more parking, relevant to obesity..... I may have posted this abstract previously...... ignore for the mean time?.......
Nutrition 1997 May;13(5):403-11
Hypothalamic neuronal histamine: implications of its homeostatic control
of energy metabolism.
Sakata T, Yoshimatsu H, Kurokawa M
Department of Internal Medicine, School of Medicine, Oita Medical University, Japan.
In a series of studies on histaminergic functions in the hypothalamus, probes to manipulate activities of histaminergic neuron
systems were applied to assess its physiologic and pathophysiologic implications using non-obese normal and Zucker obese
rats, an animal model of genetic obesity. Food intake is suppressed by either activation of H1-receptor or inhibition of the
H3-receptor in the ventromedial hypothalamus (VMH) or the paraventricular nucleus, each of which is involved in satiety
regulation. Histamine neurons in the mesencephalic trigeminal sensory nucleus modulate masticatory functions, particularly eating
speed through the mesencephalic trigeminal motor nucleus, and activation of the histamine neurons in the VMH suppress intake
volume of feeding at meals. Energy deficiency in the brain, i.e., intraneuronal glucoprivation, activates neuronal histamine in the
hypothalamus. Such low energy intake in turn accelerates glycogenolysis in the astrocytes to prevent the brain from energy
deficit. Thus, both mastication and low energy intake act as afferent signals for activation of histaminergic nerve systems in the
hypothalamus and result in enhancement of satiation. There is a rationale for efficacy of a very-low-calorie conventional
Japanese diet as a therapeutic tool for weight reduction. Feeding circadian rhythm is modulated by manipulation of
hypothalamic histamine neurons. Hypothalamic histamine neurons are activated by an increase in ambient temperature.
Hypothalamic neuronal histamine controls adaptive behavior including a decrease in food intake and ambulation, and an
increase in water intake to maintain body temperature to be normally constant. In addition, interleukin-1 beta, an endogenous
pyrogen, enhanced turnover of neuronal histamine through prostaglandin E2 in the brain. Taken together, the histamine neuron
system in the hypothalamus is essential for maintenance of thermoregulation through the direct and indirect control of adaptive
behavior. Behavioral and metabolic abnormalities of obese Zucker rats including hyperphagia, disruption of feeding circadian
rhythm, hyperlipidemia, hyperinsulinemia, and disturbance of thermoregulation are essentially derived from a defect in
hypothalamic neuronal histamine. Abnormalities produced by depletion of neuronal histamine from the hypothalamus in normal
rats mimic those of obese Zuckers. Grafting the lean Zucker fetal hypothalamus into the obese Zucker pups attenuates those
abnormalities. These findings indicate that histamine nerve systems in the brain play a crucial role in maintaining homeostatic
energy balance. |
