC) and waist-to-height ratio (WHtR)] in preadolescence by sex. METHODS: Subjects were fourth-grade school children (aged 9 to 10 years) from elementary schools in Ina-town, Japan, in 2010. Measurements of height, weight, %BF and WC were conducted for each subject. We obtained data on height and weight of subjects at birth, age 1.5 years and age 3 years from the Maternal and Child Health handbook. Rapid weight gain was defined as a change in weight-for-age standard deviation score greater than 0.67 from birth to age 1.5 years (infancy) or from age 1.5 to 3 years (early childhood). RESULTS: All anthropometric variables (BMI, %BF, WC and WHtR) at age 9 to 10 years were significantly higher in the rapid weight gain during both infancy and early childhood period group than in the no rapid weight gain group, regardless of sex. When compared with the no rapid weight gain group, rapid weight gain during early childhood period had significantly higher BMI and WC in boys and BMI, %BF and WC in girls. Compared with the no rapid weight gain group, the rapid weight gain during infancy group had a significantly higher WC in boys and significantly higher BMI and WC in girls. CONCLUSION: Rapid weight gain during both infancy and early childhood was related to higher anthropometric measurements, including WHtR, among Japanese preadolescents, regardless of sex. This study suggests that rapid weight gain during infancy and early childhood may be a risk factor for general/abdominal obesity later in life.

Influence of eating quickly and eating until full on anthropometric gains in girls: A population-based, longitudinal study.

BACKGROUND: In examining childhood overweight/obesity, there is a need to consider both eating quickly and eating until full. This longitudinal study investigated the influence of eating quickly and/or eating until full on anthropometric variables and becoming overweight/obese among Japanese schoolgirls. METHODS: Study participants were fourth-grade schoolgirls (aged 9 or 10 years) in Ina Town, Japan. Physical examinations and a questionnaire survey were performed at baseline (fourth grade) and after 3 years (seventh grade). Height, weight, and waist circumference were measured in the physical examinations, while the data on eating quickly and eating until full were collected in the questionnaire survey. Analysis of variance and analysis of covariance were used to compare the differences in each anthropometric variable between fourth and seventh grade among groups. RESULTS: Data on 425 non-overweight/obese schoolgirls in fourth grade were analyzed. Gains in anthropometric variables (body mass index, waist circumference, and waist-to-height ratio) from fourth to seventh grade were significantly larger in the "eating quickly and eating until full" group than in the "not eating quickly and not eating until full" group. In contrast, there were no significant differences in the gains between the "eating quickly or eating until full" group and the "not eating quickly and not eating until full" group. The proportion of overweight/obese girls in seventh grade was higher in the "eating quickly and eating until full" group than in the other groups. CONCLUSIONS: Eating quickly and eating until full had a substantial impact on excess gains in anthropometric variables among schoolgirls, suggesting that modifying these eating behaviors may help prevent non-overweight/obese girls from the excess gains. Accordingly, school health programs need to focus on not eating quickly and/or not eating until full to prevent overweight/obesity; it is necessary to emphasize "the risk of overweight/obesity associated with these eating behaviors" in schools.

Rapid weight gain during early childhood is associated with overweight in preadolescence: a longitudinal study in Japan.

BACKGROUND: The objective of this study was to examine the relationship between rapid weight gain during early childhood and overweight in preadolescence by sex. METHOD: Study subjects were 676 boys and 620 girls in fourth grade (aged 9 or 10 years) from elementary schools in Ina-town, Japan, during 2010-2012. Height and weight of subjects at birth, age 1.5 and 3 years, were collected from the Maternal and Child Health Handbook, while values at 9-10 years were measured. Rapid weight gain was defined as a change in weight-for-age standard deviation score greater than 0.67 from birth to age 1.5 years (0-1.5 years) or from age 1.5 to 3 years (1.5-3 years). RESULTS: After adjustment for confounding factors, compared with no rapid weight gain, rapid weight gain during 0-1.5 years and 1.5-3 years or rapid weight gain during 1.5-3 years but not during 0-1.5 years significantly increased the odds ratio (OR) for overweight at age 9-10 years in boys (OR, 6.21; 95% confidence interval [CI], 2.84-13.58 and OR, 3.31; 95% CI, 1.67-6.54, respectively) and girls (OR, 7.55; 95% CI, 2.99-19.07 and OR, 3.42; 95% CI, 1.38-8.49, respectively). CONCLUSION: The present study suggests that rapid weight gain during early childhood was associated with being overweight in preadolescence, regardless of sex.

