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Underreporting is a problem in dietary surveys, and data on Japanese individuals with obesity are lacking. In addition, in dietary surveys of individuals with obesity, underreporting and extreme energy restrictive practices for short periods of time have been reported, and blood total ketone levels (ketone bodies) may be able to distinguish between these factors. The present study aimed to examine the relationship between underreporting [energy intake (EI)/basal metabolic rate estimate (BMR)] and ketone bodies in obese Japanese women. The participants included 91 women with obesity aged 47±9 years with a body mass index (BMI) of 29.8±3.9 kg/m² who met the exclusion criteria out of 164 individuals who participated in an institutional cohort study baseline survey between September 2006 and September 2015. The current study defined the relationship between EI/BMR, BMI and the participants' ketone body levels. EI/BMR

We aimed to clarify food intake and dietary patterns that affect urinary sodium excretion (urinary salt excretion) among young women. We used 2012 to 2018 data from the health and nutrition testing on admission, which is a part of ongoing epidemiological studies, for students enrolling in the Faculty of Nutrition Science, Nakamura Gakuen University. Fasting urine samples were collected from the participants, and their estimated daily salt excretion was calculated using the Tanaka equation. The dietary assessment used was the semi‐quantitative food frequency questionnaire, and we confirmed its validity. The participants included 2218 women aged 18 to 20 years who were classified into four groups according to urinary salt excretion (g/d) from their spot urine: Q(1)

The authors investigated interannual differences in the sodium excretion levels of young healthy Japanese women as estimated from spot urine analysis at Nakamura Gakuen University from 1995 to 2015. Participants included 4931 women aged 18 to 20 years who were classified into three time periods according to year of health check: first (1995-2001), second (2002-2007), and third (2008-2015). Estimated daily urinary sodium and potassium excretion levels and the sodium to potassium ratio were 120.6±31.9 mmol, 35.2±8.1 mmol, and 3.5±0.9, respectively. Adjusted for body weight, sodium excretion, and potassium excretion significantly decreased in the second and third period compared with the first period (P

Protein S, a nonenzymatic cofactor to activated protein C, presents in two forms in plasma, free form and in a complex with C4b-binding protein. The aim of this study was to determine the association of plasma protein S levels with the variables related to cardiovascular disease risk. The relationships between plasma protein S levels with lipids, inflammation markers, and adiposity were first examined on middle-aged obese women (n = 62), then on young nonobese women (n = 160) to verify the findings in the obese women. Total and free protein S antigen levels in middle-aged obese women, approximately half being in a postmenopausal state and suffered from dyslipidemia, correlated negatively with estradiol and positively with triglycerides, total cholesterol, LDL cholesterol, apoA-II, apoB, apoC-II, apoC-III, apoE, hemoglobin A1c, and protein C, whereas there was no correlation with HDL cholesterol, apoA-I, BMI, visceral fat area, blood pressure, or factor VII activity. Multiple linear regression analyses revealed that protein C, apoC-II, and fibrinogen were significant predictors of total protein S antigen levels, accounting for 51.9% of variance, and apoC-II as a singular significant predictor for free protein S antigen levels (12.3% of variance). In young nonobese women, most being normolipidemic, apoC-II was also selected as a significant predictor of total protein S antigen levels, but not of free protein S antigen levels. The positive relationship between plasma protein S levels and apoC-II, a key regulator of triglycerides hydrolysis, may contribute to the pathogenesis of increased concentrations of plasma protein S.

This study aimed to investigate whether accumulation of subcutaneous abdominal fat has a beneficial correlation with lipid metabolism in premenopausal and/or postmenopausal Japanese women. The study enrolled 146 premenopausal women, ranging in age from 19 to 54 years, and 82 postmeno-pausal women, ranging in age from 47 to 66 years. Fat distribution, including abdominal visceral fat area (VFA) and abdominal subcutaneous fat area (SFA), were measured in an outpatient clinic by magnetic resonance imaging. Homogeneity of the regression slopes for SFA to total cholesterol ( P = 0.030), low-density lipoprotein cholesterol ( P = 0.020), apolipoprotein B (apoB) ( P = 0.001), and the ratio of apoB to apolipoprotein A-I (apoA-I) ( P = 0.003) were not found between premenopausal and postmenopausal women, even after adjustment for both VFA and age. However, the regression slopes for VFA to all measured lipid parameters, as well as apolipoproteins, were homogeneous between the premenopausal and postmeno-pausal groups. Abdominal SFA in postmenopausal women correlated negatively with total cholesterol ( P = 0.007), low-density lipoprotein cholesterol ( P = 0.002), apoB ( P < 0.001), and the ratio of apoB to apoA-I ( P = 0.001), after adjustment for age and VFA, but this was not the case in premenopausal women. The mechanisms involved in the beneficial effects of subcutaneous fat accumulation in postmenopausal women remain obscure, but upregulated aromatase expression, derived from adipose tissue, may possibly improve lipid and apolipoprotein metabolism.

