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Biomedical subjects

N Sakane

Publications and source records attributed to N Sakane.

54 records · Page 3Linked to original sources
PubMed1995

Probucol prevents the progression of fatty liver in MSG obese mice.

We investigated the effect of Probucol in preventing fatty liver in monosodium-L-glutamate (MSG) treated obese mice and control mice fed a high fat diet. MSG mice became significantly obese 9 weeks after birth with higher levels of serum blood glucose, total cholesterol, HDL-cholesterol, GPT, and cholinesterase, and had greater triglyceride contents in their livers relative to control mice. Morphologically, MSG obese mice also had a marked fatty liver. Administration of Probucol mixed with the high fat diet for 2 weeks significantly decreased the serum levels of total cholesterol and HDL-cholesterol, and liver triglyceride contents in both MSG and control mice. Morphologically, the livers were less fatty after Probucol treatment. These results suggest that Probucol prevents the development of fatty liver, and in addition reduces hypercholesterolemia.

Animals↗
PubMed1995

A case of primary hyperparathyroidism that had been treated under a diagnosis of depression for 10 years.

A 66 year old man who had been treated under a diagnosis of depression for 10 years was referred to the Kyoto Prefectural University of Medicine, Kyoto because of general fatigue and appetite loss. The patient was diagnosed as having primary hyperparathyroidism (PHPT) based on the increased parathyroid hormone (PTH) and serum calcium levels. Computed tomography revealed solitary adenoma of parathyroid gland. The resection of this solitary adenoma improved the PTH and serum calcium concentrations to normal ranges, which resulted in an improvement in his depressive state. This case suggests that ionic calcium levels contribute to the mental symptoms associated with PHPT. As PHPT is curable, the possibility of PHPT should be taken into account when patients have depressive symptoms.

Aged↗
PubMed1995

Acromegalic gigantism with low serum level of growth hormone and elevated serum insulin-like growth factor-I.

In a case of acromegalic gigantism with hyperprolactinemia is reported, the basal serum growth hormone (GH) levels ranged from 1.2 to 1.9 ng/ml. Serum GH response to either insulin-induced hypoglycemia or GH-releasing hormone was blunted. Frequent blood sampling showed non-pulsatile GH secretion. Serum prolactin and insulin-like growth factor-I (IGF-I) levels were elevated. After unsuccessful surgery, bromocriptine treatment normalized serum prolactin without affecting serum GH and IGF-I levels. Combined administration of octreotide with bromocriptine reduced serum GH and IGF-I levels. In this case, non-pulsatile GH secretion and enhanced tissue sensitivity to GH may induce hypersecretion of IGF-I and cause clinical acromegalic gigantism.

Acromegaly↗
PubMed1995

Thermogenic, anti-obesity effects of bofu-tsusho-san in MSG-obese mice.

OBJECTIVE: To investigate the hypothesis that anti-obesity action of bofu-tsusho-san (TJ-62) works via activating the brown adipose tissue thermogenesis and inhibiting the phosphodiesterase activity. DESIGN: MSG obese mice and lean controls were fed a diet including 1.4% or 4.7% TJ-62 of weight of food for 8 weeks. Another group of MSG obese mice were fed with 1-ephedrine (1-E) + d-pseudoephedrine (d-PE) of equivalent amounts as contained in TJ-62 (4.7%) for 8 weeks. Yet another group of MSG obese mice were further supplemented with Glycyrrhizae Radix (GR) extract + Forsythiae Fructus (FF) extract + Schizonepetae Spica (SS) extract (that inhibited phosphodiesterase activity) of amounts contained in TJ-62 (4.7%) for 8 weeks. MEASUREMENTS: The following were measured: The concentration of ephedrine and its congeners in TJ-62; the inhibitory effect of TJ-62 on phosphodiesterase activity; body weight; food intake; retroperitoneal white adipose tissue (RWAT) weight; interscapular brown adipose tissue (IBAT) weight; mitochondrial protein content in IBAT; cytochrome c oxidase activity in IBAT; guanosine-5'-diphosphate (GDP) binding in IBAT mitochondria. RESULTS: One gram of TJ-62 contained 3.33 mg of 1-E and 0.73 mg of d-PE. One mg of TJ-62 was equivalent to 2.5 mg of caffeine in the inhibitory effect on phosphodiesterase activity. After feeding with TJ-62, GDP binding was significantly increased in a dose dependent manner. Body weight and RWAT weight decreased in both MSG obese mice and lean controls. Food intake was not changed by TJ-62. Feeding with 1-E + d-PE produced responses of about 70% of those of TJ-62. These responses were, furthermore, enhanced by the addition of the three extracts to the levels that were similar to those produced by TJ-62. CONCLUSION: Bofu-tsusho-san (TJ-62) works via activating the BAT thermogenesis and inhibiting the phosphodiesterase activity in mice.

