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| ヒスタミンは食欲を抑える神経伝達物質で、同時に脂肪を燃焼してエネルギーの代謝を促進する働きがあります。神経伝達物質のヒスタミンはアミノ酸のヒスチジンから作られ、アミノ酸のヒスチジンが不足すると脂肪を増やし肥満の原因になります。
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| Histamine is an important brain neurotransmitter
that suppresses food intake. Brain histamine also increases
energy expenditure by stimulating fat use via activation of
the sympathetic nervous system. Histamine is made from L-histidine
and there is a direct relationship between blood L-histidine
and brain histamine. A deficiency of L-histidine leads to increased
weight and increased storage of fat in fat body stores. In addition,
a deficiency of L-histidine leads to decreased energy use further
complicating the ability to lose weight when there really is
a deficiency of L-histidine. This article discuss the relationship
between histamine deficiency and obesity.The article also discusses
the role of histamine in regulation of leptin metabolism. This
article provides strong evidence that a deficiency of histamine
is strongly related to obesity. The Editors |
Fulop,A.K.; Foldes,A.; Buzas,E.; Hegyi,K.;
Miklos,I.H.; Romics,L.; Kleiber,M.; Nagy,A.; Falus,A.; Kovacs,K.J.
Laboratory of Molecular Neuroendocrinology, Institute of Experimental
Medicine, H-1083 Budapest, Hungary
Endocrinology 144:4306-4314:2003
Histamine has been referred to as an anorexic factor that decreases
appetite and fat accumulation and affects feeding behavior.
Tuberomammillary histaminergic neurons have been implicated
in central mediation of peripheral metabolic signals such as
leptin, and centrally released histamine inhibits ob gene expression.
Here we have characterized the metabolic phenotype of mice that
completely lack the ability to produce histamine because of
targeted disruption of the key enzyme in histamine biosynthesis
(histidine decarboxylase, HDC). Histochemical analyses confirmed
the lack of HDC mRNA, histamine immunoreactivity, and histaminergic
innervation throughout the brain of gene knockout mouse. Aged
histamine-deficient (HDC-/-) mice are characterized by visceral
adiposity, increased amount of brown adipose tissue, impaired
glucose tolerance, hyperinsulinemia, and hyperleptinemia. Histamine-deficient
animals are not hyperphagic but gain more weight and are calorically
more efficient than wild-type controls. These metabolic changes
presumably are due to the impaired regulatory loop between leptin
and hypothalamic histamine that results in orexigenic dominance
through decreased energy expenditure, attenuated ability to
induce uncoupling protein-1 mRNA in the brown adipose tissue
and defect in mobilizing energy stores. Our results further
support the role of histamine in regulation of energy homeostasis |
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