Serum levels of n-3 PUFA and colorectal cancer risk in Chinese population.

Circulating n-3 PUFA, which integrate endogenous and exogenous n-3 PUFA, can be better used to investigate the relationship between n-3 PUFA and disease. However, studies examining the associations between circulating n-3 PUFA and colorectal cancer (CRC) risk were limited, and the results remained inconclusive. This case­control study aimed to examine the association between serum n-3 PUFA and CRC risk in Chinese population. A total of 680 CRC cases and 680 sex- and age-matched (5-year interval) controls were included. Fatty acids were assayed by GC. OR and 95 % CI were calculated using multivariable logistic regression after adjustment for potential confounders. Higher level of serum α-linolenic acid (ALA), docosapentaenoic acid (DPA), DHA, long-chain n-3 PUFA and total n-3 PUFA were associated with lower odds of CRC. The adjusted OR and 95 % CI were 0·34 (0·24, 0·49, Pfor trend < 0·001) for ALA, 0·57 (0·40, 0·80, Pfor trend < 0·001) for DPA, 0·48 (0·34, 0·68, Pfor trend < 0·001) for DHA, 0·39 (0·27, 0·56, Pfor trend < 0·001) for long-chain n-3 PUFA and 0·31 (0·22, 0·45, Pfor trend < 0·001) for total n-3 PUFA comparing the highest with the lowest quartile. However, there was no statistically significant association between EPA and odds of CRC. Analysis stratified by sex showed that ALA, DHA, long-chain n-3 PUFA and total n-3 PUFA were inversely associated with odds of CRC in both sexes. This study indicated that serum ALA, DPA, DHA, long-chain n-3 PUFA and total n-3 PUFA were inversely associated with odds of having CRC in Chinese population.

Serum flavin mononucleotide but not riboflavin is inversely associated with the risk of colorectal cancer.

Vitamin B2 is essential for DNA methylation, stability and repair, which may influence the development and pathogenesis of several cancers. However, data regarding the associations of circulating vitamin B2 with colorectal cancer risk are limited. The purpose of this study was to investigate the associations between serum vitamin B2 and colorectal cancer risk, particularly among participants with different serum levels of vitamin B6 or folate. A hospital-based case-control study, including 1009 colorectal cancer cases and 1182 controls matched by age and sex, was conducted in Guangdong Province, China. Vitamin B2 including riboflavin and flavin mononucleotide (FMN), the vitamin B6 indicator pyridoxal-5'-phosphate (PLP) and folate in serum samples were measured by ultra-high-performance liquid chromatography-tandem mass spectrometry. Vitamin B2 sum was calculated as the sum of riboflavin plus FMN. A significant inverse association was observed between serum FMN, but not serum riboflavin or vitamin B2 sum, and colorectal cancer risk. The adjusted odds ratio (OR) and 95% confidence interval (95% CI) of serum FMN, by comparing the highest with the lowest quartile, was 0.63 (0.46-0.85, Ptrend = 0.001). Stratified analysis by serum PLP and folate levels indicated that serum FMN was inversely associated with colorectal cancer risk among participants with lower serum PLP or higher folate levels. This study added supporting data to the limited evidence that vitamin B2 could play a preventive role in colorectal carcinogenesis among the Chinese population, primarily by FMN. Individuals with a lower PLP level or an adequate folate level could be more sensitive to the protective role of vitamin B2.

Association of plant-based dietary patterns with the risk of colorectal cancer: a large-scale case-control study.

Plant-based diets are associated with a lower risk of colorectal cancer, but the risk might differ by the quality of plant-based diets. This study aimed to investigate the association between different types of plant-based dietary patterns and colorectal cancer risk in the Chinese population. We conducted a case-control study with 2799 eligible colorectal cancer cases and 2799 sex- and age-matched controls in Guangzhou, China. A validated food frequency questionnaire was used to collect dietary data, from which we derived plant-based diet indices, including the plant-based diet index (PDI), the healthy PDI (hPDI), and the unhealthy PDI (uPDI). The PDI, hPDI, and uPDI assess the adherence to overall, healthy, and unhealthy plant-based dietary patterns, respectively. The odds ratios (ORs) and 95% confidence intervals (CIs) for colorectal cancer risk were estimated using unconditional logistic regression models. Higher adherence to the PDI, particularly the hPDI, was associated with a lower risk of colorectal cancer, whereas greater adherence to the uPDI was associated with a higher risk of colorectal cancer. Compared with the lowest quintile, the adjusted ORs in the highest quintile were 0.79 (95% CI: 0.66-0.95) for the PDI, 0.45 (95% CI: 0.38-0.55) for the hPDI, and 1.45 (95% CI: 1.18-1.78) for the hPDI, respectively. In stratified analysis, the inverse association between the PDI and colorectal cancer risk was not observed in women, and the positive association between the uPDI and colorectal cancer risk was not observed in men. In conclusion, these results support recommendations that shifting to a healthy plant-based dietary pattern is important for the prevention of colorectal cancer, particularly in the Chinese population that habitually consumes plant foods.