Adipose Tissue↗
PubMed1994

Anti-obesity and anti-diabetic effects of CL 316,243, a highly specific beta 3-adrenoceptor agonist, in yellow KK mice.

The anti-obesity and anti-diabetic effects of CL 316,243, a highly specific beta 3-adrenoceptor agonist (beta 1: beta 2: beta 3 = 0:1:100,000), were evaluated in obese diabetic yellow KK mice and C57Bl control mice. The study compound was fed through a gastric tube at a rate of 0.1 mg/kg/day for 2 weeks. The following parameters were compared in the treated and control animals given distilled water: brown adipose tissue thermogenesis, resting metabolic rate, insulin receptors in adipocytes, and blood glucose and serum insulin levels during a glucose overloading test. CL 316,243 significantly increased brown adipose tissue thermogenesis and resting metabolic rate in both yellow KK mice and C57Bl controls. The amount of white adipose tissue decreased, although food intake was not affected. The effects contributed to the mitigation of obesity in yellow KK mice. CL 316,243 also increased the concentration of insulin receptors and decreased the levels of serum insulin and blood glucose during the glucose overloading test in yellow KK mice. These observations suggest that CL 316,243 possesses anti-obesity and anti-diabetic effects and consequently may be useful for treating obesity as well as non-insulin-dependent diabetes mellitus in obese persons, without causing excessive side effects.

Animals↗
PubMed1994

Effect of nicotine on sympathetic nervous system activity of mice subjected to immobilization stress.

We tested the hypothesis that nicotine possesses an antistress action by measuring the turnover of norepinephrine (NE), a reliable indicator of sympathetic nervous system activity, in the interscapular brown adipose tissue (IBAT) and heart of mice treated with nicotine injections, immobilization stress, or nicotine + immobilization stress, vs. untreated controls. Nicotine enhanced the sympathetic activity in the IBAT and heart, and induced a loss of body weight. Immobilization-related stress accelerated sympathetic activity in the IBAT and heart more strongly than did nicotine loading alone. Pretreatment with nicotine suppressed the sympathetic activity induced by immobilization stress to the same extent as that observed after administering nicotine alone. Thus, these results appeared to support our hypothesis.

Adipose Tissue, Brown↗
PubMed1994

Effect of CL 316,243, a novel beta 3-adrenoceptor agonist, on insulin secretion in perfused mouse pancreas.

In order to clarify the insulin-release mechanism of beta 3-adrenoceptor agonist, we examined the effect of CL 316,243, a highly specific beta 3-adrenoceptor agonist having a relative potency of beta 1:beta 2:beta 3 = 0:1:100,000, on insulin secretion in perfused mouse pancreas. The application of 0.2 mM and 0.5 mM CL 316,243 produced significant insulin secretion from within 1 min, which lasted until 2 min after its withdrawal. DL-propranolol and ICI 118551 at 0.2 mM partially inhibited the insulin secretion induced by the 0.2 mM CL 316,243, but 0.2 mM metoprolol had no effect on the insulin release produced by 0.2 mM CL 316,243. We conclude that beta 3-adrenoceptor agonist stimulates insulin secretion via beta 3-action in the perfused mouse pancreas.

Adrenergic beta-Agonists↗
PubMed1994

Anti-obesity effect of CL 316,243, a highly specific beta 3-adrenoceptor agonist, in mice with monosodium-L-glutamate-induced obesity.

