Wang Li-jian, Zhou Lü, Yuan Bo, Wang Ling
Department of Physiology, Institute of Basic Medical Science, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking Union Medical College, Beijing 100005, China.
Zhonghua Yi Xue Za Zhi. 2006 Aug 29;86(32):2266-70.
To observe the role of leptin on the regulation of inter-digestive migrating motor complex (MMC) and gastric motility of postprandial period, as well as the serum leptin level and its relationship with motilin during different fast and postprandial periods.
Strain gauges were implanted on the serosa of corpus, antrum and pylorus in 50 conscious Wistar rats to record the gastric motility activities. Canula was inserted in the external jugular vein for drug perfusion and blood sampling. The rats were randomly divided into 5 groups: (1) Group 1 to observe the relationship between the postprandial fasting MMC and MMC after feeding. MMC on the empty stomach was recorded, soon afterwards test meal was fed, then the gastric motility was recorded for 60 minutes. Blood samples were collected during the phases I, II, III, and IV, 3 minutes after feeding and then every 5 minutes to test the serum leptin and motilin. (2) Leptin group. After the recording of the first MMC, leptin was perfused during the second MMC to observe its effect on the stomach motility. (3) Anti-leptin serum group. During the second MMC, 5 minutes before feeding and 60 minutes after feeding, anti-leptin serum was perfused to observe its effect on the postprandial stomach motility. (4) Leptin + atropine group. During the first MMC perfusion of atropine was followed by perfusion of leptin. and (5) leptin + cholecystokinin (CCK)-A receptor blocker group. Perfusion of CCK-A receptor blocker was followed by perfusion of leptin. Serum leptin and motilin levels were measured by radioimmunoassay.
Typical MMC with phase I, II, III, and IV was recorded in the fasting rats. The phase III of antral MMC could migrate to the pylorus. During the postprandial period, the gastric motility patterns were persistent rhythmic peristaltic contractions. When the stomach was empty, the mean concentration of serum leptin was (5.6 +/- 1.0) microg/L, (11.4 +/- 2.1) microg/L, and (2.1 +/- 0.7) microg/L during the phase I, II and III respectively, being the highest in the phase II, significantly higher than those in the phase I and III (both P < 0.01). During digestive period, the serum concentration of leptin began to increase 3 minutes after the meal and reached its peak of (28.1 +/- 4.4) microg/L 10 minutes after the meal. The serum concentration of leptin remained on a high level till 30 minutes later (compared with that in the inter-digestive period, P < 0.01). On the contrary, the serum concentration of motilin was the highest in the phase III of MMC and the lowest in the digestive period. Intravenous infusion of leptin (2.5 microg x kg(-1) x 10 min) turned the inter-digestive pattern of gastric motility to digestive period pattern with corpus distension and contraction of antrum and pylorus. The effects of leptin on gastric motility were blocked by anti-leptin serum, atropine, and CCK-A receptor blocker loxiglumide.
Leptin is a hormone to promote the inter-digestive MMC phase II and postprandial digestive motility activities of stomach, the concentration fluctuation of which will cause satiety related delay of gastric emptying. The effect of leptin on gastric motility is mediated by cholinergic nerve and CCK-A receptors.
观察瘦素在调节消化间期移行性复合运动(MMC)及餐后胃动力中的作用,以及不同禁食和餐后时段血清瘦素水平及其与胃动素的关系。
将应变片植入50只清醒Wistar大鼠胃体、胃窦和幽门的浆膜上,记录胃动力活动。经颈外静脉插入套管用于药物灌注和采血。大鼠随机分为5组:(1)第1组观察餐后禁食MMC与进食后MMC的关系。记录空腹时的MMC,随后给予试餐,然后记录60分钟的胃动力。在MMC的I、II、III、IV期、进食后3分钟及随后每5分钟采集血样,检测血清瘦素和胃动素。(2)瘦素组。记录第一次MMC后,在第二次MMC期间灌注瘦素,观察其对胃动力的影响。(3)抗瘦素血清组。在第二次MMC期间,进食前5分钟和进食后60分钟灌注抗瘦素血清,观察其对餐后胃动力的影响。(4)瘦素+阿托品组。在第一次MMC期间先灌注阿托品,随后灌注瘦素。(5)瘦素+胆囊收缩素(CCK)-A受体阻断剂组。先灌注CCK-A受体阻断剂,随后灌注瘦素。采用放射免疫法测定血清瘦素和胃动素水平。
在禁食大鼠中记录到具有I、II、III、IV期的典型MMC。胃窦MMC的III期可向幽门移行。餐后时段,胃动力模式为持续有节律的蠕动收缩。空腹时,血清瘦素平均浓度在MMC的I期、II期和III期分别为(5.6±1.0)μg/L、(11.4±2.1)μg/L和(2.1±0.7)μg/L,II期最高,显著高于I期和III期(均P<0.01)。消化期,血清瘦素浓度在进食后3分钟开始升高,进食后10分钟达到峰值(28.1±4.4)μg/L。血清瘦素浓度在30分钟后仍维持在高水平(与消化间期相比,P<0.01)。相反,胃动素血清浓度在MMC的III期最高,在消化期最低。静脉输注瘦素(2.5μg·kg⁻¹·10min)使胃动力的消化间期模式转变为消化期模式,表现为胃体扩张和胃窦及幽门收缩。抗瘦素血清、阿托品和CCK-A受体阻断剂洛西肽可阻断瘦素对胃动力的作用。
瘦素是一种促进消化间期MMC II期和餐后胃消化动力活动的激素,其浓度波动会导致与饱腹感相关的胃排空延迟。瘦素对胃动力的作用由胆碱能神经和CCK-A受体介导。