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1.
Int J Obes (Lond) ; 38(6): 812-7, 2014 Jun.
Article in English | MEDLINE | ID: mdl-24213309

ABSTRACT

BACKGROUND: Brown adipose tissue (BAT) is involved in the regulation of whole-body energy expenditure and adiposity. Some clinical studies have reported an association between BAT and blood glucose in humans. OBJECTIVE: To examine the impact of BAT on glucose metabolism, independent of that of body fatness, age and sex in healthy adult humans. METHODS: Two hundred and sixty healthy volunteers (184 males and 76 females, 20-72 years old) underwent fluorodeoxyglucose-positron emission tomography and computed tomography after 2 h of cold exposure to assess maximal BAT activity. Blood parameters including glucose, HbA1c and low-density lipoprotein (LDL)/high-density lipoprotein-cholesterol were measured by conventional methods, and body fatness was estimated from body mass index (BMI), body fat mass and abdominal fat area. The impact of BAT on body fatness and blood parameters was determined by logistic regression with the use of univariate and multivariate models. RESULTS: Cold-activated BAT was detected in 125 (48%) out of 260 subjects. When compared with subjects without detectable BAT, those with detectable BAT were younger and showed lower adiposity-related parameters such as the BMI, body fat mass and abdominal fat area. Although blood parameters were within the normal range in the two subject groups, HbA1c, total cholesterol and LDL-cholesterol were significantly lower in the BAT-positive group. Blood glucose also tended to be lower in the BAT-positive group. Logistic regression demonstrated that BAT, in addition to age and sex, was independently associated with BMI, body fat mass, and abdominal visceral and subcutaneous fat areas. For blood parameters, multivariate analysis after adjustment for age, sex and body fatness revealed that BAT was a significantly independent determinant of glucose and HbA1c. CONCLUSION: BAT, independent of age, sex and body fatness, has a significant impact on glucose metabolism in adult healthy humans.


Subject(s)
Adipose Tissue, Brown/metabolism , Adipose Tissue/metabolism , Adiposity/physiology , Cold Temperature , Energy Metabolism/physiology , Glucose/metabolism , Glycated Hemoglobin/metabolism , Adipose Tissue, Brown/diagnostic imaging , Adipose Tissue, Brown/physiology , Adult , Aged , Body Composition , Female , Fluorodeoxyglucose F18 , Humans , Male , Middle Aged , Positron-Emission Tomography , Radiopharmaceuticals , Tomography, X-Ray Computed
8.
Br J Anaesth ; 101(5): 659-65, 2008 Nov.
Article in English | MEDLINE | ID: mdl-18791189

ABSTRACT

BACKGROUND: The alpha(2)-adrenoceptor agonist clonidine is used in combination with lidocaine for anaesthesia. Lidocaine inhibits axonal transport and neurite growth, whereas alpha(2)-adrenoceptor agonists have neurotrophic effects. Here we have investigated whether clonidine reduces lidocaine-induced inhibition of axonal transport in cultured mouse dorsal root ganglion neurones. METHODS: Axonal transport of organelles and neurite growth were assessed by video microscopy in cells treated with clonidine and lidocaine for 1 h. Stable responses were achieved within this period. RESULTS: Clonidine (10 and 100 microM) increased and lidocaine (10, 100 microM, and 1 mM) decreased axonal transport. The inhibitory effects of lidocaine were reduced by simultaneous treatment with clonidine. The actions of clonidine were antagonized by the alpha(2)-adrenoceptor antagonist yohimbine. Since clonidine was reported to block N-type channels, we further investigated the role of ion channels in the antagonistic action of clonidine on the lidocaine response. The action of lidocaine on axonal transport was not mimicked by the Na+ channel blocker tetrodotoxin and not blocked by the Na+ channel activator veratridine. The action of lidocaine was not blocked by the L-type Ca2+ channel blocker nifedipine, but was blocked by the N-type channel blocker omega-conotoxin MVIIA. These effects on axonal transport correlated with the effects on neurite growth. CONCLUSIONS: Inhibition of axonal transport induced by lidocaine, which may be mediated by N-type channel activation, can be blocked by clonidine. Clonidine may alleviate the effects of lidocaine on neuronal dysfunction.


