| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Outline of Final Research Achievements |
Overconsumption beyond multiple physiological control is an issue to produce prevalence of obesity and metabolic diseases. To explore its neurobiological mechanisms, we examined changes in feeding inhibitory mechanisms in mice showing binge-like sugar overconsumption. We found circulating concentration of a gut hormone, peptide YY (PYY), secreted after an intra-gastric (IG) infusion of sucrose significantly decreased in mice with bingeing in comparison to that in control animals. In addition, c-fos expression in the brainstem in response to the IG stimulation or peripheral PYY administration were also reduced in the bingeing group. Peripheral administration of PYY, cholecystokinin, or glucagon-like peptide-1 suppressed the expression of the sugar bingeing. Our results suggest that sugar overconsumption is partly due to blunted feeding inhibition based on dysfunction of gut hormone secretion and gut-brain interaction via hormonal and neural signals during postingestive processes.
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