Section on Clinical Psychoneuroendocrinology and Neuropsychopharmacology, Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA; Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA; Department of Behavioral and Social Sciences, Brown University, Providence, RI, USA.
Psychoneuroendocrinology. 2013 Dec;38(12):3085-91. doi: 10.1016/j.psyneuen.2013.09.005. Epub 2013 Sep 13.
Ghrelin is a 28-amino acid peptide produced mainly by mucosal neuroendocrine cells lining the fundus of the stomach. Preclinical and clinical studies suggest that ghrelin plays a role in alcoholism. Furthermore, human laboratory studies indicate that acute oral administration of alcohol results in reduced circulating ghrelin. As ghrelin is primarily produced in the stomach, one question never previously explored is whether alcohol administered intravenously (IV) results in similar decrease in ghrelin levels. Thus, this study analyzed the potential effects of IV alcohol administration on plasma ghrelin levels in healthy nonsmoking social drinkers (n=44) who received either a 180-min IV infusion of 6% (v/v) alcohol or 0.9% normal saline in two separate counterbalanced sessions. At each session, participants arrived having fasted for ~7 h and received a light breakfast 60 min before the infusion. The percent change (%Δ) in ghrelin levels was 4.5-fold less in the alcohol condition than the saline condition. In fact, there was only a modest change in ghrelin levels from baseline in the IV alcohol condition (9.6%Δghrelin) while in the IV saline condition there was a robust change (43.4%Δghrelin). There was a trend toward significance in %Δghrelin in the alcohol condition compared to the placebo condition (F[1,33]=3.3, p=0.07). While the exact mechanisms by which alcohol influences ghrelin levels are unclear, alcohol may act directly in the stomach by inhibiting ghrelin secretion and/or release, and may also attenuate ghrelin levels systemically. Although IV alcohol did not reduce circulating ghrelin levels, as seen in previous studies with oral alcohol administration, the present findings suggest that, despite bypassing the stomach, alcohol still attenuated circulating ghrelin levels, i.e. the fasting-induced increase in circulating ghrelin was blunted by IV alcohol administration. These findings lead us to hypothesize that alcohol might affect ghrelin signaling not only via a local effect on the stomach mucosa, but also via a systemic effect.
胃饥饿素是一种由胃底黏膜神经内分泌细胞产生的 28 个氨基酸肽。临床前和临床研究表明，胃饥饿素在酒精中毒中发挥作用。此外，人体实验室研究表明，急性口服酒精会导致循环胃饥饿素减少。由于胃饥饿素主要在胃中产生，因此以前从未探讨过一个问题，即静脉内（IV）给予酒精是否会导致胃饥饿素水平类似的降低。因此，这项研究分析了在健康非吸烟社交饮酒者（n=44）中 IV 给予酒精对血浆胃饥饿素水平的潜在影响，这些参与者在两个单独的平衡会话中分别接受 6%（v/v）酒精或 0.9%生理盐水的 180 分钟 IV 输注。在每个会话中，参与者禁食约 7 小时，并在输注前 60 分钟接受清淡早餐。在酒精条件下，胃饥饿素水平的变化百分比（%Δ）比生理盐水条件低 4.5 倍。事实上，在 IV 酒精条件下，胃饥饿素水平仅从基线略有变化（9.6%Δghrelin），而在 IV 生理盐水条件下则有明显变化（43.4%Δghrelin）。与安慰剂条件相比，酒精条件下的%Δghrelin 有显著趋势（F[1,33]=3.3，p=0.07）。虽然酒精影响胃饥饿素水平的确切机制尚不清楚，但酒精可能通过抑制胃饥饿素的分泌和/或释放而直接在胃中起作用，并且还可能系统地减弱胃饥饿素水平。尽管 IV 酒精没有像以前的口服酒精给药研究那样降低循环胃饥饿素水平，但目前的研究结果表明，尽管绕过了胃，但酒精仍然减弱了循环胃饥饿素水平，即 IV 酒精给药减弱了空腹引起的循环胃饥饿素增加。这些发现使我们假设，酒精可能不仅通过对胃黏膜的局部作用，而且还通过全身作用来影响胃饥饿素信号。
