Clinical nutrition ESPEN · 2025
Suppressive effect of myristic acid on postprandial blood glucose elevation in healthy adults with high blood glucose levels: A double-blinded, randomized, placebo-controlled, parallel-group study.
СтатьяРандомизированное исследованиеНазвание и аннотация: Перевод в очереди
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Sato Toshiro, Nishimura Saki, Aoki Ryosuke, Iwasaki Masashi, Sano Hiroaki, Kobayashi Hirofumi, Sakai Hiromichi, Takara Tsuyoshi, Sakane Fumio
Аннотация
BACKGROUND AND AIMS: Long-term oral administration of myristic acid has been shown to ameliorate hyperglycemia in a mouse model of type 2 diabetes (Nagoya-Shibata-Yasuda mice). However, its effects on human hyperglycemia remains unclear. This study aimed to evaluate the effects of myristic acid on postprandial blood glucose levels in healthy adults with high blood glucose levels.
METHODS: This randomized, double-blinded, placebo-controlled clinical trial assigned 100 healthy individuals with high postprandial blood glucose levels (maximum postprandial blood glucose concentration (Cmax) in the oral glucose tolerance test (OGTT): 140-199 mg/dL) to receive low (730 mg/day, 20 participants), medium (970 mg/day, 30 participants), or high (1,460 mg/day, 20 participants) daily doses of myristic acid or a placebo intervention (30 participants) for 12 weeks. Soft capsules packed with transesterified oil containing myristic acid were used as the test foods. The primary outcome was the effect of medium-dose myristic acid treatment on the incremental area under the curve (iAUC) of the OGTT. Secondary outcomes were the effects of medium-dose myristic acid treatment on the Cmax in the OGTT, blood glucose levels at 0, 30, 60, 90, and 120 min in the OGTT, and fasting blood insulin levels. In addition, the effects of high- and low-dose myristic acid treatments on the iAUC in the OGTT, Cmax in the OGTT, blood glucose levels at 0, 30, 60, 90, and 120 min in the OGTT, and fasting blood insulin levels were determined as secondary outcomes.
RESULTS: The iAUC in the medium-dose group was significantly (approximately 20 %) lower than that in the placebo group (medium-dose: 78.8 ± 7.4 (estimated marginal mean ± standard error) mg/dL · h, placebo: 101.4 ± 7.8 mg/dL · h, Δ = -22.7 mg/dL · h, P = 0.041). The glucose level at 60 min after glucose loading in the OGTT in the medium-dose group was markedly lower than that in the placebo group (Δ = -23.0 mg/dL, P = 0.010). The iAUC (high-dose: 82.0 ± 7.1 mg/dL · h, placebo: 102.2 ± 6.1 mg/dL · h, Δ = -20.2 mg/dL · h, P = 0.038), Cmax (Δ = -11.4 mg/dL, P = 0.041), and glucose concentration at 60 min after glucose loading (Δ = -21.8 mg/dL, P = 0.003) in the high-dose group in the OGTT were significantly lower than those in the placebo group; however, similar findings were not observed for the low-dose group. Fasting blood insulin levels in the medium-dose (Δ = 2.2 μU/mL, P = 0.029) and high-dose (Δ = 1.1 μU/mL, P = 0.059) groups were greater than those in the placebo group. No adverse events related to the test food were observed.
CONCLUSIONS: We demonstrated for the first time that oral intake of myristic acid has postprandial blood glucose-lowering effects in humans. Although excessive intake of saturated fatty acids should be avoided, our findings indicate that consuming small amounts of myristic acid may help mitigate risk factors associated with T2D development and is beneficial for maintaining health, by lowering postprandial blood glucose levels. However, future long-term studies of myristic acid are warranted to investigate any impact on diabetes progression.
TRIAL REGISTRATION: This study was registered at www.umin.ac.jp/ctr (Registry number: UMIN000054038).
METHODS: This randomized, double-blinded, placebo-controlled clinical trial assigned 100 healthy individuals with high postprandial blood glucose levels (maximum postprandial blood glucose concentration (Cmax) in the oral glucose tolerance test (OGTT): 140-199 mg/dL) to receive low (730 mg/day, 20 participants), medium (970 mg/day, 30 participants), or high (1,460 mg/day, 20 participants) daily doses of myristic acid or a placebo intervention (30 participants) for 12 weeks. Soft capsules packed with transesterified oil containing myristic acid were used as the test foods. The primary outcome was the effect of medium-dose myristic acid treatment on the incremental area under the curve (iAUC) of the OGTT. Secondary outcomes were the effects of medium-dose myristic acid treatment on the Cmax in the OGTT, blood glucose levels at 0, 30, 60, 90, and 120 min in the OGTT, and fasting blood insulin levels. In addition, the effects of high- and low-dose myristic acid treatments on the iAUC in the OGTT, Cmax in the OGTT, blood glucose levels at 0, 30, 60, 90, and 120 min in the OGTT, and fasting blood insulin levels were determined as secondary outcomes.
RESULTS: The iAUC in the medium-dose group was significantly (approximately 20 %) lower than that in the placebo group (medium-dose: 78.8 ± 7.4 (estimated marginal mean ± standard error) mg/dL · h, placebo: 101.4 ± 7.8 mg/dL · h, Δ = -22.7 mg/dL · h, P = 0.041). The glucose level at 60 min after glucose loading in the OGTT in the medium-dose group was markedly lower than that in the placebo group (Δ = -23.0 mg/dL, P = 0.010). The iAUC (high-dose: 82.0 ± 7.1 mg/dL · h, placebo: 102.2 ± 6.1 mg/dL · h, Δ = -20.2 mg/dL · h, P = 0.038), Cmax (Δ = -11.4 mg/dL, P = 0.041), and glucose concentration at 60 min after glucose loading (Δ = -21.8 mg/dL, P = 0.003) in the high-dose group in the OGTT were significantly lower than those in the placebo group; however, similar findings were not observed for the low-dose group. Fasting blood insulin levels in the medium-dose (Δ = 2.2 μU/mL, P = 0.029) and high-dose (Δ = 1.1 μU/mL, P = 0.059) groups were greater than those in the placebo group. No adverse events related to the test food were observed.
CONCLUSIONS: We demonstrated for the first time that oral intake of myristic acid has postprandial blood glucose-lowering effects in humans. Although excessive intake of saturated fatty acids should be avoided, our findings indicate that consuming small amounts of myristic acid may help mitigate risk factors associated with T2D development and is beneficial for maintaining health, by lowering postprandial blood glucose levels. However, future long-term studies of myristic acid are warranted to investigate any impact on diabetes progression.
TRIAL REGISTRATION: This study was registered at www.umin.ac.jp/ctr (Registry number: UMIN000054038).