Trans triacylglycerols from dairy products and industrial hydrogenated oil exhibit different effects on the function of human umbilical vein endothelial cells via modulating phospholipase A2/arachidonic acid metabolism pathways.

Dairy fat intake has been considered as a risk factor for cardiovascular disease. Rodent models show that trans fatty acids in industrial hydrogenated oil and ruminant milk have different effects on cardiovascular diseases. One of the main reasons is that the distributions of trans fatty acids in triacylglycerols from dairy products and from industrial hydrogenated oil are different, which affects lipid absorption and metabolism. This study investigated the effects of 1,3-olein-2-elaidin (OEO, representing industrial hydrogenated oil triacylglycerols) and 1-vaccenic-2,3-olein (OOV, representing ruminant triacylglycerols in dairy products) on the function of human umbilical vein endothelial cells (HUVEC), including cell viability, lactate dehydrogenase (LDH) exudation rate, and nitric oxide secretory and nitric oxide synthase relative activity. We found that the detrimental effect of OEO on HUVEC was significantly greater than that of OOV. The results also showed that the absorption rate of OEO in HUVEC (78.25%) was significantly greater than that of OOV (63.32%). Mechanistically, based on phospholipidomics analysis, we found that calcium-independent phospholipase A2 (iPLA2) played a key role with regard to the OOV-mediated arachidonic acid (ARA)/COX-2/PG pathway, whereas secretory phospholipase A2 (sPLA2) and cytoplasmic phospholipase A2 (cPLA2) are responsible for the OEO-mediated ARA/COX-2/PG pathway. Moreover, OEO had a greater effect on the protein expression of COX-2 and PG secretion than OOV. In addition, iPLA2, sPLA2, and cPLA2 could mediate the ARA/CYP4A11 pathway in OOV-treated HUVEC, but only iPLA2 could mediate this pathway in HUVEC treated with OEO. We also found that sPLA2 could mediate the ARA/5-LOX pathway in HUVEC treated with OOV, but none of these 3 forms of PLA2 could mediate this pathway in HUVEC treated with OEO. On the other hand, after OOV treatment, trans-11 C18:1 was converted to beneficial forms of fatty acids in HUVEC, including conjugated linoleic acid (CLA) and trans-9 C16:1. In conclusion, we elucidated the potential mechanisms that might account for the diverse effects of triacylglycerols from industrial hydrogenated oil and ruminant milk on the function of HUVEC.

9t18:1 and 11t18:1 activate the MAPK pathway to regulate the expression of PLA2 and cause inflammation in HUVECs.

trans fatty acids (TFAs) have been reported to promote vascular diseases mainly by promoting apoptosis and inflammation of vascular endothelial cells. However, it has been reported in recent years that elaidic acid (9t18:1) and vaccenic acid (11t18:1) may have different effects on vascular health. This study investigated the effects of 9t18:1 and 11t18:1 on human umbilical vein endothelial cell (HUVEC) function and the possible mechanism of inflammation by analyzing the changes in the phospholipid composition and the relationship between phospholipase A2 (PLA2) and MAPK pathway. Here we found that the effect of 11t18:1 on cell viability, membrane damage and cellular inflammation was significantly lower than that of 9t18:1 (p < 0.05). And 9t18:1 and 11t18:1 had different effects on phospholipid composition. Both 9t18:1 and 11t18:1 significantly increased the protein expression of PLA2. Moreover, the MAPK pathway regulated the expression of PLA2, inflammatory cytokines and cyclooxygenase-2 (COX-2) and the secretion of prostaglandin E2 (PGE2) in HUVECs induced by 9t18:1 and 11t18:1. In conclusion, 9t18:1 and 11t18:1 activated the MAPK pathway which regulated the expression of PLA2 to cause inflammation in HUVECs.

9c11tCLA modulates 11t18:1 and 9t18:1 induced inflammations differently in human umbilical vein endothelial cells.

Endothelial inflammation is recognized as the initial stage of a multistep process leading to coronary heart disease (CHD). Recently, the different effects of industrial trans fatty acids (elaidic acid, 9t18:1) and ruminant trans fatty acids (vaccenic acid, 11t18:1) on CHD have been reported in epidemiological and animal studies, however, the mechanism was not fully studied. Therefore, the objective of this study was to explore the underlying mechanism by which 9t18:1 and 11t18:1 affect human umbilical vein endothelial cells (HUVECs) inflammation. We found that 9c11t-CLA modulated the inflammation of HUVECs induced by 9t18:1 and 11t18:1. Fatty acid composition, pro-inflammatory factors, phosphorylation of MAPKs, and the TLR4 level in HUVECs altered by 11t18:1 induction, collectively suggest that the bio-conversion of 11t18:1 to 9c11tCLA might be the cause why 11t18:1 and 9t18:1 have distinct influences on endothelial injuries. It was concluded that it is biosynthesis of 9c11t CLA from11t18:1, and the modulation of TLR4-MAPK pathway by 9c11t CLA, which at least partially account for the slight effect of 11t18:1 on endothelial inflammation.