Osto M, Wielinga P Y, Alder B, Walser N, Lutz T A
Institute of Veterinary Physiology, and Zurich Center for Integrative Human Physiology, Vetsuisse Faculty University of Zurich, Winterthurerstrasse 260, 8057, Zurich, Switzerland.
Physiol Behav. 2007 Aug 15;91(5):566-72. doi: 10.1016/j.physbeh.2007.03.017. Epub 2007 Mar 30.
Amylin is a pancreatic hormone that is considered to be a satiating signal acting on neurons of the area postrema (AP) in the hindbrain. The adiposity signals leptin and insulin act in the hypothalamus to influence feeding. They also enhance the hindbrain's responsivity to satiating signals, e.g. cholecystokinin (CCK). The orexigenic hormone ghrelin is thought to use the same hypothalamic pathways as leptin and insulin, with opposite actions on feeding behaviour. In fact, CCK and ghrelin also seem to interact in the control of feeding. Because CCK's anorectic effect depends on endogenous amylin, the aim of this study was therefore to evaluate a possible functional interaction between amylin and these hormones on short-term food intake in rats. The experiments were performed with male Wistar rats. Intracerebroventricular injection (i3vt) of an orexigenic dose of ghrelin (5 ng/5 microl) reduced but did not completely reverse the intraperitoneal amylin (5 microg/kg)-induced inhibition of food intake. In comparison, administration of a sub-threshold dose of ghrelin (3 ng/5 microl) did not affect the anorexigenic action of peripheral amylin. Leptin administered into the third ventricle (i3vt; 3.5 microg/5 microl) and intraperitoneal amylin (5 microg/kg) synergistically reduced food intake in chow-fed rats. I3vt insulin, administered at a sub-threshold dose (0.5 mU/5 microl), significantly enhanced the response to peripheral amylin. These results indicate that the lipostatic signals leptin and insulin may synergize with amylin to reduce food intake. In contrast, under the conditions tested, the orexigenic hormone ghrelin does not seem to influence the feeding response to peripheral amylin.
胰淀素是一种胰腺激素，被认为是一种作用于后脑最后区（AP）神经元的饱腹感信号。肥胖信号瘦素和胰岛素在下丘脑中发挥作用以影响进食。它们还增强后脑对饱腹感信号的反应性，例如胆囊收缩素（CCK）。促食欲激素胃饥饿素被认为与瘦素和胰岛素使用相同的下丘脑途径，但对进食行为有相反的作用。事实上，CCK和胃饥饿素在进食控制中似乎也相互作用。由于CCK的厌食作用依赖于内源性胰淀素，因此本研究的目的是评估胰淀素与这些激素在大鼠短期食物摄入上可能存在的功能相互作用。实验用雄性Wistar大鼠进行。脑室内注射（i3vt）促食欲剂量的胃饥饿素（5 ng/5 μl）可减少但不能完全逆转腹腔注射胰淀素（5 μg/kg）诱导的食物摄入抑制。相比之下，给予阈下剂量的胃饥饿素（3 ng/5 μl）不影响外周胰淀素的厌食作用。向第三脑室注射（i3vt；3.5 μg/5 μl）的瘦素与腹腔注射的胰淀素（5 μg/kg）协同降低了喂食大鼠的食物摄入量。以阈下剂量（0.5 mU/5 μl）给予的i3vt胰岛素显著增强了对外周胰淀素的反应。这些结果表明，脂肪稳态信号瘦素和胰岛素可能与胰淀素协同作用以减少食物摄入量。相比之下，在所测试的条件下，促食欲激素胃饥饿素似乎不影响对外周胰淀素的进食反应。
