School of Agriculture, Hokkaido University, Sapporo, Japan.
Graduate School of Agriculture, Hokkaido University, Sapporo, Japan.
J Nutr. 2021 May 11;151(5):1320-1328. doi: 10.1093/jn/nxab013.
Dietary calcium has been proposed to reduce appetite in human studies. Postprandial satiety is mainly controlled by gut hormones. However, the effect of calcium on appetite and the role of gut hormones remain unclear.
We examined whether oral administration of calcium reduces food intake in rats and investigated the underlying mechanism.
Male Sprague Dawley rats (8-12 wk old) were used after an overnight fastifffng. In a series of 2 trials with 1-wk interval between challenges, food intake was measured 0.5-24 h after oral gavage of a vehicle (saline containing 1.5% carboxymethyl cellulose) as the control treatment, or the vehicle containing various calcium compounds [calcium chloride (CaCl2), calcium carbonate, calcium lactate, in a random order] at 150 mg calcium/kg dose. A conditional taste aversion test was conducted. In separate experiments, plasma calcium and gut hormone concentrations were measured 15 or 30 min after oral administration of the calcium compounds. In anesthetized rats, portal peptide-YY (PYY) concentrations were measured after intraluminal administration of a liquid meal with or without additional calcium.
Oral CaCl2 reduced food intake acutely (30 min, ∼20%, P < 0.05) compared with control rats, without taste aversion. Plasma PYY concentration was higher (100%, P < 0.05) in CaCl2-preloaded rats than in control rats, 15 min after administration. In anesthetized rats, luminal meal + CaCl2 induced a 4-fold higher increase in plasma PYY than the control treatment did. Oral administration of a calcium-sensing receptor (CaSR) agonist suppressed food intake (∼30%, P < 0.05), but CaCl2 and CaSR agonist did not suppress food intake under treatment with a PYY receptor antagonist. Furthermore, the CaSR antagonist attenuated the effect of CaCl2 on food intake.
CaCl2 suppresses food intake partly by increasing CaSR-mediated PYY secretion in rats. Our findings could at least partially explain the satiating effect of calcium.
已有研究提出膳食钙可减少人体的食欲。餐后饱腹感主要受肠道激素控制。然而，钙对食欲的影响以及肠道激素的作用尚不清楚。
我们在大鼠中研究了口服钙是否能减少食物摄入，并探讨了其潜在机制。
雄性 Sprague Dawley 大鼠（8-12 周龄）禁食过夜后用于实验。在为期 1 周的 2 项试验中，大鼠口服灌胃载体（含 1.5%羧甲基纤维素的生理盐水）作为对照处理后，0.5-24 h 测量食物摄入量，或随机给予载体中添加不同钙化合物[氯化钙（CaCl2）、碳酸钙、乳酸钙]（剂量为 150 mg 钙 /kg）。进行条件性味觉厌恶测试。在单独的实验中，在口服钙化合物后 15 或 30 min 测量血浆钙和肠道激素浓度。在麻醉大鼠中，经腔内置入含或不含额外钙的液体餐后，测量门静脉肽 YY（PYY）浓度。
与对照大鼠相比，口服 CaCl2 可急性（30 min 时约减少 20%，P<0.05）减少食物摄入，且无味觉厌恶。与对照大鼠相比，给予 CaCl2 预负荷后 15 min 时大鼠的血浆 PYY 浓度更高（100%，P<0.05）。在麻醉大鼠中，与对照处理相比，腔内置入餐食+CaCl2 可使血浆 PYY 增加 4 倍。口服钙敏感受体（CaSR）激动剂可抑制食物摄入（约 30%，P<0.05），但 CaCl2 和 CaSR 激动剂在 PYY 受体拮抗剂存在时不能抑制食物摄入。此外，CaSR 拮抗剂减弱了 CaCl2 对食物摄入的作用。
CaCl2 通过增加 CaSR 介导的 PYY 分泌部分抑制大鼠的食物摄入。我们的发现至少可以部分解释钙的饱腹感效应。