Interaction between Habitual Green Tea and Coffee Consumption and ACTN3 Genotype in Association with Skeletal Muscle Mass and Strength in Middle-Aged and Older Adults.

BACKGROUND: Recent studies have suggested the potential benefits of habitual coffee and green tea consumption on skeletal muscle health. However, it remains unclear whether these benefits are modified by genetic factors, particularly the alpha-actinin-3 (ACTN3) genotype, which is associated with the skeletal muscle phenotype. This study aimed to investigate the interaction between habitual coffee or green tea consumption and the ACTN3 genotype in association with skeletal muscle mass (SMM) and strength. METHODS: This cross-sectional study was conducted on 1,023 Japanese middle-aged and older adults (619 females, aged 45-74 years) living in the community. SMM was gauged using a bioelectrical impedance spectroscopy device, and handgrip strength (HGS) was used to measure muscle strength. The ACTN3 genotype (RR, RX, and XX) was determined from blood samples. Sex-specific linear regression models were used to analyze the interactions between coffee or green tea consumption and the ACTN3 genotype in association with SMM and HGS. RESULTS: In females, a significant interaction was observed between green tea consumption and the ACTN3 genotype in association with HGS (P interaction < 0.05). Furthermore, stratified analysis revealed a positive association between green tea consumption and HGS, specifically in females with the ACTN3 XX genotype (P trend < 0.05). In males, no significant interactions were observed between coffee or green tea consumption and the ACTN3 genotype in association with SMM or HGS (P interaction > 0.05). CONCLUSION: Our findings suggest that the skeletal muscle strength benefits associated with habitual green tea consumption may be contingent upon sex and the ACTN3 genotype.

Dose-Response Relationships between Diet Quality and Mortality among Frail and Non-Frail Older Adults: A Population-Based Kyoto-Kameoka Prospective Cohort Study.

OBJECTIVES: Although better diet quality is inversely associated with mortality risk, the association between diet quality and mortality remains unclear in frail and non-frail older adults. Thus, we aimed to examine this association in older Japanese adults. DESIGN: A prospective cohort study. SETTING AND PARTICIPANTS: We used the data of 8,051 Japanese older adults aged ≥65 years in the Kyoto-Kameoka study. MESUREMENTS: Dietary intake was estimated using a validated food frequency questionnaire. Diet quality was evaluated by calculating the adherence scores to the Japanese Food Guide Spinning Top (range, 0 [worst] to 80 [best]), which were stratified into quartiles. Frailty status was assessed using the validated self-administered Kihon Checklist (KCL) and the Fried phenotype (FP) model. Survival data were collected between February 15, 2012 and November 30, 2016. Statistical analysis was performed using the multivariate Cox proportional hazard analysis and the spline model. RESULTS: During the median 4.75-year follow-up (36,552 person-years), we recorded 661 deaths. After adjusting for confounders, compared with the bottom adherence score quartile, the top quartile was associated with lower hazard ratio (HR) of mortality in frailty (HR, 0.73; 95% confidence interval [CI], 0.54-1.00) and non-frailty, as defined by the KCL (HR, 0.72; 95% CI, 0.52-1.01). In the spline model, regardless of frailty status defined by the KCL and FP model, adherence score showed a strongly dose-dependent inverse association with mortality up to approximately 55 points; however, no significant differences were observed thereafter. This association was similar to the results obtained in individuals with physical, cognitive, and depression as domains of KCL in the spline model. CONCLUSIONS: Our findings demonstrate an L-shaped association between diet quality and mortality in both frail and non-frail individuals. This study may provide important knowledge for improving poor diet quality in older individuals with frailty or domains of frailty.

