Laboratory of Nutrition, Azabu University School of Veterinary Medicine, Sagamihara, Japan.
Anim Sci J. 2009 Dec;80(6):655-61. doi: 10.1111/j.1740-0929.2009.00683.x.
The aim of the present study was to elucidate the mechanism by which ketone bodies increase antidiuretic hormone (ADH) secretion. Four male Holstein calves (5 weeks of age) were utilized. Four levels of butyrate (0 g, 11 g, 22 g and 44 g) were administrated intra-ruminally in a 4 x 4 Latin square design and cerebrospinal fluid (CSF, six-position lumbar puncture), blood plasma and urine were collected. The concentration of total plasma and CSF protein was 5.5-5.6 g/dL and 27.5-28.3 mg/dL, respectively. CSF concentrations of a specific ketone body, 3-hydroxybutyric acid, were significantly higher in the 22 g and 44 g butyrate groups than in the control group. CSF concentrations of ADH in the 11 g and 44 g butyrate groups were significantly higher than in the control group. Plasma concentration of 3-hydroxybutyric acid was increased by intraruminal administration of butyrate within 15 min in a dose-dependent manner, and it was higher in the 22 g and 44 g butyrate group than in the control group from 15 min to 4 h. With the exception of the 11 g butyrate group, plasma concentrations of ADH also increased in response to butyrate treatment, and it was higher in the 44 g butyrate group than in the 22 g butyrate group from 15 min to 1.5 h. The duration of the elevated plasma concentrations of ADH was shorter than that of the plasma concentration of 3-hydroxybutyric acid. The relationship between the plasma concentrations of ADH and 3-hydroxybutyric acid was statistically significant but the correlation between the two concentrations was not high. Butyrate treatment elevated the plasma concentration of ADH and also resulted in reduced urine volume and increased urine osmolality. Haematocrit (Ht) values, and the osmolality of CSF and plasma were not different among the groups. Our results suggested that the increased ADH secretion observed in suckling calves fed dry feeds was caused by butyrate-derived ketone body that crossed the blood-brain barrier rapidly.
本研究旨在阐明酮体增加抗利尿激素 (ADH) 分泌的机制。选用 4 头 5 周龄荷斯坦公犊。采用 4x4 拉丁方设计,通过瘤胃内给 4 个不同水平的丁酸盐(0 g、11 g、22 g 和 44 g),收集脑脊液(六部位腰椎穿刺)、血桨和尿液。总血浆和 CSF 蛋白浓度分别为 5.5-5.6 g/dL 和 27.5-28.3 mg/dL。22 g 和 44 g 丁酸盐组 CSF 中特定酮体 3-羟丁酸的浓度明显高于对照组。11 g 和 44 g 丁酸盐组 CSF 中 ADH 的浓度明显高于对照组。丁酸盐瘤胃内给药 15 分钟内可使血桨 3-羟丁酸浓度呈剂量依赖性升高,22 g 和 44 g 丁酸盐组 15 分钟至 4 小时高于对照组。除 11 g 丁酸盐组外,ADH 血桨浓度也随丁酸盐处理而升高,15 分钟至 1.5 小时 44 g 丁酸盐组高于 22 g 丁酸盐组。升高的 ADH 血桨浓度持续时间短于 3-羟丁酸的血桨浓度。ADH 与 3-羟丁酸的血桨浓度之间存在统计学显著相关性,但两者之间的相关性不高。丁酸盐处理可升高 ADH 血桨浓度,减少尿流量,增加尿渗透压。各组的血球压积(Ht)值、CSF 和血桨渗透压无差异。结果表明,给哺乳期干饲料的犊牛补充丁酸盐会导致血脑屏障快速通过的丁酸盐衍生的酮体增加 ADH 分泌。