The effects of CL 316,243, a highly specific beta 3-adrenoceptor agonist (relative selectivities of 0, 1 and 100,000 for beta 1-, beta 2- and beta 3-receptors, respectively), were evaluated in mice with monosodium L-glutamate (MSG)-induced obesity as well as in control mice injected with physiological saline instead of MSG. Both MSG- and saline-treated mice were divided into three groups and at 8 weeks of age received either CL 316,243 (0.1 or 1.0 mg/kg) or distilled water through a gastric tube for 2 weeks. CL 316,243 not only reduced white adipose tissue mass but also activated brown adipose tissue and systemic metabolism, and hence reduced body mass without affecting food intake. Furthermore, CL 316,243 decreased hyperglycemia and hypertriglyceridemia in MSG-treated mice. However, at the higher dose, CL 316,243 also increased liver triglyceride in MSG-treated mice. These observations suggest that CL 316,243 exerts an anti-obesity effect in mice with MSG-induced obesity and consequently may prove efficacious in the treatment of human obesity.

Adrenergic beta-Agonists↗
PubMed1994

The alpha/beta-adrenergic receptor blocker arotinolol activates the thermogenesis of brown adipose tissue in monosodium-L-glutamate-induced obese mice.

We have found previously that arotinolol, an alpha/beta-adrenergic blocker, increases blood flow in brown adipose tissue (BAT) in a similar extent as BRL 26830A, a beta 3-adrenoceptor agonist. We tested the hypothesis that arotinolol activates thermogenesis in BAT, leading to weight loss in monosodium-L-glutamate-induced (MSG-induced) obese mice and saline-treated controls. Six weeks of standard animal feed (CE-2) containing arotinolol hydrochloride (350 mg/kg CE-2), which reduced mean blood pressure in MSG-treated mice, significantly increased the mitochondrial protein content in BAT, and activated the specific and total binding of guanosine-5'-diphosphate (GDP) in BAT mitochondria, leading to a reduction of obesity in both MSG- and saline-treated mice vs. the control groups fed with CE-2 diet alone. However, six weeks of CE-2 diet containing propranolol hydrochloride (525 mg/kg CE-2) a non-selective beta-blocker, markedly reduced the specific and total binding of GDP in BAT mitochondria, leading to weight gain in both MSG- and saline-treated mice. These findings support the hypothesis, that arotinolol activates BAT thermogenesis, leading to weight loss.

Adipose Tissue↗
PubMed1994

Usefulness of mazindol in combined diet therapy consisting of a low-calorie diet and Optifast in severely obese women.

We conducted a double-blind test to examine whether or not the addition of mazindol, an appetite suppressor, to combined diet therapy [low-calorie diet + Optifast: 4600-3928kj(1100-940 kcal)/day] enhances the weight-reduction effect and reduces dropout from treatment in women with severe obesity. All of the patients were enrolled in the combined diet therapy and exercise [1255kj(300 kcal/day)] for 7 months. At the end of the first month, the patients were given, at random, three tablets of either 0.5 mg mazindol (18 women) or placebo (18 women) per day, in three doses for three months, in addition to the diet and exercise therapies. At 7 months, the key for the double-blind test was opened by the controller. Four of the 18 patients in the placebo group dropped out of the programme at 2 months after drug treatment, because they could not endure the intense hunger. Therefore, data for these 4 patients were excluded from evaluation. However, none of the patients treated with mazindol + combined diet therapy dropped out. The body weight and body-fat ratio showed marked reduction (p < 0.01 vs. premedication weight). The percent weight loss and percent reduction in body-fat ratio in the mazindol group was significantly (p < 0.01) greater than those found in the placebo group, which also showed a significant decrease in body weight and body-fat ratio (p < 0.01 vs. pre-medication weight) during the same period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Mechanism of anti-obesity action of benidipine hydrochloride in mice.

Benidipine hydrochloride, a dihydropyridine calcium antagonist, decreases body weight and also has a hypotensive effect. The mechanism of its inhibitory effect on body weight is unclear, although this agent increases blood flow in brown adipose tissue, which functions as a main thermogenic organ. The hypothesis that benidipine hydrochloride activates brown adipose tissue to induce body weight loss was tested on mice made obese by pretreatment with monosodium-L-glutamate (MSG). When benidipine hydrochloride was incorporated in the diet (1.0 mg per gram of food) for 4 weeks, binding of guanosine-5'-diphosphate in brown adipose tissue mitochondria was significantly increased. Body weight and body fat decreased in both MSG obese mice and in lean controls. Results support the hypothesis and suggest the possibility that benidipine hydrochloride may be useful for treating obese hypertensive patients.

