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Toshihide Yoshida

Publications and source records attributed to Toshihide Yoshida.

28 records · Page 2Linked to original sources
PubMed2003

[The knack of treatment for obese patients with hypertension and diabetes mellitus: combined the newest tailor-made diet therapy with the usual stress-management therapy].

The 5-10% body weight loss often leads to amelioration or cure of hypertension and diabetes mellitus in obese patients. But, the effect of diet therapy on obese patients differs in each individual because of the differences in energy expenditure, such as the resting metabolic rate (RMR). We have recently reported that obese Japanese with the missense mutation (Trp64Arg) of the beta 3-adrenergic receptor (beta 3-AR) gene and/or the uncoupling protein 1 (UCP1) gene mutation (A-3826G) have difficulties in weight loss by the reducing RMR, while Japanese with beta 2-AR gene mutation (Arg16Gly) have an under-weight condition through increased RMR. Here I introduce the importance of tailor-made diet therapy to improve obesity based on analysis of gene polymorphisms and in order to maintain this tailor-made diet therapy, I emphasize that the stress-management therapy should be needed to remove mental problems which caused obesity.

Carrier Proteins↗
PubMed2003

123I-Metaiodobenzylguanidine uptake in the nape of the neck of children: likely visualization of brown adipose tissue.

UNLABELLED: The distribution of radioiodinated metaiodobenzylguanidine (MIBG) has been studied primarily in patients with neuroendocrine tumors-in pediatrics, particularly with neuroblastomas. Sometimes, symmetric accumulation in which no tumor is identified is seen in the nape-of-the-neck region. We estimated visually whether accumulation was found in the nape of the neck and studied the characteristics of the accumulation. METHODS: Retrospectively, we investigated 266 (123)I-MIBG scintigraphic studies performed on pediatric patients who had been treated for neuroendocrine tumors or who were suspected of having such tumors. RESULTS: Accumulation in the nape of the neck was seen in 32 of 266 studies (12%); in none of these cases was the accumulation identified as a tumor by other imaging modalities or follow-up studies. In the same individuals, the accumulation varied and it was observed more often during winter. CONCLUSION: Symmetric (123)I-MIBG accumulations in the nape-of-the-neck region observed in children are thought to be related to the uptake in brown adipose tissue.

3-Iodobenzylguanidine↗
PubMed2002

Proinsulin C-peptide activates cAMP response element-binding proteins through the p38 mitogen-activated protein kinase pathway in mouse lung capillary endothelial cells.

Proinsulin C-peptide has been reported to have some biological activities and to be possibly involved in the development of diabetic microangiopathy. In the present study, we examined the effects of C-peptide on the mitogen-activated protein kinase pathway in LEII mouse lung capillary endothelial cells. Stimulation of the cells with C-peptide increased both p38 mitogen-activated protein kinase (p38MAPK) and extracellular signal-regulated kinase (ERK1/2) activities and activity-related site-specific phosphorylation of the respective kinases in a concentration-dependent manner, but failed to activate c-Jun N-terminal kinase. Stimulation of the cells with C-peptide also induced site-specific phosphorylation of cAMP response element (CRE)-binding protein (CREB)/activating transcription factor 1 (ATF1), and thereby binding of these transcription factors to CRE. Among three CREB kinases tested, phosphorylation of mitogen-activated protein kinase-activated protein kinase 2 (MAPKAP-K2) was induced after stimulation with C-peptide. The phosphorylation of CREB, ATF1 and MAPKAP-K2 were inhibited by SB203580, a p38MAPK inhibitor, but not by PD98059, an ERK kinase inhibitor. These results indicate that C-peptide activates p38MAPK followed by MAPKAP-K2 to enhance DNA-CREB/ATF1 interactions.

Animals↗
PubMed2002

[The tailor-made diet therapy to improve obesity].

As the white adipose tissue, especially abdominal fat is an endocrine organ secreting adipocytokines, which induce insulin resistance, hypertension, and arteriosclerotic diseases, reduction of the abdominal fat is important. But effect of the diet therapy differs in each individual, because of the difference of energy expenditure. Since the relationship between the missense mutation (Trp64Arg) of the beta 3-adrenergic receptor (beta 3-AR) gene and low energy expenditure in the obese Pima Indians was made clear, gene polymorphisms that mediate body weight are reported one after another. We also reported that one third of Japanese have the Trp64Arg mutation of beta 3-AR gene, which may produce obesity or difficulties in weight loss. Here we introduce the obesity-related genes, and report the importance of Tailor-made diet therapy based on molecular genetics to improve obesity.

Adrenergic beta-3 Receptor Agonists↗
PubMed2002

(123)I- or (125)I-metaiodobenzylguanidine visualization of brown adipose tissue.