Adequate Protein Intake on Comprehensive Frailty in Older Adults: Kyoto-Kameoka Study.

OBJECTIVES: Defining an adequate protein intake in older adults remains unresolved. We examined the association between calibrated protein intake and comprehensive frailty by sex in the Kyoto-Kameoka study. DESIGN: Cross-sectional study of baseline data. SETTING AND PARTICIPANTS: The study included 5679 Japanese participants aged 65 years or older. METHODS: Calibration coefficients were estimated from food frequency questionnaires and 7-day dietary records as a reference. Comprehensive frailty was evaluated using the 25-item Kihon Checklist (KCL) and defined as a total KCL score of ≥7points. Sex-specific calibrated protein intakes were presented as % of energy, per kg of actual body weight (BW), and per kg of ideal BW. RESULTS: Multiple logistic regression analysis showed that calibrated protein intake is inversely associated with comprehensive frailty. The association between protein intake and comprehensive frailty was also evaluated using curve fitting with non-linear regression, a weak U-shaped association was found in males and an L-shaped association in females. Men had a low prevalence of frailty at a calibrated protein intake of 15-17% energy from protein, 1.2 g/kg actual BW/day, or 1.4 g/kg ideal BW/day, and women had a low prevalence of frailty at 17-21% energy from protein or 1.6 g/kg ideal BW/day, with the prevalence of frailty remaining unchanged at higher protein intakes. Meanwhile, the inverse relationship between protein intake per ABW and frailty showed a gradual decrease at 1.4 g/kg ABW/day for protein in women. CONCLUSIONS AND IMPLICATIONS: A non-linear relationship was found between calibrated protein intake and frailty, with a U-shaped association in men and an L-shaped association in women. Adequate protein intake in healthy Japanese older adults was higher than the current recommended daily allowance.

Cellular levels of thioredoxin associated with drug sensitivity to cisplatin, mitomycin C, doxorubicin, and etoposide.

Thioredoxin, a cellular thiol, functions as a self-defense mechanism in response to environmental stimuli, including oxidative stress. We first determined cellular levels of thioredoxin in several human bladder and prostatic cancer cell lines resistant to cis-diamminedichloroplatinum(II) (cisplatin). All cisplatin-resistant cell lines had much higher levels of thioredoxin than those in their drug-sensitive parental counterpart. We then, by introducing thioredoxin antisense expression plasmids into human bladder cancer T24 cells, established two bladder cancer cell lines that had decreased levels of thioredoxin. These thioredoxin antisense transfectants showed increased sensitivity to cisplatin and also to other superoxide-generating agents, i.e., doxorubicin, mitomycin C, etoposide, and hydrogen peroxide, as well as to UV irradiation, but not to the tubulin-targeting agents, vincristine, and colchicine. Cellular levels of thioredoxin thus appear to limit sensitivity to various superoxide-generating anticancer drugs in cancer cells.

Enhanced coexpression of thioredoxin and high mobility group protein 1 genes in human hepatocellular carcinoma and the possible association with decreased sensitivity to cisplatin.

Thioredoxin (TRX), a disulfide-reducing intracellular protein, functions as a cellular defense mechanism against oxidative stress. In this study, we asked whether expression of TRX, glutathione-thiol transferase pi, and high mobility group protein 1 (HMG-1) genes is enhanced in human hepatocellular carcinoma and whether expression of these genes is associated with sensitivity to cisplatin. Both TRX and HMG-1 were co-overexpressed in almost all cancerous lesions in comparison to normal tissue in surgically resected hepatocellular carcinomas of 20 patients. Tumor sensitivity to cisplatin [cis-diamminedichloroplatinum (II)], but not to mitomycin C or doxorubicin, correlated with mRNA levels of TRX in cancer tissue. TRX and HMG-1 may be useful tumor markers, and TRX might be also a useful marker for sensitivity to cisplatin in human hepatocellular carcinomas.

Differential induction of constitutive and inducible nitric oxide synthases by distinct inflammatory stimuli in bovine aortic endothelial cells.

