Российская академия наук


СORRECTION OF FOOD INTAKE IN MICE GENETICALLY PREDISPOSED TO HYPERPHAGIA AND OBESITY



страница110/848
Дата10.12.2019
Размер1.98 Mb.
1   ...   106   107   108   109   110   111   112   113   ...   848
СORRECTION OF FOOD INTAKE IN MICE GENETICALLY PREDISPOSED TO HYPERPHAGIA AND OBESITY

Bazhan N.M., Yakovleva T.V., Makarova E.N., Kazantseva A.Y.

The establishment of the Russian Academy of Sciences, Institute of cytology and genetics, Novosibirsk, Russia, bazhan-nm@yandex.ru


Now obesity and obesity-related pathologies, such as type 2 diabetes have taken the character of world-wide epidemic. The obesity development is known to be depended on interaction of genetic and environmental factors. Food intake is known to changed during the individual development. Pregnancy and lactation are characterized by increased and emotional stress – decreased appetite. The aim of the study was to investigate whether physiological states with relatively high and low food intake will affect the development of genetically-determined hyperphagia and obesity. C57Bl/6J mice carrying lethal yellow mutation at the Agouti locus (Ay/a mice) predisposed to the obesity and diabetes 2 development were used. The Ay mutation reduces melanocortin (MC) system activity which controls energy balance under the rest conditions. Mice of standard C57Bl/6J genotype (a/a mice) served as metabolic control. Repeating emotional stress (0,5h restraint х 3 times a week x 5 weeks) hampered development of obesity and 2 type diabetes in the Ay/a mice. Acute (1 h restraint) emotional stresses inhibited feeding and decreased plasma insulin levels only in the Ay/a mice. Anorexia in stressed Ay/a mice was independent of pathways involving hypothalamic orexigenic neuropeptide AgRP, NPY and HPA axis and might be associated with increased anorexic signal through corticotrophin-releasing factor 2 receptor (CRFR2) in the hypothalamus. Pregnancy and lactation eliminated hereditary hyperphagia, delayed obesity and diabetes development in the Ay/a mice. Lactation induced hyperphagia was independent on the pathways involving hypothalamic orexigenic neuropeptide AgRP, NPY. So, pregnancy and lactation (high food intake) similar to emotional stress (low food intake) prevented the development of genetically determined obesity and improved glucose metabolism in the Ay/a mice. One can assume that MC system, disturbed by the Ay mutation does not play a leading role in the feeding regulation during lactation and emotional stress. Other hypothalamic systems help to keep appétit and consequently glucose metabolism on the new levels appropriated to new physiological needs. These adaptations masked the genetically determined hyperphagia caused by the disturbance in the MC signaling, hampered obesity development and improved glucose metabolism in Ay/a mice.

The study was supported by the RFBR 09-04-00447, 10-04-00331, 11-04-01956.

Каталог: news
news -> Умеренные когнитивные нарушения у больных с сосудистым поражением головного мозга 14. 01. 11 нервные болезни
news -> 15-й международный медицинский форум «качество и безопасность оказания медицинской помощи» нижегородская ярмарка россия, Нижний Новгород
news -> Сборник материалов
news -> Разработка технологии вкусоароматических добавок с применением сенсорных технологий
news -> «казұму 85 жыл: жетістіктері мен келешегі» халықаралық ғылыми-тəжірибелік конференция аясындағы «клиникалық фармация: халықаралық ТƏжірибе мен қазақстанның денсаулық сақтаудағы даму ерекшеліктері»
news -> Программа международной научно-практической конференции 14-15 апреля 2016 г. Курск 2016
news -> Российская академия наук отделение физиологических наук


Поделитесь с Вашими друзьями:
1   ...   106   107   108   109   110   111   112   113   ...   848




База данных защищена авторским правом ©zodorov.ru 2020
обратиться к администрации

    Главная страница