UNLABELLED: (123)I-Metaiodobenzylguanidine (MIBG) accumulations that do not correspond to any tumor are observed occasionally on the medial aspect of the upper back or shoulder of children. The true nature of such accumulations is unknown, and we hypothesized that they represent interscapular brown adipose tissue (IBAT) visualized by scintigraphy. METHODS: Wistar rats (7 wk old) received MIBG labeled with (123)I or (125)I. Autoradiography was performed, and concentrations of the tracer in the interscapular subcutaneous tissue were identified histopathologically. The effects of 6-hydroxydopamine, reserpine, and beta 3-adrenergic receptor agonist (CL316,243) on the accumulation were investigated to elucidate the mechanism of uptake into BAT. RESULTS: Autoradiography showed well-defined distinct accumulation in the subcutaneous tissue on the upper back, and hematoxylin-eosin and anti-uncoupling protein 1 antibody staining confirmed that it was BAT. The percentage injected dose per gram in BAT was as high as that in the heart and was quite different from the concentration in white adipose tissue. Preadministration of 6-hydroxydopamine or reserpine resulted in lower MIBG concentrations in BAT. Activation of the beta 3-adrenergic receptor accelerated the washout of MIBG in BAT and caused an increase in concentration in white adipose tissue. CONCLUSION: MIBG accumulates in the adrenergic nervous system in BAT, and IBAT is distinguished from the surrounding white adipose tissue. To our knowledge, BAT has not been visualized previously. We showed that MIBG scintigraphy might be suitable for the investigation of BAT and treatment of human obesity.

3-Iodobenzylguanidine↗
PubMedDate not supplied

Effects of caffeine on the uncoupling protein family in obese yellow KK mice.

1. The hypothesis that caffeine upregulates uncoupling protein (UCP)-1, UCP-2 and UCP-3 expression, which contribute to thermogenesis, was investigated in obese mice. 2. The mRNA levels of UCP-1, -2 and -3 in brown adipose tissue (BAT), UCP-2 in white adipose tissue (WAT), and UCP-2 and -3 in skeletal muscle were measured using real-time quantitative reverse transcription-polymerase chain reaction analysis in obese yellow KK mice 4 h after the subcutaneous administration of either 60 mg/kg caffeine or physiological saline. Plasma free fatty acids, adrenaline, noradrenaline and dopamine levels were also measured. 3. In caffeine-injected obese mice, UCP-1 mRNA levels were significantly increased by 1.5-fold in BAT, UCP-2 mRNA levels were increased by 1.8- and 2.5-fold in BAT and skeletal muscles, respectively, and UCP-3 mRNA levels were increased 1.7- and 3.4-fold in BAT and skeletal muscles, respectively, compared with control mice injected with physiological saline. There was no difference in UCP-2 mRNA levels in WAT between the two groups. 4. Plasma free fatty acids and adrenaline levels were significantly elevated in mice treated with caffeine compared with those injected with physiological saline. 5. It was concluded that caffeine upregulates the expression of UCP-1, UCP-2 and UCP-3 in BAT and UCP-2 and UCP-3 in skeletal muscles, which may contribute to thermogenesis in obese mice.

Adipose Tissue↗
PubMedDate not supplied

Effect of ultrasonic stimulation on mRNA abundance of uncoupling protein (UCP) 2 and UCP 3 in gastrocnemius muscle of rats.

1. The hypothesis that ultrasonic stimulation upregulates uncoupling protein (UCP) 2 and UCP3 in gastrocnemius muscle by a different mechanism of exercise was investigated in Wister rats. 2. The ultrasnonic-stimulated group was given ultrasonic stimulation to the leg (1 MHz frequency, 1 W/cm2 intensity, 10 min continuously). 3. The exercise group was given exercise training by swimming for 10 min in plastic barrels filled with warm water. 4. After 3 h, rats were killed and the gastrocnemius muscle was removed rapidly, weighed and frozen in liquid nitrogen for real-time quantitative reverse transcription-polymerase chain reaction analysis. 5. In gastrocnenius muscles of ultrasonic-stimulated rats, UCP3 mRNA abundance was significantly increased 3.6-fold and UCP2 mRNA abundance was significantly increased 2.2-fold compared with control rats. 6. In gastrocnenius muscles of exercised rats, UCP3 mRNA abundance was significantly increased 3.5-fold compared with control rats, but no change in UCP2 mRNA abundance was observed. 7. Plasma free fatty acid (FFA) levels were also significantly increased in the ultrasonic stimulation group, as well as the exercise group, compared with the control group. 8. These findings show that ultrasonic stimulation lipolyses subcutaneous fat into FFA and glycerol and upregulates UCP2 and UCP3 mRNA by a mechanism different to that of exercise.

Animals↗