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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Peroxisome Proliferator-Activated Receptor gamma Controls Ingestive Behavior, Agouti-Related Protein, and Neuropeptide Y mRNA in the Arcuate Hypothalamus
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Peroxisome Proliferator-Activated Receptor gamma Controls Ingestive Behavior, Agouti-Related Protein, and Neuropeptide Y mRNA in the Arcuate Hypothalamus

机译：过氧化物酶体增殖物激活的受体γ控制弓形下丘脑的摄食行为，刺痛相关蛋白和神经肽Y mRNA。

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Peroxisome proliferator-activated receptor gamma (PPAR gamma) is clinically targeted for type II diabetes treatment; however, rosiglitazone (ROSI), a PPAR gamma agonist, increases food intake and body/fat mass as side-effects. Mechanisms for these effects and the role of PPAR gamma in feeding are not understood. Therefore, we tested this role in Siberian hamsters, a model of human energy balance, and C57BL/6 mice. We tested the following: (1) how ROSI and/or GW9662 (2-chloro-5-nitro-N-phenylbenzamide; PPAR gamma antagonist) injected intraperitoneally or into the third ventricle (3V) affected Siberian hamster feeding behaviors; (2) whether food deprivation (FD) co-increases agouti-related protein (AgRP) and PPAR gamma mRNA expression in Siberian hamsters and mice; (3) whether intraperitoneally administered ROSI increases AgRP and NPY in ad libitum-fed animals; (4) whether intraperitoneally administered PPAR gamma antagonism blocks FD-induced increases in AgRP and NPY; and finally, (5) whether intraperitoneally administered PPAR gamma modulation affects plasma ghrelin. Third ventricular and intraperitoneally administered ROSI increased food hoarding and intake for 7 d, an effect attenuated by 3V GW9662, and also prevented (intraperitoneal) FD-induced feeding. FD hamsters and mice increased AgRP within the arcuate hypothalamic nucleus with concomitant increases in PPAR gamma exclusively within AgRP/NPY neurons. ROSI increased AgRP and NPY similarly to FD, and GW9662 prevented FD-induced increases in AgRP and NPY in both species. Neither ROSI nor GW9662 affected plasma ghrelin. Thus, we demonstrated that PPAR gamma activation is sufficient to trigger food hoarding/intake, increase AgRP/NPY, and possibly is necessary for FD-induced increases in feeding and AgRP/NPY. These findings provide initial evidence that FD-induced increases in AgRP/NPY may be a direct PPAR gamma dependent process that controls ingestive behaviors.
机译：过氧化物酶体增殖物激活受体γ（PPARγ）在临床上是针对II型糖尿病的治疗目标;但是，PPARγ激动剂罗格列酮（ROSI）会增加食物的摄入量和体重。这些作用的机制以及PPARγ在喂养中的作用尚不清楚。因此，我们在西伯利亚仓鼠，人类能量平衡模型和C57BL / 6小鼠中测试了这一作用。我们测试了以下内容：（1）腹膜内或第三脑室（3V）注射的ROSI和/或GW9662（2-氯-5-硝基-N-苯基苯甲酰胺; PPARγ拮抗剂）如何影响西伯利亚仓鼠的进食行为; （2）食物剥夺（FD）是否在西伯利亚仓鼠和小鼠中共同增加了刺豚鼠相关蛋白（AgRP）和PPARγmRNA表达; （3）腹膜内施用的ROSI是否增加了随意喂养动物的AgRP和NPY; （4）腹膜内给予的PPARγ拮抗作用是否阻断FD诱导的AgRP和NPY的增加;最后，（5）腹膜内施用的PPARγ调节是否会影响血浆生长素释放肽。第三次心室和腹膜内施用的ROSI可增加食物ho积和摄入量，持续7天，这种作用被3V GW9662削弱，并且还阻止了（腹膜内）FD诱导的进食。 FD仓鼠和小鼠在弓状下丘脑核内增加了AgRP，同时在AgRP / NPY神经元内仅增加了PPARγ。 ROSI与FD相似地增加了AgRP和NPY，而GW9662阻止了FD诱导的两种物种中AgRP和NPY的增加。 ROSI和GW9662均不影响血浆生长素释放肽。因此，我们证明了PPARγ激活足以触发食物ard积/摄入，增加AgRP / NPY，并且可能是FD引起的进食和AgRP / NPY增加的必要条件。这些发现提供了初步证据，表明FD诱导的AgRP / NPY升高可能是直接的PPAR依赖γ的过程，可控制摄食行为。

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