Nutr Res Pract.  2022 Jun;16(3):285-297. 10.4162/nrp.2022.16.3.285.

Dietary supplementation with Korean pine nut oil decreases body fat accumulation and dysregulation of the appetite-suppressing pathway in the hypothalamus of high-fat diet-induced obese mice

Affiliations
  • 1Major of Food and Nutrition, Division of Applied Food System, Seoul Women's University, Seoul 01797, Korea
  • 2Department of Food and Nutrition, College of Human Ecology, Seoul National University, Seoul 08826, Korea
  • 3Research Institute of Human Ecology, Seoul National University, Seoul 08826, Korea

Abstract

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.
RESULTS
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 Ghsr (ghrelin receptor) and ,Agrp (agouti-related peptide) (P < 0.05), which are expressed when energy consumption is low to induce appetite as well as the appetitesuppressing neuropeptides Pomc and Cartpt (P = 0.079 and 0.056, respectively). Korean PNO downregulated jejunal Cd36 and epididymal Lpl 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 Apoa4 and upregulate epididymal Adrb3 mRNA levels, suggesting that PNO may decrease chylomicron synthesis and induce lipolysis.
CONCLUSIONS
In summary, Korean PNO attenuated body fat accumulation, and appeared to prevent HFD-induced dysregulation of the hypothalamic appetite-suppressing pathway.

Keyword

Neuropeptides; gastrointestinal hormones; intestinal absorption; adipose tissue; lipid metabolism

Figure

  • Fig. 1 Fecal triacylglycerol, non-esterified fatty acid, and cholesterol levels. Data are presented as means ± SEM, n= 7–14 for each group. Two-way analysis of variance was used to determine the significant effect of fat amount and oil type. Different letters indicate significant difference at P < 0.05 by Fisher's LSD multiple comparison test.SC, 10% soybean oil; PC, 10% pine nut oil; SHFD, 10% soybean oil + 35% lard; PHFD, 10% pine nut oil + 35% lard; TAG, triacylglycerol; NEFA, non-esterified fatty acid; CHOL, cholesterol.

  • Fig. 2 The mRNA expression levels of neuropeptides (hypothalamic Npy, Agrp, Pomc, and Cartpt). Data are presented as means ± SEM, n= 5-6 for each group. Two-way analysis of variance was used to determine the significant effect of fat amount and oil type. Different letters indicate significant difference at P < 0.05 by Fisher's LSD multiple comparison test. All values are normalized to the levels of house-keeping gene Gapdh and expressed as relative mRNA level compared to the average expression level of SC group.mRNA, messenger RNA; SC, 10% soybean oil; PC, 10% pine nut oil; SHFD, 10% soybean oil + 35% lard; PHFD, 10% pine nut oil + 35% lard; Npy, neuropeptide Y; Agrp, agouti-related peptide; Pomc, pro-opiomelanocortin-alpha; Cartpt, cocaine- and amphetamine-regulated transcript prepropeptide; Gapdh, glyceraldehyde 3-phosphate dehydrogenase.

  • Fig. 3 Correlation between body weight and hypothalamic neuropeptide mRNA levels. Correlation between body weight and (A) Npy, (B) Agrp, (C) Pomc, and (D) Cartpt mRNA levels. Pearson's correlation was used to determine the linear relationship between variables.mRNA, messenger RNA; Npy, neuropeptide Y; Agrp, agouti-related peptide; Pomc, pro-opiomelanocortin-alpha; Cartpt, cocaine- and amphetamine-regulated transcript prepropeptide.

  • Fig. 4 The mRNA expression levels of genes associated with intestinal lipid metabolism (jejunal Cd36, Fabp2, Dgat2, and Apoa4). Data are presented as means ± SEM, n= 5–6 for each group. Two-way analysis of variance was used to determine the significant effect of fat amount and oil type. Different letters indicate significant difference, P < 0.05. All values are normalized to the levels of house-keeping gene Gapdh and expressed as relative mRNA level compared to the average expression level of SC group.mRNA, messenger RNA; SC, 10% soybean oil; PC, 10% pine nut oil; SHFD, 10% soybean oil + 35% lard; PHFD, 10% pine nut oil + 35% lard; Cd36, fatty acid translocase; Fabp2, fatty acid binding protein 2, intestinal; Dgat2, diacylglycerol O-acyltransferase 2; Apoa4, apolipoprotein A-IV; Gapdh, glyceraldehyde 3-phosphate dehydrogenase.

  • Fig. 5 The mRNA expression levels of genes associated with lipid metabolism in the white adipose tissue (epididymal Lpl, Plin1, Udp2, Adrb3, Pparg, Ppargc1a, and Ppard). Data are presented as means ± SEM, n = 5–6 for each group. Different letters indicate significant difference, P < 0.05. All values are normalized to the levels of house-keeping gene Gapdh and expressed as relative mRNA level compared to the average expression level of SC group.mRNA, messenger RNA; SC, 10% soybean oil; PC, 10% pine nut oil; SHFD, 10% soybean oil + 35% lard; PHFD, 10% pine nut oil + 35% lard; Lpl, lipoprotein lipase; Plin1, perilipin 1; Ucp2, mitochondrial uncoupling protein 2; Adrb3, β3 adrenergic receptor; Pparg, peroxisome proliferator-activated receptor gamma; Ppargc1a, peroxisome proliferator-activated receptor gamma coactivator 1 alpha; Ppard, peroxisome proliferator-activated receptor delta; Gapdh, glyceraldehyde 3-phosphate dehydrogenase.


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