ヒスチジンから合成される神経ヒスタミンは, レプチンにより賦活化され摂食を抑制し, 脂肪分解を促進することが動物実験で報告されている。本研究は, 中高年肥満女性において, ヒスチジン摂取が摂食を抑制し, 脂肪分解を促進し, 血清レプチン濃度に影響を及ぼすか否かについて検討を行った。対象者は3カ月間の減量プログラムに参加した中高年肥満女性118名である。減量前後に, 採血, 体重測定, 食事調査を行った。減量後のタンパク質当りヒスチジン摂取量とエネルギー摂取量の間には有意な負の相関が認められた。この関係は, 血清レプチン濃度で補正後も成立した。また, 減量後のタンパク質当りヒスチジン摂取量と血清遊離脂肪酸濃度の間には有意な正の相関が認められた。以上のことより, 中高年肥満女性においてヒスチジン摂取が摂食を抑制し, 脂肪分解を促進する可能性が示唆され, ヒスチジンが肥満の予防, 改善に有効なアミノ酸であることが考察された。

中高年肥満女性を閉経前群, 閉経後群に分け, LDL-コレステロール (LDL-C) および内臓脂肪に影響を及ぼす食事因子を, 3カ月間の減量指導による内臓脂肪減少時および減量指導終了より1年後の内臓脂肪増加時について検討した。減量指導開始時に, BMIは群間に有意差を認めないにも関わらず, 内臓脂肪, LDL-Cは閉経後群が閉経前群に比し有意に高値を示した。減量指導後, 体重, BMI, 内臓脂肪は両群ともに有意に低値を示し, LDL-Cは閉経前群でのみ有意に低下し, 閉経後群は低下傾向を示したが有意ではなかった。LDL-Cの減少に内臓脂肪が正の相関を示し, 閉経後群で有意であった。重回帰分析の結果より, 閉経後群のLDL-Cの減少に内臓脂肪と砂糖摂取量, 脂質エネルギー比が正の関連を認め, 内臓脂肪の減少には嗜好飲料類摂取量が閉経の有無に関係なく有意な正の関連を認めた。減量指導終了より1年後, 標準体重当りエネルギー摂取量は両群ともに有意に増加し, 内臓脂肪は増加傾向を示し, LDL-Cは両群ともに有意に上昇した。内臓脂肪の増加に砂糖摂取量が正の相関を閉経後群で示し, エネルギー補正後も有意であった。以上より, 中高年肥満女性のLDL-Cの減少に内臓脂肪が正に関与し, 内臓脂肪の変動にはショ糖および脂質が閉経の有無に関係なく正に関与することが示唆された。

Insulin resistance is thought to raise blood pressure. Recently, a significant positive relationship between mean blood pressure and plasma leptin levels, but there have been no reports dealing with the relationship between blood pressure and either insulin resistance or serum leptin levels after weight loss. In the present work, we attempted to clarify the relationship between changes in blood pressure and either the serum leptin level or the insulin level in 102 moderately obese females (mean body mass index (BMI), 29.5 +/- 0.5 kg/m2; age, 47.0 +/- 0.9) during a 3 month period. No differences in age, fat-mass, homeostasis model assessment (HOMA), the summation of insulin (sigmaIRI), plasma renin activity (PRA) or 24 h norepinephrine excretion (24hU-NE) were observed between the hypertensive (HT) group (n = 31) and normotensive (NT) group (n = 71) before weight loss, but the basal serum leptin was significantly higher in the HT (16.8 +/- 1.1 ng/ml) than in the NT group (15.2 +/- 0.8 ng/ml), after adjusting for abdominal total fat. After a 3 month weight reduction program, the total abdominal fat, serum leptin and sigmaIRI significantly decreased in both groups. The systolic blood pressure (SBP)/diastolic blood pressure (DBP) significantly decreased from 144/84 to 130/77 mmHg only in the HT but not in the NT group. The PRA decreased in both groups, while the 24hU-NE significantly decreased only in the HT group. The changes in the leptin level were significantly correlated with the changes in both sigmaIRI and HOMA after weight loss in the two groups, respectively. Finally, a statistically significant positive correlation was observed between the changes in the leptin and the changes in the mean blood pressure (MBP) (r = 0.412, p < 0.05) only in the HT group. Multiple regression analysis revealed that the changes in MBP were independently associated with the changes in 24hU-NE and the changes in either sigmaIRI or HOMA in all subjects. However, a statistically significant positive correlation was observed between the changes in MBP and the changes in leptin levels even after adjusting for the total abdominal fat, 24hU-NE and either sigmaIRI or HOMA (both expressed as a percentage of the baseline value) in a multiple regression analysis only in the HT group. These results suggest that leptin may play a role in the pathophysiology of obese hypertension.

