Departamento de Fisiologia, Universidade Federal de São Paulo (Unifesp), Rua Botucatu, n° 862 - 2° andar, Vila Clementino, São Paulo, SP 04023-062, Brazil.
Lipids Health Dis. 2013 Dec 26;12:188. doi: 10.1186/1476-511X-12-188.
Brain glucose sensing may contribute to energy homeostasis control. The prefrontal cortex (PFC) participates in the hedonic component of feeding control. As high-fat diets may disrupt energy homeostasis, we evaluated in male Wistar rats whether intake of high-fat fish-oil diet modified cortical glucose extracellular levels and the feeding induced by intracerebroventricular glucose or PFC glucoprivation.
Glucose levels in PFC microdialysates were measured before and after a 30-min meal. Food intake was measured in animals receiving intracerebroventricular glucose followed, 30-min. later, by 2-deoxy-D-glucose injected into the PFC.
The fish-oil group showed normal body weight and serum insulin while fat pads weight and glucose levels were increased. Baseline PFC glucose and 30-min. carbohydrates intake were similar between the groups. Feeding-induced PFC glucose levels increased earlier and more pronouncedly in fish-oil than in control rats. Intracerebroventricular glucose inhibited feeding consistently in the control but not in the fish-oil group. Local PFC glucoprivation with 2-DG attenuated glucose-induced hypophagia.
The present experiments have shown that, following food intake, more glucose reached the prefrontal cortex of the rats fed the high-fat fish-oil diet than of the rats fed the control diet. However, when administered directly into the lateral cerebral ventricle, glucose was able to consistently inhibit feeding only in the control rats. The findings indicate that, an impairment of glucose transport into the brain does not contribute to the disturbances induced by the high-fat fish-oil feeding.
脑葡萄糖感应可能有助于能量稳态控制。前额叶皮层(PFC)参与进食控制的享乐成分。由于高脂肪饮食可能会破坏能量稳态,我们在雄性 Wistar 大鼠中评估了高脂肪鱼油饮食是否改变了大脑皮层葡萄糖细胞外水平,以及脑室内葡萄糖或 PFC 糖剥夺引起的进食。
在 30 分钟的进食后,测量 PFC 微透析物中的葡萄糖水平。在接受脑室内葡萄糖的动物中测量食物摄入量,30 分钟后,将 2-脱氧-D-葡萄糖注入 PFC。
鱼油组体重和血清胰岛素正常,而脂肪垫重量和葡萄糖水平升高。两组之间的 PFC 葡萄糖基线和 30 分钟碳水化合物摄入量相似。鱼油组的 PFC 葡萄糖水平在进食诱导下更早且更明显地升高。脑室内葡萄糖一致抑制了对照组的进食,但在鱼油组则不然。用 2-DG 局部 PFC 糖剥夺减弱了葡萄糖诱导的摄食减少。
本实验表明,在进食后,摄入高脂肪鱼油饮食的大鼠的前额叶皮层中到达的葡萄糖比摄入对照饮食的大鼠更多。然而,当直接注入侧脑室时,葡萄糖仅能在对照组大鼠中一致地抑制进食。这些发现表明,葡萄糖向大脑的转运受损不会导致高脂肪鱼油喂养引起的紊乱。