Exposure to various combinations of cytokines and lipopolysaccharide (LPS) has been reported to increase NO production in vascular endothelial cells. The molecular entity of the newly expressed nitric oxide synthase (NOS) in endothelial cells, however, has not yet been examined in detail. In this report, we carried out biochemical characterizations and molecular identification of NOS isoform(s) expressed in cytokine/LPS-treated bovine aortic endothelial cells (BAEC). The increased NOS activity in tumor necrosis factor-alpha (TNF-alpha)/LPS-treated BAEC was localized mainly in the cytosolic fraction and Ca2+-independent, whereas that in interferon-alpha,beta(IFN-alpha,beta)/LPS-treated BAEC was preferentially in the membrane fraction and Ca2+-dependent, suggesting that TNF-alpha/LPS increased an inducible NOS (iNOS)-like activity, and IFN-alpha,beta/LPS increased an endothelial constitutive NOS (ecNOS)-like activity. Correspondingly, the different responses to the cytokine/LPS pretreatment were demonstrated in semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) using primers specific for iNOS or ecNOS, that is, TNF-alpha/LPS elicited the expression of iNOS mRNA whereas IFN-alpha,beta/LPS increased that of ecNOS mRNA. A nuclear run-on transcription assay and an inhibition experiment by actinomycin D indicated that the apparent increase of ecNOS in the IFN-alpha,beta/LPS-treated BAEC was at least in part ascribed to the transcriptional activation. The nucleotide sequences of the amplified PCR products in TNF-alpha/LPS- and IFN-alpha,beta/LPS-treated BAEC were 93% and 99% identical to the corresponding regions of human hepatocyte iNOS and bovine ecNOS, respectively. These findings indicated that, in cytokine/LPS-treated BAEC, two NOS isoforms whose molecular natures were closely homologous to the conventional isoforms of iNOS and ecNOS were differently induced in response to distinct inflammatory stimuli.

Cloning and sequencing of the cDNA encoding human glutaredoxin.

Glutaredoxin (thioltransferase) is a small, heat-stable protein, which is involved in thiol/disulfide exchange reactions. We have isolated a cDNA that encodes glutaredoxin from a human brain cDNA library. The encoded protein contains 106 amino acids with a calculated molecular mass of 11.76 kDa and an isoelectric point of 8.09. The amino acid sequence deduced from the cDNA is more than 80% identical to those of other mammalian glutaredoxins.

Expression of thioredoxin and thioredoxin reductase in placentae of pregnant mice exposed to lipopolysaccharide.

We have previously shown that thioredoxin and thioredoxin reductase were immunohistochemically localized in cytotrophoblasts, decidua and stromal cells in the stem villi of human placenta and that the addition of exogenous thioredoxin and thioredoxin reductase to mitochondrial fractions from human placenta displayed a protective effect on fumarase activity against oxidative stress. In this study, to investigate further the roles of thioredoxin and thioredoxin reductase in protecting pregnancy against oxidative stress, we examined the effect of lipopolysaccharide (LPS), which induces a variety of cytokines and produces radical oxygen species, on the expression of thioredoxin and thioredoxin reductase in mouse placenta. We focused on the placental protective effect in the second trimester, when the onset of placental dysfunction might occasionally lead to a critical state for the fetus. Thus we analysed placentae from mice on day 13 of pregnancy at various time points after they were injected with LPS (50 microg/kg i.p.) or saline as a control. The expressions of thioredoxin and thioredoxin reductase were evaluated by Western blotting and immunohistochemistry. Western blot analysis revealed that LPS approximately quadrupled the expression of both thioredoxin and thioredoxin reductase in the placentae of pregnant mice. When both proteins were localized immunohistochemically, it was found that the decidua and the diploid trophoblasts in the basal zone were intensively stained. Furthermore, the expression of 4-hydroxy-2-nonenal (HNE)-modified proteins, which are markers of oxidative stress, was enhanced in placenta by LPS. Our study suggests that the induced thioredoxin and thioredoxin reductase might protect the placenta from the stress induced by LPS.