The aim of our study was to investigate the association between nutrient factors and the osteo-sono assessment index (OSI) for calcaneus of young Japanese women. The subjects consisted of 965 young women aged from 18 to 22 years studying at the Department of Food and Nutrition at Nakamura-Gakuen University. The OSI was measured by ultrasonic bone absorptiometry. We found that age, weight, height, exercise, as well as the daily intakes of calcium, phosphorus, protein, energy and sodium were the main factors related to OSI in young women. Positive associations were observed between the OSI and the weight, exercise and daily intakes of calcium, protein and energy, whereas while negative associations were seen between the OSI and the age, height and daily intakes of phosphorus and sodium. In addition, all of these factors were also independently related to the OSI.

We investigated whether amino acid substitution of tryptophan by arginine at the residue 64 (64 Arg) of beta 3-adrenergic receptor affects on the degree of reduction in the abdominal fat distribution during a 3-month weight reduction program in either pre- or postmenopausal Japanese women. Beta 3-adrenergic receptor gene polymorphism was examined in 90 Japanese obese women by restriction-enzyme cleavage conformation. The visceral and subcutaneous fat area was measured by magnetic resonance imaging. The baseline body mass index, body weight, fat mass and abdominal subcutaneous and total fat area in 15 obese postmenopausal women with a beta 3-adrenergic receptor (64 Arg) were significantly higher than those in 25 postmenopausal obese women with a beta 3-adrenergic receptor (64 Trp/64 Trp). In contrast, no such differences were found in the 50 premenopausal obese women. After a 3-month weight reduction period, the ratio of visceral to subcutaneous fat areas tended to be lower in both pre-and post-menopausal women with a beta 3-adrenergic receptor (64 Arg), but statistically significant in only the premenopausal obese women (p

The serum cholesterol level at a young age is considered to be a significant factor in the high prevalence of coronary heart disease. Seven hundred and ninety-six females, mean age 18.9 (18∼22), participated in both blood sampling and a nutritional survey. The nutritional survey was carried out in 1995 by the 24-hour recall method to determine the individual food consumption. The BMI, serum total cholesterol, HDL-cholesterol and triglyceride were 20.8 (SE 0.08) kg/m 2 , 181 (SE 1.0) mg/dL, 60 (SE 0.4) mg/dL, 66 (SE 1.2) mg/dL, respectively. Higher than normal levels of total cholesterol (>200 mg/dL) and Lp(a) (>30mg/dL) were obtained in 22.1% and 19.3% of the subjects, respectively. The total energy intake was 1700 kcal/day, twenty-seven % of which was derived from fat and 46% from cereals. In a multiple regression analysis, the serum total cholesterol and LDL-cholesterol were found to be significantly associated with the BMI as well as the simple carbohydrate and fat energy ratio, respectively, whereas the HDL showed a significantly negative correlation with the BMI. The triglyceride level was associated with the BMI. These results suggests that the BMI, fat energy ratio and simple carbohydrate intake, such as cakes and beverages, appear to be the main factors influencing of hyperlipidemia in young Japanese females.

