Resting state hypothalamic response to glucose predicts glucose-induced attenuation in the ventral striatal response to food cues
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منابع مشابه
Biphasic Response to Luteolin in MG-63 Osteoblast-Like Cells under High Glucose‑Induced Oxidative Stress
Background: Clinical evidence indicates the diabetes-induced impairment of osteogenesis caused by a decrease in osteoblast activity. Flavonoids can increase the differentiation and mineralization of osteoblasts in a high-glucose state. However, some flavonoids such as luteolin may have the potential to induce cytotoxicity in osteoblast-like cells. This study was performed to investigate whether...
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background: clinical evidence indicates the diabetes-induced impairment of osteogenesis caused by a decrease in osteoblast activity. flavonoids can increase the differentiation and mineralization of osteoblasts in a high-glucose state. however, some flavonoids such as luteolin may have the potential to induce cytotoxicity in osteoblast-like cells. this study was performed to investigate whether...
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One of the early steps in the regionalization of the CNS is the subdivision of the forebrain into dorsal and basal telencephalic ventricular zones. These ventricular zones give rise to the cortex and striatum respectively, in the mature brain. Previous work suggests that while neural precursors are able to move within both the dorsal cortical and basal striatal ventricular zones, they are unabl...
متن کاملInsulin blunts the response of glucose-excited neurons in the ventrolateral-ventromedial hypothalamic nucleus to decreased glucose.
Insulin signaling is dysfunctional in obesity and diabetes. Moreover, central glucose-sensing mechanisms are impaired in these diseases. This is associated with abnormalities in hypothalamic glucose-sensing neurons. Glucose-sensing neurons reside in key areas of the brain involved in glucose and energy homeostasis, such as the ventromedial hypothalamus (VMH). Our results indicate that insulin o...
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ژورنال
عنوان ژورنال: Appetite
سال: 2017
ISSN: 0195-6663
DOI: 10.1016/j.appet.2017.05.038