Localization of thioredoxin reductase and thioredoxin in normal human placenta and their protective effect against oxidative stress.

Recent studies have indicated that oxidative stress is involved in the pathogenesis of pre-eclampsia. Oxidative stress damages systemic tissues, and placental damage may result in intrauterine growth retardation and fetal distress. Thus, this study attempted to elucidate the placental localization of thioredoxin and thioredoxin reductase, substances that may reduce oxidative stress. Furthermore, it studied the defence mechanism of the thioredoxin-thioredoxin reductase system against oxidative stress in mitochondria of normal human placenta where reactive oxygen species are primarily produced. The examination of thioredoxin reductase activity in subcellular fractions of human placenta indicated that thioredoxin reductase was located not only in cytoplasm, but also in mitochondria. The existence of thioredoxin and thioredoxin reductase in human placenta was confirmed immunologically using antibodies raised against thioredoxin and thioredoxin reductase. Thioredoxin and thioredoxin reductase were localized histochemically in cytotrophoblasts, decidua, and stromal cells in the stem villi. The addition of exogenous thioredoxin and thioredoxin reductase to fumarase in mitochondria of human placenta displayed a protective effect against oxidative stress. In conclusion, this study confirmed the intracellular localization and the tissue distribution of thioredoxin and thioredoxin reductase in human placenta. Moreover, the complete thioredoxin-thioredoxin reductase system in human placenta may protect the placenta from damage caused by oxidative stress.

Expression of mitochondrial thioredoxin-dependent antioxidant protein, SP-22, in normal human and inflammatory mouse placentae.

The aim of this study was to elucidate whether a novel mitochondrial antioxidant protein, SP-22, is localized in placenta and whether its expression is induced in placenta of lipopolysaccharide (LPS)-exposed mouse. Western blot analysis of normal human placenta indicated that the SP-22 protein was located in the mitochondrial fraction. Immunohistochemical analysis of SP-22 in normal placenta showed that immunoreactive SP-22 was distributed mostly in cytotrophoblastic cells but with almost no signal in syncytiotrophoblasts. The positive signals were also detected in the decidual cells and stromal cells in stem villi of normal placenta. We also examined LPS-mediated inflammatory placenta on day 13 of pregnancy at various time points after LPS injection (50 microg/kg, intraperitoneally). Western blot analysis indicated that LPS approximately quadrupled the expression of SP-22 in placenta of LPS-exposed mouse. When the SP-22 protein was localized immunohistochemically, the decidua and the diploid trophoblasts in the basal zone were intensively stained in placenta of LPS-exposed mouse compared to the control. The localization and inducible expression of SP-22 protein in placenta suggest a possible role in antioxidant system in mitochondria of normal and inflammatory placentae.

Enhanced protein levels of protein thiol/disulphide oxidoreductases in placentae from pre-eclamptic subjects.

Recent studies have indicated that pre-eclampsia is closely associated with oxidative stress both in maternal circulation and in the placenta. Protein thiol/disulphide oxidoreductases, such as thioredoxin, glutaredoxin, and protein disulphide isomerase have recently been found to eliminate reactive oxygen species (ROS) and regenerate oxidatively damaged proteins. Protein thiol/disulphide oxidoreductases may also play a role in combating pre-eclampsia. In this study, we examined the accumulation of 4-hydroxy-2-nonenal (HNE)-modified proteins, which are markers of lipid peroxidation, in human placentae of normal and pre-eclamptic subjects. We also examined the protein levels of thioredoxin, glutaredoxin, and protein disulphide isomerase in placentae. Immunoblotting and immunohistochemistry showed that HNE-modified proteins accumulated to a greater extent in pre-eclamptic placentae than in normal placentae. In both normal and pre-eclamptic placentae, thioredoxin, glutaredoxin, and protein disulphide isomerase were detected in the trophoblasts of the floating villi. The levels of these proteins were increased approximately 2- to 3-fold in the pre-eclamptic placentae compared to the normal placentae. These results indicated that the pre-eclamptic placentae were exposed to oxidative stress and that the protein thiol/disulphide oxidoreductases were adaptively induced in pre-eclamptic placentae, suggesting possible roles for thioredoxin, glutaredoxin, and protein disulphide isomerase in protecting placental functions against oxidative stress caused by pre-eclampsia.