We examined whether or not the oral administration of L-nitroarginine methylester (L-NAME), an inhibitor of nitric oxide (NO) synthase, promotes cholesterol-induced arteriosclerosis in the aorta and the coronary artery. Thirty-six male Japanese white rabbits were fed 0.5% cholesterol-containing laboratory chow and randomly assigned to the following three groups: (1) water, (2) 80 microg/ml L-NAME and (3) 400 microg/ml L-NAME in drinking water. The rabbits were fed a 0.5% cholesterol-containing diet for 8 months. During the 8-month period, the concentration of total cholesterol and L-nitroarginine in the serum and the mean blood pressure were measured. The concentration of NO3 in the serum was also measured. After sacrifice, the aortic surface involvement (AI%), the ratio of the thickened intima to the media and the contents of the total cholesterol of the aorta, the maximum % stenosis of the subepicardial large coronary artery, the % frequency of the nearly completely occlusive distal small coronary artery and the area of the myocardial fibrosis were all measured. We found no statistical difference among the three groups regarding the degree of arteriosclerotic lesions of the aorta and of the large coronary artery, and the area of myocardial fibrosis, as well as the serum cholesterol exposure index (the area under the curve of the serum total cholesterol concentration) and the mean blood pressure. However, the serum concentration of L-nitroarginine was approximately 50 and 200 microM/l in groups 2 and 3, respectively. The concentration of NO3 in the serum in group 1 was significantly higher than that in groups 2 and 3. We thus conclude, that the oral administration of L-NAME in the rabbits fed a cholesterol-containing diet for 8 months failed to promote arteriosclerotic lesions in the aorta and the coronary artery, even though the serum concentration of L-nitroarginine increased sufficiently to inhibit NO synthase in the arterial endothelium and the NO3 concentration in the serum decreased in the rabbits given L-NAME.

The aim of the present study is primarily to re-examine an animal model of acute myocardial infarction (AMI) and arterial thrombosis, developed by Constantinides and his colleagues in the 1960s, in both heritable hyperlipidemic rabbits and normal rabbits because they did not study these rabbits. The groups in this study consisted of 29 normal rabbits and 29 Watanabe heritable hyperlipidemic (WHHL) rabbits. These rabbits were administered Russell's viper venom (RVV) as a procoagulant, intraperitoneally with serotonin or angiotensin II or saline, intravenously. As a control, 10 normal and 17 WHHL rabbits were administered intravenously with either angiotensin II or saline. These treatments were given on 2 successive days. AMI lesion was found in 8 of 29 normal and 7 of 29 WHHL rabbits receiving RVV and angiotensin or serotonin. Angiotensin II promoted the incidence of aortic thrombosis associated with segmental medial necrosis and an intimal disruption in WHHL rabbits receiving RVV. In the normal rabbits, angiotensin II in addition to RVV induced segmental medial necrosis of the aorta, but angiotensin II alone did not. Thus, we postulated that a synergistic effect of RVV as a cytotoxic substance and a sudden increase in the aortic wall tension by angiotensin II might thus result in acute aortic medial necrosis. The conclusion was that no close correlation between coronary arteriosclerosis and AMI was found in this animal model. The intravenous administration of angiotensin promoted aortic medial necrosis even in normal rabbits treated with RVV and then accelerated aortic thrombosis in the WHHL rabbits treated with RVV.

To investigate the causal relationship between lesions of either the proximal large or the distal small coronary arteries and myocardial fibrosis, the hearts and the aortas of 99 cholesterol-fed rabbits with either intermittent or continuous hyperlipidemia for 8 months or more, 44 Watanabe-heritable hyperlipidemic (WHHL) rabbits and 20 normal rabbits were studied histologically. The size and location of the myocardial fibrosis correlated closely with the almost completely occlusive distal small coronary artery which mainly consisted of macrophages, necrosis and calcification but did not correlate with the maximum % stenosis of the large proximal subepicardial coronary arteries in the cholesterol-fed-rabbits. Myocardial fibrosis and almost completely occlusive lesions of the distal small coronary arteries were very rare in the WHHL rabbits, and the maximum % stenosis of the proximal coronary artery and aortic lesions in the WHHL rabbits tended to be greater than those in the cholesterol-fed rabbits. Thus, we are still not certain as to whether or not, the organic stenosis of the subepicardial coronary artery is responsible for myocardial fibrosis in WHHL-rabbits. In conclusion, a causal relationship was observed between myocardial fibrosis and the occlusive lesions of the distal small coronary arteries in cholesterol-fed rabbits, while the arteriosclerotic lesions of the small coronary artery in cholesterol-fed rabbits completely differed from those observed in WHHL-rabbit.

