Department of Animal Science, Cornell University, Ithaca, NY 14853.
Institute for Animal Science, Physiology and Hygiene Unit, University of Bonn, 53115 Bonn, Germany.
J Dairy Sci. 2017 Nov;100(11):9418-9427. doi: 10.3168/jds.2017-13274. Epub 2017 Aug 23.
In transition dairy cows, plasma levels of the insulin-sensitizing hormone adiponectin fall to a nadir at parturition and recover in early lactation. The transition period is also characterized by rapid changes in metabolic and hormonal factors implicated in other species as positive regulators of adiponectin production (i.e., negative energy balance, lipid mobilization) and others as negative regulators (i.e., reduced leptin and insulin and increased growth hormone and plasma fatty acids). To assess the role of onset of negative energy balance and lipid mobilization after parturition, dairy cows were either milked thrice daily (lactating) or never milked (nonlactating) for up to 4 wk after parturition. Plasma adiponectin was 21% higher across time in nonlactating than lactating cows. Moreover, nonlactating cows recovered plasma adiponectin at similar rates as lactating cows even though they failed to lose body condition. Next, we assessed the ability of individual hormones to alter plasma adiponectin in transition dairy cows. In the first experiment, dairy cows received a constant 96-h intravenous infusion of either saline or recombinant human leptin starting on d 8 of lactation. In the second experiment, dairy cows were studied in late pregnancy (LP, starting on prepartum d -31) and again in early lactation (EL, starting on d 7 postpartum) during a 66-h period of basal sampling followed by 48 h of hyperinsulinemic-euglycemia. In the third experiment, cows were studied either in LP (starting on d -40 prepartum) or EL (starting on d 7 postpartum) during a 3-h period of basal sampling followed by 5 d of bovine somatotropin treatment. Plasma adiponectin was reduced by an average of 21% in EL relative to LP in these experiments, but neither leptin, insulin, or growth hormone treatment affected adiponectin in LP or EL. Finally, the possibility that plasma fatty acids repress plasma adiponectin was evaluated by intravenous infusion of a lipid emulsion in nonpregnant, nonlactating cows in the absence or presence of glucagon for 16 consecutive hours. The intralipid infusion increased plasma fatty acid concentration from 102 to over 570 µM within 3 h but had no effect on plasma adiponectin irrespective of presence or absence of glucagon. Overall, these data suggest that energy balance around parturition may regulate plasma adiponectin but do not support roles for lipid mobilization or sustained changes in the plasma concentration of leptin, insulin, growth hormone, or fatty acids.
在过渡奶牛中，胰岛素增敏激素脂联素的血浆水平在分娩时降至最低点，并在泌乳早期恢复。过渡期的特点还包括代谢和激素因素的快速变化，这些因素在其他物种中被认为是脂联素产生的正调节剂（即负能平衡、脂质动员），而其他因素则是负调节剂（即瘦素和胰岛素减少，生长激素和血浆脂肪酸增加）。为了评估分娩后负能平衡和脂质动员的起始在过渡奶牛中的作用，奶牛要么每天挤奶三次（泌乳），要么在分娩后最多 4 周内从不挤奶（非泌乳）。非泌乳奶牛的血浆脂联素在整个时间内比泌乳奶牛高 21%。此外，非泌乳奶牛的血浆脂联素恢复速度与泌乳奶牛相似，尽管它们没有失去体况。接下来，我们评估了单个激素在过渡奶牛中改变血浆脂联素的能力。在第一个实验中，奶牛从泌乳第 8 天开始接受为期 96 小时的生理盐水或重组人瘦素的恒速静脉输注。在第二个实验中，奶牛在妊娠晚期（LP，从产前第 31 天开始）和泌乳早期（EL，从产后第 7 天开始）进行研究，在基础采样 66 小时后进行 48 小时的高胰岛素-正常血糖。在第三个实验中，奶牛在 LP（从产前第 40 天开始）或 EL（从产后第 7 天开始）期间进行 3 小时的基础采样，然后进行 5 天的牛生长激素治疗。在这些实验中，EL 中血浆脂联素比 LP 平均降低 21%，但无论是瘦素、胰岛素还是生长激素治疗都没有影响 LP 或 EL 中的脂联素。最后，通过在非妊娠、非泌乳奶牛中连续 16 小时静脉输注脂肪乳剂，评估血浆脂肪酸是否抑制血浆脂联素的可能性，无论是否存在胰高血糖素。在 3 小时内，静脉内输注脂肪乳剂将血浆脂肪酸浓度从 102µM 增加到 570µM 以上，但无论是否存在胰高血糖素，对血浆脂联素均无影响。总的来说，这些数据表明分娩前后的能量平衡可能调节血浆脂联素，但不支持脂质动员或瘦素、胰岛素、生长激素或脂肪酸血浆浓度的持续变化发挥作用。