Enhancement of mitochondrial oxidative stress and up-regulation of antioxidant protein peroxiredoxin III/SP-22 in the mitochondria of human pre-eclamptic placentae.

A growing body of evidence indicates that the pathogenesis of pre-eclampsia is closely associated with oxidative stress occurring in mitochondria. In the present study, we evaluated the degree of mitochondrial lipid peroxidation by assessing the accumulation of 4-hydroxy-2-nonenal (HNE)-modified proteins and examined the expression of mitochondrial antioxidant protein peroxiredoxin III/SP-22 in normal and pre-eclamptic human placentae. The accumulation of HNE-modified proteins increased to a greater extent in both the mitochondria and cytosol of pre-eclamptic placentae than in those of normal placentae. Moreover, the accumulation of HNE-modified proteins was much more evident in the mitochondria than in the cytosol, indicating that lipid peroxidation occurred mainly in the mitochondria of pre-eclamptic placentae. The mRNA expression of peroxiredoxin III/SP-22 was increased about 2-fold in pre-eclamptic placentae compared to normal placentae. The protein levels of peroxiredoxin III/SP-22 were approximately 4-fold higher in pre-eclamptic placentae than in normal placentae. Immunohistochemistry of placental tissues showed that the levels of peroxiredoxin III/SP-22 protein were increased in the trophoblasts of floating villi, stromal cells of stem villi, and decidual cells in pre-eclamptic placentae. These results indicate that peroxiredoxin III/SP-22 plays a crucial role in the protection of placental function from oxidative stress occurring in mitochondria of pre-eclamptic placentae.

17beta-estradiol induces protein thiol/disulfide oxidoreductases and protects cultured bovine aortic endothelial cells from oxidative stress.

OBJECTIVE: To examine whether or not estrogens induced the expression of protein thiol/disulfide oxidoreductases such as protein disulfide isomerase (PDI), thioredoxin (Trx), Trx reductase, and glutaredoxin (Grx) in vascular endothelial cells. METHODS: The regenerative effects of the protein thiol/disulfide oxidoreductases, PDI, Trx and Grx, on oxidatively damaged proteins were assayed using H2O2-inactivated glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as a reporter enzyme. The induction of protein thiol/disulfide oxidoreductases and the accumulation of protein adducts generated by lipid peroxidation were examined by Western blotting in estrogen-treated bovine aortic endothelial cells (BAECs). RESULTS: Reduced PDI, Trx and Grx regenerated the H2O2-inactivated GAPDH in vitro. The levels of these protein disulfide oxidoreductases in BAECs were increased by pretreatment with 0.01-10 micromol/l 17beta-estradiol, the largest increase (about fourfold of the control) being found for PDI. Other sex hormones such as progesterone and testosterone did not affect the contents of these oxidoreductases in BAECs. 4-Hydroxy-2-nonenal (HNE)-protein adducts, which are generated by lipid peroxidation, were accumulated in BAECs exposed to paraquat, whereas the pretreatment of BAECs with 17beta-estradiol suppressed their accumulation. CONCLUSIONS: The estrogen-mediated induction of the protein thiol/disulfide oxidoreductases such as PDI, Trx, Trx reductase and Grx suggested a possible involvement of these oxidoreductases in the antioxidant protection of estrogen observed in the vascular system.

A weight reduction and weight maintenance program with long-lasting improvement in left ventricular mass and blood pressure.

