Short-term fasting selectively suppresses leptin pulse mass and 24-hour rhythmic leptin release in healthy midluteal phase women without disturbing leptin pulse frequency or its entropy control (pattern orderliness)
Short-term fasting selectively suppresses leptin pulse mass and 24-hour rhythmic leptin release in healthy midluteal phase women without disturbing leptin pulse frequency or its entropy control (pattern orderliness)
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DOI：
10.1210/jc.85.1.207
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发表时间：
2000-01-01
影响因子：
5.8
通讯作者：
Veldhuis, JD
中科院分区：
文献类型：
--
作者：
Bergendahl, M;Iranmanesh, A;Veldhuis, JD
营养信号强烈调节神经内分泌轴，如LH， GH和TSH的释放，部分可能是通过脂肪细胞衍生的神经活性肽瘦素。反过来，瘦素的释放受急性（禁食）和长期（脂肪储存）营养状态的控制。在这里，我们研究了短期（2.5天）禁食对正常月经周期中激素充足的黄体中期健康年轻女性瘦素释放的神经内分泌影响。8名女性在不同的月经周期中，在随机安排的2.5天禁食和进食期间，每隔10分钟进行24小时的血液采样。用无模型聚类分析量化脉搏性瘦素释放，用近似熵统计量化瘦素模式的有序性，用余弦分析量化昼夜节律性。禁食期间平均（24小时）血清瘦素浓度下降4.6倍；即从15.2 +/- 2.3到3.4 +/- 0.6 μ g/L （P = 0.0007）。聚类分析发现，在进食和禁食状态下，每24 h瘦素峰值分别为13.9 +/- 1.1和14.3 +/- 1.1 (P = NS)，瘦素峰间间隔不变（89 +/- 5.4 vs 92 +/- 5.3 min）。瘦素峰面积下降4.2倍（155 +/- 21 μ s）。37 +/- 7个面积单位，P = 0.004)，这是由于瘦素脉冲增量幅度减少（4.4 +/- 0.7 vs. 1.0 +/- 0.13 μ g/L, P = 0.001.1）。24小时瘦素节律的余弦振幅和中间值（平均值）下降了4倍，而峰期（昼夜瘦素峰值的时间）保持不变。瘦素释放的近似熵是稳定的，从而表明瘦素释放模式在禁食中保持有序。交叉相关分析显示瘦素- gh呈正（空腹）和负（空腹）关系，但瘦素- lh无相关性。总之，短期（2.5天）禁食通过选择性减弱瘦素脉冲面积和增量幅度的机制，深刻抑制健康女性在性类固醇充足的黄体中期24小时血清瘦素浓度和搏动性瘦素释放。相反，控制24小时瘦素释放的脉冲产生、昼夜节律决定和熵控制机制不会因月经期的急性营养限制而改变。瘦素- gh（而非瘦素- lh）表现出营养依赖性的正相关性（进食）和负相关性（禁食）。在男性、儿童或绝经后妇女短期营养限制期间，是否有类似的神经内分泌机制监督瘦素信号的改变尚不清楚。
Nutritional signals strongly regulate neuroendocrine axes, such as those subserving release of LH, GH, and TSH, presumptively in part via the adipocyte-derived neuroactive peptide leptin. In turn, leptin release is controlled by both acute (fasting) and long-term (adipose store) nutrient status. Here, we investigate the neuroendocrine impact of short-term (2.5-day) fasting on leptin release in healthy young women studied in the steroid-replete midluteal phase of the normal menstrual cycle. Eight women each underwent 24-h blood sampling at 10-min intervals during a randomly ordered 2.5-day fasting vs. fed session in separate menstrual cycles. Pulsatile leptin release was quantified by model-free Cluster analysis, the orderliness of leptin patterns by the approximate entropy statistic, and nyctohemeral leptin rhythmicity by cosinor analysis. Mean (24-h) serum leptin concentrations fell by 4.6-fold during fasting; namely, from 15.2 +/- 2.3 to 3.4 +/- 0.6 mu g/L (P = 0.0007). Cluster analysis identified 13.9 +/- 1.1 and 14.3 +/- 1.1 leptin peaks per 24 h in the fed and fasting states (P = NS), and unchanging leptin interpeak intervals (89 +/- 5.4 vs. 92 +/- 5.3 min). Leptin peak area declined by 4.2-fold (155 +/- 21 us. 37 +/- 7 area units, P = 0.004), due to a reduction in incremental leptin pulse amplitude (4.4 +/- 0.7 vs. 1.0 +/- 0.13 mu g/L, P = 0.001.1). The cosine amplitude and mesor (mean) of the 24-h leptin rhythm decreased by 4-fold, whereas the acrophase (timing of the nyctohemeral leptin peak) remained fixed. The approximate entropy of leptin release was stable, thus indicating preserved orderliness of leptin release patterns in fasting. Cross-correlation analysis revealed both positive (fed) and negative (fasting) leptin-GH relationships, but no leptin-LH correlations.In summary, short-term (2.5-day) fasting profoundly suppresses 24-h serum leptin concentrations and pulsatile leptin release in the sex steroid-sufficient midluteal phase of healthy women via mechanisms that selectively attenuate leptin pulse area and incremental amplitude. In contrast, the pulse-generating, nyctohemeral phase-determining, and entropy-control mechanisms that govern 24-h leptin release are not altered by acute nutrient restriction at this menstrual phase. Leptin-GH (but not leptin-LH) showed nutrient-dependent positive (fed) and negative (fasting) cross-correlations. Whether similar neuroendocrine mechanisms supervise altered leptin signaling during short-term nutrient restriction in men, children, or postmenopausal women is not known.