1. The effects of nipradilol, a beta-adrenoceptor antagonist which possesses a nitroxy group, on cytosolic Ca2+ concentration ([Ca2+]i), and on tension development were simultaneously measured by front-surface fluorometry and fura-2-loaded strips in the proximal portion of pig coronary arteries. 2. Nipradilol reduced in a concentration-dependent manner both the [Ca2+]i and tension, irrespective of whether the strips were unstimulated or exposed to either high K+ or histamine containing solutions. However, both in the case of contractions induced by high K+-depolarization and histamine stimulation, for a given [Ca2+]i elevation the tension which developed in the presence of nipradilol was smaller than that generated in its absence, so that the [Ca2+]i-tension curves during the contraction were shifted to the right. 3. In the absence of extracellular Ca2+, the [Ca2+]i elevation due to the release of Ca2+ from histamine-sensitive store was inhibited by nipradilol. Nipradilol had no effect on the [Ca2+]i elevation due to the release of Ca2+ from caffeine-sensitive stores; however, it did inhibit the caffeine-induced increase in tension. A derivative of nipradilol, which lacked a nitroxy molecule (Nip(-N)), had no effect on the [Ca2+]i and tension elevated by histamine or caffeine in the absence of extracellular Ca2+. 4. The beta-adrenoceptor agonist, isoprenaline, reduced [Ca2+]i tension when applied to steady state contractions induced by high K+, or at the peak level of tension to histamine. The reduction of [Ca2+]i and tension induced by isoprenaline was inhibited by Nip(-N) in a concentration-dependent manner and nipradilol inhibited the isoprenaline-induced relaxation with bell-shaped concentration-response curves. At lower concentrations, nipradilol acted as a beta-blocker, the IC50- value being smaller than that of Nip(-N), and at higher concentrations, it acted as a nitrovasodilator. 5. Thus, it is suggested that, at lower concentrations, nipradilol, an antianginal drug, acts as a beta-adrenoceptor antagonist. At higher concentrations, it relaxes the proximal portion of the coronary artery by directly reducing [Ca2+]i and the Ca2+-sensitivity of the myofilaments, apparently due to the presence of the nitroxy molecule.

A 3-year follow-up study on 334 young Japanese females enrolled in a university at the age of 18 years revealed that discontinuation of leisure time impact-loading exercises performed in junior high and/or high school was associated with increased risk of reduction in calcaneus osteo-sono assessment index (OSI). Bone strength rapidly increases during puberty and reaches its peak by the end of adolescence. The aim of this study was to determine the lifestyle factors that influence the maintenance of calcaneus OSI in young adult females around the time when peak bone mass is attained. Annual health checkups including OSI measurements, anthropometrics, lifestyle analysis, and blood examination were performed 4 times on 334 Japanese females enrolled in a university at the age of 18 years. According to the slope of OSI change during the 3-year follow-up, the subjects were grouped into two categories: OSI loss (the lowest tertile) and OSI gain/stable (the second and third tertiles). At the baseline assessment, the OSI loss group had higher OSI and height and an earlier menarche age than the OSI gain/stable group. Performing leisure time impact-loading exercise in junior high and/or high school but discontinuing it at university was associated with increased risk of OSI loss, independent of OSI, height and weight at the age of 18 years, weight change during follow-up, age of menarche, energy-adjusted nutrient intake, and alcohol drinking; the odds ratios were 4.1–4.9 compared with those performing impact-loading exercise at university. In particular, duration, frequency, and subjective intensity of impact-loading exercise during high school were positively associated with OSI loss. Discontinuation of leisure time impact-loading exercises performed during late adolescence is associated with an increased risk of OSI loss in young adult females during the 3-year follow-up period.

The behavioral changes associated with seizures induced by auditory stimulation in magnesium (Mg)-deficient rats originate in deep brain structures and secondarily project to neocortex. In the present study, we examined the roles of N-methyl-D-aspartate (NMDA) receptors in this seizure model. The intraperitoneal administration of the competitive NMDA receptor blocker DL-2-amino-7-phosphonoheptanoic acid (36 and 72 mg/kg) and the non-competitive NMDA receptor blocker MK-801 (1.35 and 2.7 mg/kg), completely prevented the induction of seizure and bradyarrhythmia or sudden death resulting from seizure. Therefore, the white-noise-induced seizures in Mg-deficient rats are linked to increased neuronal excitability via the NMDA receptor.