Obesity is a major risk factor for cardiovascular disease and is associated with hypertension and increased left ventricular mass (LVM). Maintenance of reduced weight has been a matter of recent concerns in the treatment of obese subjects. This study was conducted to confirm the effect of the addition of exercise to diet on maintenance of body weight in a weight reduction program. In addition, this study was conducted to estimate whether LVM changes in parallel with a change in body weight during a long-term follow-up after a weight-reduction program. Twenty-two normotensive (NT) obese subjects and 14 mild hypertensive (HT) obese subjects ranging in age from 22 to 51 years participated in a 12-week supervised weight-reduction program involving mild exercise and a mild hypocaloric diet. After this 12-week intervention, they were advised to maintain their modified lifestyle during a 1-year follow-up period. After the 12-week intervention, the mean reductions in body weight (BW) in the NT and HT groups were 4.1 kg (P < .0001) and 5.8 kg (P < .0001), respectively. LVM in the NT and HT groups was significantly reduced from 154 g to 136 g (P < .005) and from 169 g to 152 g (P < .002), respectively. One year after intervention, the mean gains in BW in the NT and HT groups were 2.3 kg (not significant, NS) and 0.4 kg (NS), respectively. The mean gains in LVM in the NT and HT groups were 8 g (NS) and 7 g (NS), respectively. It was also shown that blood pressures in the HT group were significantly decreased after the 12-week intervention and there was no significant change in blood pressure in the HT group 1 year after intervention. In conclusion, reduced body weight was maintained for 1 year after a 12-week supervised weight-reduction program in both normotensive and mild hypertensive obese subjects. Reduced left ventricular mass was maintained for a long period in both normotensive and mild hypertensive obese subjects and lowered blood pressure was maintained in the mild hypertensive obese subjects.

Possible differences in the regenerative roles played by thioltransferase and thioredoxin for oxidatively damaged proteins.

A possible involvement of thioltransferase (also known as glutaredoxin) in the regenerative reaction of proteins inactivated by oxidative stress were examined in vitro using the enzyme purified from bovine liver. Thioltransferase at physiological concentrations, together with glutathione, glutathione reductase and NADPH, regenerated the oxidatively damaged proteins with a comparable potency to that of thioredoxin. Experiments performed with protein substrates with their critical cysteine residues oxidized differently, that is, phosphofruktokinase and glyceraldehyde 3-phosphate dehydrogenase with mixed disulfide bonds and glyceraldehyde 3-phosphate dehydrogenase with sulfenyl or sulfinyl groups, indicated that thioltransferase regenerated the proteins inactivated by mixed disulfide formation more efficiently than thioredoxin, whereas thioredoxin preferentially regenerated the proteins inactivated by monothiol oxidation to sulfenic or sulfinic acid. These findings suggested that thioltransferase exerted regenerative effects on oxidatively damaged proteins like its cognate protein, thioredoxin, but with different substrate specificity, and their relative contribution to the regeneration reaction is dependent on the form of the oxidized thiols of the damaged proteins.

Effects of a community-based lifestyle-modification program on cardiovascular risk factors in middle-aged women.

We investigate the effectiveness of a community-based lifestyle-modification program for reducing blood pressure and other cardiovascular risk factors in sedentary Japanese middle-aged women. Among an initial cohort of 210 middle-aged sedentary women, 195 subjects completed a community-based 12-week lifestyle-modification program for reducing cardiovascular risk factors. Blood pressure, body weight and the serum lipid profile were measured both at baseline and at the end of the 12-week lifestyle-modification program. The program consisted of mild aerobic exercise and a mild hypocaloric diet. After the 12-week program, both systolic and diastolic blood pressure were significantly reduced, especially in subjects who were hypertensive at baseline. Desirable changes in body weight and the serum lipid profile were also found after the 12-week program. Multiple linear regression analysis revealed that, in obese subjects, the decrease in systolic blood pressure was correlated with both the initial systolic blood pressure and the change in estimated maximum oxygen consumption. In addition, the decrease in diastolic blood pressure was correlated with the initial diastolic blood pressure and the change in body weight. On the other hand, in non-obese subjects, the decrease in blood pressure was correlated with the initial blood pressure and the change in salt intake. A community-based lifestyle-modification program that consisted of mild aerobic exercise and a mild hypocaloric diet was considered to be practically effective for reducing multiple cardiovascular risk factors. Individuals who already have one or more mild cardiovascular risk factors still could be good candidates for a community-based lifestyle-modification program.