期刊
JOURNAL OF PHYSIOLOGICAL SCIENCES
卷 61, 期 2, 页码 103-113出版社
SPRINGER TOKYO
DOI: 10.1007/s12576-010-0127-6
关键词
Feeding regulation; Ketosis; Monocarboxylate transporter 1; Energy sensing; Paraventricular nucleus
类别
资金
- Ministry of Education, Culture, Sports, Science, and Technology [18208025]
- Grants-in-Aid for Scientific Research [21688021, 18208025] Funding Source: KAKEN
Uncontrolled type 1 diabetes leads to hyperphagia and severe ketosis. This study was conducted to test the hypothesis that ketone bodies act on the hindbrain as a starvation signal to induce diabetic hyperphagia. Injection of an inhibitor of monocarboxylate transporter 1, a ketone body transporter, into the fourth ventricle normalized the increase in food intake in streptozotocin (STZ)-induced diabetic rats. Blockade of catecholamine synthesis in the hypothalamic paraventricular nucleus (PVN) also restored food intake to normal levels in diabetic animals. On the other hand, hindbrain injection of the ketone body induced feeding, hyperglycemia, and fatty acid mobilization via increased sympathetic activity and also norepinephrine release in the PVN. This result provides evidence that hyperphagia in STZ-induced type 1 diabetes is signaled by a ketone body sensed in the hindbrain, and mediated by noradrenergic inputs to the PVN.
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