1. We examined temporal changes in the relationship between cytosolic calcium concentrations ([Ca2+]i) and developed tension during histamine-induced contractions of strips of the coronary artery of the pig, by making use of simultaneous measurements of fura-2 fluorescence and force. 2. The relationship between [Ca2+]i and developed tension observed with cumulative applications of extracellular Ca2+ ([Ca2+]o), ranging from 0 mM to 10 mM, during 118 mM K(+)-depolarization was similar to that observed in chemically skinned strips of the porcine coronary artery, as noted by other investigators. [Ca2+]i at 0 mM [Ca2+]o, at 50% of maximum, and at maximum tension development were 76 nM, 424 nM, and 3050 nM, respectively. 3. Cumulative applications of histamine induced dose-dependent increases in [Ca2+]i and tension and the extent of tension for a given change in [Ca2+]i increased, i.e. greater effectiveness of [Ca2+]i-tension relationship, than seen with K(+)-depolarization. 4. When histamine 10(-5) M was applied, [Ca2+]i abruptly rose and reached the first peak within several seconds. After a slight dip at 30 s, [Ca2+]i reached a second peak at 3 min, and then gradually declined. On the other hand, tension developed rapidly reached a maximum at 4 min, then gradually declined. The relation between [Ca2+]i and tension in the early, rising phase of contraction was similar to that obtained during depolarization. At the time of maximum tension development, the relation was greater than that observed during depolarization, which persisted in the phase of declining tension. 5. To examine the role of protein kinase C in the increased effectiveness of [Ca2+]i-tension relation of histamine-induced contractions, we used 1-(5-isoquinolinesulphonyl)-2-methylpiperazine (H-7), as an inhibitor. Exposure of strips to H-7, i0-' M, reduced the effectiveness of [Ca2+]i-tension relation toward the level observed during depolarization, while it had no effect on the [Ca2 ]i-tension relation in the early phase of contraction either in the presence or absence of extracellular Ca2 + 6. In intact smooth muscle of the coronary artery of the pig, the relationship between [Ca2+]i and developed tension varies during contraction. Histamine, a receptor-mediated stimulus, induced a greater tension for a given change in [Ca2+]i during the steady state of contraction than did depolarization. The greater effectiveness of contraction, particularly in the later phase, seems to be mediated by activation of an H-7-sensitive mechanisms.

Background Visceral adiposity is an essential component of metabolic syndrome. Reduction of excessive visceral fat prevents metabolic syndrome and improves atherosclerotic diseases. This study aimed to identify dietary patterns and physical exercise during the training-education period that predict visceral adiposity regain during the follow-up period. Methods One hundred one moderately obese Japanese women, 23 to 67 years of age, participated in 0- to 4-month training-education and 12-month follow-up periods. Dietary patterns of food groups during training-education were analyzed by principal components analysis, and 3 major dietary patterns were derived. The change in visceral fat over the follow-up, adjusted for 4-month visceral fat area (VFA) and 4- to 16-month body mass index change, was analyzed using stepwise multiple linear regression. Results VFA and body weight decreased during training-education ( P P = 0.030) and standard deviations of daily exercise duration ( P = 0.012) during training-education predicted VFA regain during follow-up. This regain correlated negatively with combinations of bread, milk and dairy products, fruits, seeds and nuts, and mushrooms, but positively with combinations of rice, pickles, miso, alcohol, and meat. The large standard deviation of daily exercise duration during training-education showed greater VFA regain during follow-up than did the smaller standard deviation ( P = 0.023), but body mass index did not show a similar trend. Conclusion Our results revealed that daily exercise fluctuations and dietary patterns were useful predictors of visceral fat regain.

