Korean pine nut oil replacement decreases intestinal lipid uptake while improves hepatic lipid metabolism in mice.
10.4162/nrp.2016.10.5.477
- Author:
Shuang ZHU
1
;
Soyoung PARK
;
Yeseo LIM
;
Sunhye SHIN
;
Sung Nim HAN
Author Information
1. Department of Food and Nutrition, College of Human Ecology, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul 08826, Korea. snhan@snu.ac.kr
- Publication Type:Original Article
- Keywords:
Pine nut oil;
high-fat diet;
intestine;
liver;
lipid metabolism
- MeSH:
Animals;
Apolipoprotein B-48;
Diet;
Diet, High-Fat;
Intestines;
Lipid Metabolism*;
Lipolysis;
Lipoproteins;
Liver;
Metabolism;
Mice*;
Nuts*;
Real-Time Polymerase Chain Reaction;
RNA, Messenger;
Soybean Oil;
Triglycerides;
Weight Gain
- From:Nutrition Research and Practice
2016;10(5):477-486
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/OBJECTIVES: Consumption of pine nut oil (PNO) was shown to reduce weight gain and attenuate hepatic steatosis in mice fed a high-fat diet (HFD). The aim of this study was to examine the effects of PNO on both intestinal and hepatic lipid metabolism in mice fed control or HFD. MATERIALS/METHODS: Five-week-old C57BL/6 mice were fed control diets containing 10% energy fat from either Soybean Oil (SBO) or PNO, or HFD containing 15% energy fat from lard and 30% energy fat from SBO or PNO for 12 weeks. Expression of genes related to intestinal fatty acid (FA) uptake and channeling (Cd36, Fatp4, Acsl5, Acbp), intestinal chylomicron synthesis (Mtp, ApoB48, ApoA4), hepatic lipid uptake and channeling (Lrp1, Fatp5, Acsl1, Acbp), hepatic triacylglycerol (TAG) lipolysis and FA oxidation (Atgl, Cpt1a, Acadl, Ehhadh, Acaa1), as well as very low-density lipoprotein (VLDL) assembly (ApoB100) were determined by real-time PCR. RESULTS: In intestine, significantly lower Cd36 mRNA expression (P < 0.05) and a tendency of lower ApoA4 mRNA levels (P = 0.07) was observed in PNO-fed mice, indicating that PNO consumption may decrease intestinal FA uptake and chylomicron assembly. PNO consumption tended to result in higher hepatic mRNA levels of Atgl (P = 0.08) and Cpt1a (P = 0.05). Significantly higher hepatic mRNA levels of Acadl and ApoB100 were detected in mice fed PNO diet (P < 0.05). These results suggest that PNO could increase hepatic TAG metabolism; mitochondrial fatty acid oxidation and VLDL assembly. CONCLUSIONS: PNO replacement in the diet might function in prevention of excessive lipid uptake by intestine and improve hepatic lipid metabolism in both control diet and HFD fed mice.