Adipose Tissue, Brown↗
PubMed1994

Relationship between basal metabolic rate, thermogenic response to caffeine, and body weight loss following combined low calorie and exercise treatment in obese women.

To clarify whether there were any differences in basal metabolic rate (BMR) and thermogenic response to caffeine in individual obese women, and if so, whether such differences affected weight loss, the basal and resting metabolic rates at 30 min after a caffeine loading test (4 mg/kg ideal body weight, per os) were measured in 136 obese women and ten lean age-matched controls. The obese subjects were then asked to follow a combined low calorie diet and exercise regimen. There were no differences in the BMR and thermogenic responses to caffeine between the obese and lean groups. However, the BMR and the thermogenic responses to caffeine varied widely in obese subjects. After two months of treatment, body weight and percentage body fat in obese women were significantly (P < 0.001) reduced. There were significant correlations between the BMR and body weight loss (r = 0.3621, P < 0.001), between BMR/lean body mass and body weight loss (r = 0.3196, P < 0.001) and between the thermogenic response to caffeine and body weight loss (r = 0.6943, P < 0.001). When the criterion of a BMR less than 3.10 kJ/min (less than two standard deviations below the mean of the age-matched lean control) was used to define an obese group with reduced BMR, there were 30 obese subjects in this group, and their body weight was significantly decreased by treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

A case of testicular feminization syndrome with bulimia nervosa.

A 19-year-old patient with a female appearance visited our department for treatment of bulimia nervosa. The patient had primary amenorrhea. Chromosomal studies revealed a 46XY karyotype, and the plasma testosterone level was in the range of normal adult males. The patient was diagnosed as having testicular feminization syndrome. The psychological background, such as severe anxieties concerning her body, was behind the eating disorders. Examinations revealed intraabdominal testes. A bilateral gonadectomy was performed, and no androgen receptors were detected in the suprapubic skin. After the gonadectomy, the patient's mental status became much more stable, and the ability to control her eating pattern was restored. Testicular feminization with bulimia nervosa is rare in Japan. The importance of mental support and a careful follow-up to people with testicular feminization is being discussed.

Adult↗
PubMedDate not supplied

Anti-obesity and anti-diabetic effects of mazindol in yellow KK mice: its activating effect on brown adipose tissue thermogenesis.

1. The anti-obesity and anti-diabetic effects of mazindol were evaluated in obese diabetic yellow KK mice and C57Bl control mice. 2. The study compound was fed through a gastric tube at a rate of 1 or 2 mg/kg per day (0.01 mol/L HCl as control) for 2 weeks. The following parameters were compared in treated and control animals: bodyweight, food intake, white adipose tissue (WAT) weight, brown adipose tissue (BAT) weight and its thermogenesis, noradrenaline (NA) turnover, blood glucose and serum insulin levels and glucose transporter 4 (GLUT4). 3. Furthermore, bodyweight loss of mice pair-fed the same amount of food as the mazindol-treated mice for 2 weeks was measured. 4. Mazindol significantly decreased food intake and significantly increased guanosine-5'-diphosphate-binding in BAT mitochondria and NA turnover in BAT in both yellow KK and C57Bl groups. The amounts of WAT in subcutaneous, mesenteric and retroperitoneal regions and bodyweights were significantly decreased in both groups. Bodyweight loss in mice pair fed with the mazindol-treated groups was approximately 70% compared with that in the mazindol-treated groups. Furthermore, mazindol decreased the levels of blood glucose and serum insulin during the glucose overloading test in yellow KK mice, but it did not influence the GLUT4 protein concentration in WAT and muscle. 5. These observations suggest that mazindol possesses both an anti-obesity action, due to the inhibition of appetite as well as the activation of BAT thermogenesis via increased NA turnover in BAT, and an anti-diabetic action. Consequently, mazindol may be useful for the treatment of obesity as well as non-insulin-dependent diabetes mellitus in obese persons.

Adipose Tissue↗