Diabetes:上海生科院发现下丘脑AgRP神经元调控肥胖的新机制

2017-01-05 不详 上海生命科学研究院

12月19日,国际学术期刊Diabetes在线发表了中国科学院上海生命科学研究院营养科学研究所郭非凡组的研究论文:Deletion of ATF4 in AgRP neurons promotes fat loss mainly via increasing energy expenditure。该研究发现在下丘脑特异神经元AgRP神经元中,激活转录因子4(ATF4)可以调节机体能量平衡和脂质代谢

12月19日,国际学术期刊Diabetes在线发表了中国科学院上海生命科学研究院营养科学研究所郭非凡组的研究论文:Deletion of ATF4 in AgRP neurons promotes fat loss mainly via increasing energy expenditure。该研究发现在下丘脑特异神经元AgRP神经元中,激活转录因子4(ATF4)可以调节机体能量平衡和脂质代谢,为肥胖和相关代谢疾病的治疗提供潜在的药物靶点。

近年来,无论在发展中国家还是发达国家,成年人还是儿童,肥胖都广泛流行,并与一系列代谢综合征糖尿病、脂肪肝、血脂异常和心血管疾病等息息相关,对人类健康造成很大威胁。因此,研究肥胖的发展机制尤为重要。体重的变化是由能量摄入和能量消耗的不平衡导致的,中枢神经系统特别是下丘脑对能量平衡的调节起着关键作用。

大脑中包含有多种特异类型的神经元,行使着不同的功能,调节人体的行为和代谢平衡。下丘脑的弓状核(ARC)包含两大类调节代谢的神经元:一类是抑制食欲的神经元,如阿黑皮素原(POMC)神经元;一类是促进食欲的神经元,包括神经肽Y(NPY)和刺鼠肽基因相关蛋白(AgRP)神经元。AgRP神经元可以通过释放AgRP蛋白,抑制POMC神经元的活性,进而促进摄食增加;也可通过调节交感神经系统或瘦素敏感性来影响能量消耗。对特异神经元如AgRP如何调控能量代谢的研究将为发现肥胖的病因与治疗提供重要理论基础。

博士后邓嘉莉和博士生原飞翔在郭非凡指导下,利用诱导性基因敲除技术,在成年小鼠的AgRP神经元中特异敲除ATF4,发现这些小鼠变瘦,胰岛素敏感性和瘦素敏感性提高。同时,实验小鼠摄食减少,能量消耗增加,提高机体产热。高脂饮食后,AgRP特异敲除ATF4小鼠可以抵抗高脂诱导的肥胖、胰岛素抵抗和脂肪肝。进一步研究其作用机制发现,ATF4可以结合到FOXO1的启动子上直接调控其表达。在敲除小鼠的下丘脑弓状核中注射FOXO1腺病毒后,小鼠脂肪显著增加。

综上所述,该研究发现了ATF4在下丘脑AgRP神经元中调节能量平衡和脂质代谢的重要功能,暗示在治疗肥胖和代谢性疾病中ATF4有可能成为新的药物靶点。

该研究工作获得国家自然科学基金、科技部、上海市科委以及中科院等科研基金的支持。

原始出处:

Deng J, Yuan F, Guo Y, Xiao Y, Niu Y, Deng Y, Han X, Guan Y, Chen S, Guo F.Deletion of ATF4 in AgRP Neurons Promotes Fat Loss Mainly via Increasing EnergyExpenditure.Diabetes. 2016 Dec 19. pii: db160954. [Epub ahead of print]

 

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    2017-01-07 xlwang2696
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    2017-01-07 xlwang2696