A high-fat diet impairs cooling-evoked brown adipose tissue activation via a vagal afferent mechanism.
| Autor: | Madden CJ; Department of Neurological Surgery, Oregon Health and Science University, Portland, Oregon maddench@ohsu.edu., Morrison SF; Department of Neurological Surgery, Oregon Health and Science University, Portland, Oregon. |
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| Jazyk: | angličtina |
| Zdroj: | American journal of physiology. Endocrinology and metabolism [Am J Physiol Endocrinol Metab] 2016 Aug 01; Vol. 311 (2), pp. E287-92. Date of Electronic Publication: 2016 Jun 28. |
| DOI: | 10.1152/ajpendo.00081.2016 |
| Abstrakt: | In dramatic contrast to rats on a control diet, rats maintained on a high-fat diet (HFD) failed to activate brown adipose tissue (BAT) during cooling despite robust increases in their BAT activity following direct activation of their BAT sympathetic premotor neurons in the raphe pallidus. Cervical vagotomy or blockade of glutamate receptors in the nucleus of the tractus solitarii (NTS) reversed the HFD-induced inhibition of cold-evoked BAT activity. Thus, a HFD does not prevent rats from mounting a robust, centrally driven BAT thermogenesis; however, a HFD does alter a vagal afferent input to NTS neurons, thereby preventing the normal activation of BAT thermogenesis to cooling. These results, paralleling the absence of cooling-evoked glucose uptake in the BAT of obese humans, reveal a neural mechanism through which consumption of a HFD contributes to reduced energy expenditure and thus to weight gain. (Copyright © 2016 the American Physiological Society.) |
| Databáze: | MEDLINE |
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