1. By use of front-surface fluorometry and fura-2-loaded strips of the coronary artery of the pig, the effects of nitroglycerin (NG) on cytosolic Ca2+ concentrations ([Ca2+]i) and on tension development were measured simultaneously. 2. Both high K+ depolarization and histamine increased [Ca2+]i and tension in a concentration-dependent manner. However, the tension development in relation to the [Ca2+]i increase ([Ca2+]i-tension relation) observed with histamine was much greater than that observed with K+ depolarization. 3. NG reduced in a concentration-dependent manner both [Ca2+]i and tension, irrespective of whether the vascular strips were in a resting state or during exposure to high K+ or to histamine stimulation. However, the extent of reduction in tension (relaxation) was greater than that expected from the reduction in [Ca2+]i based on the [Ca2+]i-tension relationship observed with K(+)-depolarization. 4. In the absence of extracellular Ca2+, NG depleted stored Ca2+ and also inhibited Ca2+ release from histamine-sensitive stores, but had no effect on the caffeine-sensitive stores. NG inhibited the caffeine-induced tension development with no change in [Ca2+]i. 5. We suggest that NG relaxes the coronary artery of the pig by reducing [Ca2+]i and also by directly controlling contractile elements through second messengers not related to changes in [Ca2+]i.

This study examined whether charting daily weight patterns can predict weight regain in obese patients. The subjects were 98 moderately obese Japanese women aged 23 to 66 years who were obliged to precisely record their daily weights during the initial 4-month education period, but not thereafter. The patients were followed up at 8, 12, and 16 months. Abdominal fat areas and blood samples were assessed in the outpatient clinic at 0, 4, and 16 months. The standard deviations (SDs) of the differences in body weight between “after waking up” and “after breakfast” (SDa), “after dinner” (SDb), and “before going to bed” (SDc) were calculated, which were parameters reflecting the fluctuations in the daily weight patterns during the first 4 months. SDc, but not SDa or SDb, was correlated positively with weight regain at 8, 12, and 16 months (P = 0.049, P = 0.002, and P = 0.001, respectively). There were significant differences in temporal change in body weight and abdominal visceral fat between the small SDc group (SDc ≤25th percentile) and the large SDc group (SDc >75th percentile), but not for subcutaneous abdominal fat or the serum concentrations of glucose, insulin, or lipids. The results indicate that fluctuation of body weight immediately before going to bed is useful for predicting the rebound in body weight.

The purpose of this study was to investigated the effect of weight loss on blood pressure and its related variables in moderately obese Japanese females, including an investigation of the rebound phenomenon. Study I examined the effects of weight loss on blood pressure in 138 moderately obese, nondiabetic females (BMI 29.3±0.3 kg/m2; age, 46.3±0.8 years) during a 3-month therapeutic dietary and exercise program. Study II investigated the effect of weight rebound on blood pressure over an additional 21 months of exercise in 48 subjects from Study I subjects. After 3 months, the BMI significantly decreased to 27.9±0.3 kg/m2. Abdominal total fat, visceral fat (V), and subcutaneous fat (S) also decreased significantly. In addition, the summation of insulin (ΣIRI), plasma glucose (ΣPG) and HOMA during 75 g oral glucose tolerance test also all significantly decreased. Significant decreases in both the SBP and DBP were observed after the 3 month weight reduction program. Multiple regression analysis revealed that the reduction in SBP was significantly and positively associated with the reduction in log ΣIRI and the reduction in log 24h-urinary norepinephrine excretion at the end of Study I. The DBP showed a significantly positive association with the log ΣIRI. With regard to the weight rebound phenomenon, Study II showed that the SBP, DBP and ΣIRI all increased significantly, and a positive correlation was observed between the changes in the SBP and those in the log ΣIRI. However, no such correlation was observed regarding the abdominal total fat and visceral fat during both periods. These results suggest that weight loss therefore caused the BP to decrease due to both an improvement in hyperinsulinemia and a decrease in the adrenergic activity which may be involved in the urinary catecholamine. As a result, hyperinsulinemia is thus considered to play an important role in the pathogenesis of blood pressure due to obesity not only during weight loss, but also during the weight rebound phenomenon. (Hypertens Res 2001; 24: 481-487)

The aim of this study was to evaluate the relationship between changes in abdominal fat areas and the baseline serum leptin levels of Japanese obese women during weight reduction. The study was performed on 100 obese female Japanese volunteers. We measured the BMI and abdominal fat areas (visceral, subcutaneous and total) by magnetic resonance imaging and determined the fasting serum leptin levels before and after a 3 month weight reduction program. We examined whether or not a relationship exists between the baseline leptin levels and the subsequent changes in the abdominal fat areas after a weight reduction program. Multiple linear regression analysis was performed to examine the relationship between the baseline leptin levels and changes in abdominal visceral, subcutaneous, and total fat areas, and demonstrated that the baseline leptin level was a significant predictive factor for changes in the abdominal visceral fat area in both pre and postmenopausal Japanese obese women. We thus concluded the relatively higher baseline leptin levels in Japanese obese women to be associated with a relatively smaller reduction in the amount of abdominal visceral fat after undergoing a weight reduction program.

