Section of Endocrinology and Investigative Medicine, Department of Metabolism, Digestion and Reproduction, Faculty of Medicine, Imperial College London, London, UK.
Section for Nutrition Research, Department of Metabolism, Digestion and Reproduction, Faculty of Medicine, Imperial College London, London, UK.
Diabetes Obes Metab. 2021 Jan;23(1):147-157. doi: 10.1111/dom.14204. Epub 2020 Oct 21.
To investigate the effects of L-phenylalanine on gastroenteropancreatic hormone release, glucose levels, subjective appetite and energy intake in humans, and to determine whether these effects were stereoisomer-specific by comparing them with D-phenylalanine.
A dose-finding, non-randomized, unblinded, crossover study was conducted during October-December 2017 at the NIHR Imperial Clinical Research Facility in five participants, in which the tolerability of escalating doses of oral L-phenylalanine was assessed (0, 3, 6 and 10 g). Also, an acute, randomized, double-blind, placebo-controlled crossover study was conducted during January-May 2018 at the NIHR Imperial Clinical Research Facility in 11 participants, in which the effects of oral 10 g L-phenylalanine relative to D-phenylalanine and placebo on gastroenteropancreatic hormone (insulin, glucagon, glucose-dependent insulinotropic polypeptide [GIP], peptide tyrosine tyrosine [PYY], glucagon-like peptide-1) and glucose concentrations, visual analogue scales for subjective appetite and energy intake at an ad libitum meal served 70 minutes postingestion, were investigated.
L-phenylalanine was well-tolerated and increased insulin and glucagon concentrations prior to meal ingestion at several time points relative to placebo and D-phenylalanine (P < .05). L-phenylalanine also increased GIP concentrations relative to D-phenylalanine (P = .0420) and placebo (P = .0249) 70 minutes following ingestion. L-phenylalanine reduced postprandial glucose area under the curve (AUC) relative to placebo (P = .0317) but did not affect subjective appetite or energy intake (P > .05). D-phenylalanine increased postprandial PYY AUC concentrations relative to placebo (P = .0002).
Ingestion of L-phenylalanine, but not D-phenylalanine, increases insulin, glucagon and GIP concentrations without appearing to have a marked effect on appetite.
研究 L-苯丙氨酸对胃肠胰激素释放、血糖水平、主观食欲和能量摄入的影响,并通过与 D-苯丙氨酸比较来确定这些影响是否具有立体异构体特异性。
2017 年 10 月至 12 月期间,在英国帝国临床研究设施的五项参与者中进行了一项剂量发现、非随机、非盲、交叉研究,评估了口服 L-苯丙氨酸递增剂量的耐受性(0、3、6 和 10g)。此外,2018 年 1 月至 5 月期间,在英国帝国临床研究设施的 11 名参与者中进行了一项急性、随机、双盲、安慰剂对照交叉研究,研究了口服 10g L-苯丙氨酸相对于 D-苯丙氨酸和安慰剂对胃肠胰激素(胰岛素、胰高血糖素、葡萄糖依赖性胰岛素释放肽[GIP]、肽酪氨酸酪氨酸[PYY]、胰高血糖素样肽-1)和血糖浓度、主观食欲和能量摄入的影响在进餐后 70 分钟随意用餐。
L-苯丙氨酸耐受性良好,与安慰剂和 D-苯丙氨酸相比,在几个时间点上增加了进餐前的胰岛素和胰高血糖素浓度(P < 0.05)。与 D-苯丙氨酸(P = 0.0420)和安慰剂(P = 0.0249)相比,L-苯丙氨酸在进餐后 70 分钟也增加了 GIP 浓度。与安慰剂相比,L-苯丙氨酸降低了餐后血糖曲线下面积(AUC)(P = 0.0317),但对食欲或能量摄入没有影响(P > 0.05)。D-苯丙氨酸增加了餐后 PYY AUC 浓度与安慰剂相比(P = 0.0002)。
摄入 L-苯丙氨酸而非 D-苯丙氨酸会增加胰岛素、胰高血糖素和 GIP 浓度,而似乎对食欲没有明显影响。