Shin Sunhye, Park Soyoung, Lim Yeseo, Han Sung Nim
Major of Food and Nutrition, Division of Applied Food System, Seoul Women's University, Seoul 01797, Korea.
Department of Food and Nutrition, College of Human Ecology, Seoul National University, Seoul 08826, Korea.
Nutr Res Pract. 2022 Jun;16(3):285-297. doi: 10.4162/nrp.2022.16.3.285. Epub 2021 Oct 13.
BACKGROUND/OBJECTIVES: Korean pine nut oil (PNO) has been reported to suppress appetite by increasing satiety hormone release. However, previous studies have rendered inconsistent results and there is lack of information on whether dietary Korean PNO affects the expression of satiety hormone receptors and hypothalamic neuropeptides. Therefore, our study sought to evaluate the chronic effects of Korean PNO on the long-term regulation of energy balance.
MATERIALS/METHODS: Five-week-old male C57BL/6 mice were fed with control diets containing 10% kcal fat from Korean PNO or soybean oil (SBO) (PC or SC) or high-fat diets (HFDs) containing 35% kcal fat from lard and 10% kcal fat from Korean PNO or SBO (PHFD or SHFD) for 12 weeks. The expression of gastrointestinal satiety hormone receptors, hypothalamic neuropeptides, and genes related to intestinal lipid absorption and adipose lipid metabolism was then measured.
There was no difference in the daily food intake between PNO- and SBO-fed mice; however, the PC and PHFD groups accumulated 30% and 18% less fat compared to SC and SHFD, respectively. Korean PNO-fed mice exhibited higher messenger RNA (mRNA) expression of (ghrelin receptor) and (agouti-related peptide) ( < 0.05), which are expressed when energy consumption is low to induce appetite as well as the appetite-suppressing neuropeptides and ( = 0.079 and 0.056, respectively). Korean PNO downregulated jejunal and epididymal mRNA expressions, which could suppress intestinal fatty acid absorption and fat storage in white adipose tissue. Consistent with these findings, Korean PNO-fed mice had higher levels of fecal non-esterified fatty acid excretion. Korean PNO also tended to downregulate jejunal and upregulate epididymal mRNA levels, suggesting that PNO may decrease chylomicron synthesis and induce lipolysis.
In summary, Korean PNO attenuated body fat accumulation, and appeared to prevent HFD-induced dysregulation of the hypothalamic appetite-suppressing pathway.
背景/目的：据报道，红松籽油（PNO）可通过增加饱腹感激素释放来抑制食欲。然而，先前的研究结果并不一致，且缺乏关于食用红松籽油是否会影响饱腹感激素受体和下丘脑神经肽表达的信息。因此，我们的研究旨在评估红松籽油对能量平衡长期调节的慢性影响。
材料/方法：将5周龄雄性C57BL/6小鼠分为两组，一组喂食含10%千卡来自红松籽油或大豆油（SBO）的对照饮食（PC或SC），另一组喂食含35%千卡来自猪油和10%千卡来自红松籽油或大豆油的高脂饮食（PHFD或SHFD），持续12周。然后测量胃肠道饱腹感激素受体、下丘脑神经肽以及与肠道脂质吸收和脂肪组织脂质代谢相关基因的表达。
喂食PNO和SBO的小鼠每日食物摄入量没有差异；然而，与SC和SHFD组相比，PC和PHFD组的脂肪积累分别减少了30%和18%。喂食红松籽油的小鼠表现出较高的胃饥饿素受体（ghrelin receptor）和刺鼠相关肽（agouti-related peptide）信使核糖核酸（mRNA）表达（P<0.05），当能量消耗较低时会表达这些物质以诱导食欲，同时食欲抑制神经肽可卡因-安非他明调节转录肽（CART）和促肾上腺皮质激素释放激素（CRH）也有表达（分别为P = 0.079和0.056）。红松籽油下调空肠脂肪酸转运蛋白2（FATP2）和附睾脂肪酸结合蛋白（FABP）mRNA表达，这可能抑制肠道脂肪酸吸收和白色脂肪组织中的脂肪储存。与这些发现一致，喂食红松籽油的小鼠粪便中非酯化脂肪酸排泄水平更高。红松籽油还倾向于下调空肠微粒体甘油三酯转移蛋白（MTP）并上调附睾激素敏感脂肪酶（HSL）mRNA水平，表明红松籽油可能减少乳糜微粒合成并诱导脂肪分解。
总之，红松籽油减轻了体脂积累，并且似乎预防了高脂饮食引起的下丘脑食欲抑制途径失调。