In order to elucidate the mechanism of behavioral alterations in magnesium-deficient rats, changes in the electroencephalogram (EEG) and electrocardiogram (ECG) were studied during auditory stimulation and correlated with the behavioral alterations. Weanling rats were fed either a Mg-deficient diet or a control synthetic diet for 2-3 weeks before the experiment. EEGs were recorded from the hippocampus and the sensorimotor and auditory cortices, and ECGs with a telemetry system. White noise with an intensity of 100 dB was given continuously to induce behavioral changes. The Mg-deficient rats developed consistent and graded behavioral changes in response to the stimulation, showing running-jumping behavior (stage 1), followed by tonic limb convulsion (stage 2) and finally by falling down on the floor (stage 3). The EEGs also showed consistent changes with spike activity, initiating in the hippocampus (stage 2) and then spreading to the neocortices bilaterally (stage 3). These findings indicate that the behavioral changes induced by auditory stimulation in the Mg-deficient rats are due to seizures arising in deeper brain structures, particularly in the limbic system, and projecting secondarily to the neocortices. The ECG changes, mainly consisting of marked bradyarrhythmia, occurred as early as the appearance of the EEG spikes, indicating that they were also related to the seizure. We conclude therefore that Mg deficiency in rats causes increased excitability of the central nervous system, resulting in seizures possibly originated in the limbic system, later developing secondary generalization, and also causing cardiac dysfunctions.

Summary Front surface fluorometry and porcine coronary arterial strips loaded with fura-2 were used to investigate the effect of endothelin on cytosolic Ca concentrations, [Ca]i, and on contractile force, the objective being to elucidate the mechanism of action. Both in the presence and absence of extracellular Ca, endothelin induced rapid and dose-dependent increases in [Ca]i and in contraction. When caffeine-sensitive and histamine-sensitive intracellular Ca stores were depleted, in Ca-free medium, a transient contraction but no increase in [Ca]i followed the subsequent application of endothelin. This Ca-independent component was largely inhibited by the relative protein kinase C inhibitor, H-7, but not inhibited by W-7, calmodulin antagonist. This component is probably linked to activation of protein kinase C.

1. Using front-surface fluorometry with fura-2-loaded porcine coronary arterial strips, we simultaneously measured effects of a Ca2+ antagonist, diltiazem, on cytosolic Ca2+ concentrations [( Ca2+]i) and on tension development. 2. In the presence of extracellular Ca2+ (1.25 mM), histamine concentration-dependently induced abrupt (the first component) and then sustained (the second component) elevations of [Ca2+]i. In the absence of extracellular Ca2+, histamine induced transient elevations of [Ca2+]i, and the time course was similar to that of the first component observed in the presence of extracellular Ca2+. Histamine caused a greater contraction for a given change in [Ca2+]i than did potassium, at [Ca2+]i over 300 nM. 3. Diltiazem, 10(-8)M to 10(-5)M, concentration-dependently inhibited the second component of [Ca2+]i elevation and tension development induced by histamine (10(-5) M). Only at higher concentrations (over 10(-5) M) did diltiazem inhibit the first component of increases in [Ca2+]i and tension development induced by histamine, both in the presence and absence of extracellular Ca2+. 4. Diltiazem (10(-6) M) inhibited increases in [Ca2+]i and tension development induced by cumulative applications of extracellular Ca2+ during K(+)-depolarization. The curve of [Ca2+]i against tension of these Ca2(+)-induced contractions obtained in diltiazem-treated strips overlapped with that obtained in untreated strips. This suggests that diltiazem has no direct effects on contractile elements. 5. In contrast, the histamine-induced Ca2(+)-tension curve (second component) was shifted in parallel to the left by diltiazem. 6. We conclude that diltiazem, at therapeutic concentrations, specifically inhibits extracellular Ca2+- dependent increases in [Ca2 +]i, with no effects on the release of Ca2 + from intracellular store sites or on Ca2 +-sensitivity of the contractile elements involved in the contractions induced by elevations of [Ca2 +]i.