Subject(s)
Adrenergic alpha-Agonists/pharmacology , Axonal Transport/drug effects , Clonidine/pharmacology , Ganglia, Spinal/drug effects , Lidocaine/antagonists & inhibitors , Anesthetics, Local/antagonists & inhibitors , Anesthetics, Local/pharmacology , Animals , Dose-Response Relationship, Drug , Ganglia, Spinal/physiology , Lidocaine/pharmacology , Male , Mice , Mice, Inbred C57BL , Microscopy, Video , Neural Inhibition/drug effects , Neurites/drug effects , Neurites/physiology , Organelles/drug effects , Organelles/physiology
11.
Neurology ; 61(3): 392-4, 2003 Aug 12.
Article in English | MEDLINE | ID: mdl-12913206

ABSTRACT

We report of an infant with neonatal glycogen storage disease type IV (GSD IV) who was examined for severe hypotonia and cardiomyopathy. On the muscle biopsy there were many fibers with diastase-resistant polyglucosan bodies. Glycogen branching enzyme (GBE1) activity in the muscle was markedly reduced. The infant had a homozygous single nucleotide deletion in the open reading frame of GBE1 gene.


Subject(s)
Glycogen Storage Disease Type IV/diagnosis , 1,4-alpha-Glucan Branching Enzyme/analysis , 1,4-alpha-Glucan Branching Enzyme/deficiency , 1,4-alpha-Glucan Branching Enzyme/genetics , Cardiomyopathies/complications , Cardiomyopathies/diagnosis , Creatine Kinase/blood , DNA Mutational Analysis , Disease Progression , Fatal Outcome , Female , Glucans/analysis , Glycogen Storage Disease Type IV/complications , Glycogen Storage Disease Type IV/genetics , Humans , Inclusion Bodies/ultrastructure , Infant, Newborn , Muscle, Skeletal/chemistry , Muscle, Skeletal/enzymology , Muscle, Skeletal/pathology , Mutation , Polyhydramnios/complications , Polyhydramnios/diagnostic imaging , Pregnancy , Sequence Deletion , Ultrasonography
12.
Forensic Sci Int ; 129(2): 134-6, 2002 Sep 26.
Article in English | MEDLINE | ID: mdl-12243884

ABSTRACT

The allele frequencies of 18 dinucleotide repeat marker loci on the X chromosome have been analyzed in 130 Japanese individuals living in Kanagawa by means of multiplex PCR and the ABI PRISM Linkage Mapping Set MD 10 Panel 28, followed by capillary electrophoresis using the ABI PRISM 310 Genetic Analyzer.


Subject(s)
Chromosomes, Human, X/genetics , Dinucleotide Repeats/genetics , Gene Frequency/genetics , Genetics, Population , Female , Genetic Markers/genetics , Humans , Japan , Male , Polymerase Chain Reaction
13.
Bull Entomol Res ; 92(4): 295-9, 2002 Aug.
Article in English | MEDLINE | ID: mdl-12191437

ABSTRACT

Field bioassays using three different synthetic sex pheromone blends (Indian, Philippine and Japanese) based on geographic variations of Cnaphalocrocis medinalis Guenée were carried out at 11 sites in Japan and in Hangzhou, China. In all of the tests, only the Japanese pheromone blend attracted a significant number of male moths, while the Indian and Philippine pheromone blends showed no marked activity. The findings in Japan showed no evidence that moths of Philippine or Indian origin were able to migrate to Japan. The results from China also showed that most populations of C. medinalisin the Hangzhou region responded to the Japanese blend. This is consistent with the current hypothesis that most populations of C. medinalisin Japan are migrants from areas to the south of the Yangzhe Valley, including the region surrounding Hangzhou, China. Furthermore, populations in the Hangzhou region can not hibernate, but are considered migrants from the southernmost parts of China and southeast Asian countries such as Vietnam where they breed continuously. Consequently, at least some populations in these areas may respond to the Japanese pheromone blend.


Subject(s)
Moths/physiology , Pheromones/physiology , Sex Attractants/physiology , Animals , China , Japan , Male , Pheromones/chemical synthesis , Sex Attractants/chemical synthesis
18.
Ryoikibetsu Shokogun Shirizu ; (34 Pt 2): 467, 2001.
Article in Japanese | MEDLINE | ID: mdl-11528841
19.
Ryoikibetsu Shokogun Shirizu ; (34 Pt 2): 468, 2001.
Article in Japanese | MEDLINE | ID: mdl-11528842
20.
Ryoikibetsu Shokogun Shirizu ; (34 Pt 2): 476-7, 2001.
Article in Japanese | MEDLINE | ID: mdl-11528848
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