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We evaluated whether linseed oil (LO) modulates the effects of a high-carbohydrate diet (HCD) on liver inflammation, fatty acid (FA) accumulation, and lipid distribution in periportal and perivenous hepatocytes. The control group (control high-carbohydrate diet [HCD-C]) received an HCD with lard and soybean oil as the lipid source. The L10 and L100 groups received the HCD with 10% and 100% of LO as the lipid source, respectively. The animals were killed by decapitation before (day 0) and after receiving the diets. Liver FA composition, inflammation, and fibrogenesis gene expression were evaluated. Also, the percentage of lipid-occupied area in periportal end perivenous hepatocytes were measured. The L100 group exhibited a higher (P < .05) liver amount of omega-3 polyunsaturated FA (n-3 PUFA) and lower (P < .05) amounts of saturated FA (SFA), monounsaturated FA (MUFA), and omega-6 polyunsaturated FA (n-6 PUFA) compared with L10 or HCD-C mice. On day 56, interleukin 10 and type IV collagen gene expression were significantly upregulated and downregulated, respectively in L100. Also, the L100 group showed lower (P < .05) FA accumulation (i.e., total FA, SFA, MUFA, and n-6 PUFA). Also, L10 and L100 presented lower (P < .05) percentage of high lipid-containing portion in periportal and perivenous hepatocytes. We concluded that LO attenuation of liver inflammation promoted by an HCD is associated with increased liver n-3 PUFA levels, so modulating FA composition, deposition, and distribution in periportal and perivenous hepatocytes.

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OBJECTIVE: This study aimed to develop and validate a rapid, simple, accurate and precise analytical method for the quantification of L-AA in vitamin C serums. Moreover, the developed method was further applied to determine L-AA in eight different brands of vitamin C serums. A complementary study was also carried out to evaluate the stability of L-AA in the vitamin C serum samples after 15, 30, 45 and 60 days of storage at ambient temperature (15-35°C). METHODS: Ultra-high-performance liquid chromatography-tandem mass spectrometry was applied. RESULTS: Quantitative analyses were performed with a total chromatographic run time of 1.5 min by matrix-matched calibration, and the analytical curve was linear over the range of 1-1700 µg L-1 with a correlation coefficient of 0.9998. The limits of detection (LOD) and quantification (LOQ) were 0.3 and 1.0 µg L-1 , respectively. Intra- and inter-assay precisions, expressed in terms of relative standard deviation, ranged from 0.3% and 2.2%, respectively, and recoveries in concentration levels of 1 and 5 µg L-1 were 103.9% and 101.2%, respectively. The proposed analytical method was successfully applied to determine the L-AA content in eight commercial vitamin C serum samples. The stability of the target analyte in samples stored at ambient temperature (15-35°C) was evaluated throughout 60 days with a 15-day interval between analyses. At 0 days, L-AA content in samples ranged from 1.05 to 169.91 mg L-1 , which decreases over time. CONCLUSION: The proposed method could be powerful in routine analyses to ensure the quantification of L-AA in vitamin C serums since it proved to be a simple, reliable, fast, precise, accurate and sensitive analytical method.

OBJECTIF: Cette étude visait à développer et valider une méthode analytique rapide, simple, exacte et précise pour la quantification de l'acide L-ascorbique dans les sérums à la vitamine C. De plus, la méthode développée a été appliquée pour déterminer l'acide L-ascorbique dans huit différentes marques de sérums à la vitamine C. Une étude complémentaire a également été réalisée pour évaluer la stabilité de l'acide L-ascorbique dans les échantillons de sérum à la vitamine C après 15, 30, 45 et 60 jours de conservation à température ambiante (15 à 35 °C). MÉTHODES: La chromatographie en phase liquide à haute performance avec spectrométrie de masse en tandem a été employée. RÉSULTATS: Des analyses quantitatives ont été réalisées avec une durée totale d'exécution chromatographique de 1,5 minute par calibration matricielle appariée, et la courbe analytique était linéaire sur la plage de 1 à 1700 µg L-1 avec un coefficient de corrélation de 0,9998. La limite de détection (LD) et la limite de quantification (LQ) ont été déterminées à 0,3 et 1,0 µg L−1 , respectivement. Les précisions intra- et inter-essais, exprimées en termes d'écart-type relatif, étaient de 0,3 % et 2,2 %, respectivement, et les récupérations aux niveaux de concentration de 1 et 5 µg L-1 étaient de 103,9 % et 101,2 %, respectivement. La méthode analytique proposée a été employée avec succès pour déterminer la teneur en acide L-ascorbique de huit échantillons de sérum à la vitamine C commerciaux. La stabilité de l'analyte cible dans les échantillons conservés à température ambiante (15 à 35 °C) a été évaluée sur 60 jours avec un intervalle de 15 jours entre les analyses. À 0 jour, la teneur en acide L-ascorbique dans les échantillons était comprise entre 1,05 et 169,91 µg L-1 , ce qui diminue au fil du temps. CONCLUSION: La méthode proposée pourrait être puissante dans les analyses de routine pour assurer la quantification de l'acide L-ascorbique dans les sérums à la vitamine C puisqu'elle s'est avérée être une méthode analytique simple, fiable, rapide, précise, exacte et sensible.

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A high-carbohydrate diet (HCD) is a well-established experimental model of accelerated liver fatty acid (FA) deposition and inflammation. In this study, we evaluated whether canola oil can prevent these physiopathological changes. We evaluated hepatic FA accumulation and inflammation in mice fed with a HCD (72.1% carbohydrates) and either canola oil (C group) or soybean oil (S group) as a lipid source for 0, 7, 14, 28, or 56 days. Liver FA compositions were analyzed by gas chromatography. The mRNA expression of acetyl-CoA carboxylase 1 (ACC1) was measured as an indicator of lipogenesis. The mRNA expression of F4/80, tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß, IL-6, and IL-10, as mediators of liver inflammation, were also measured. The C group stored less n-6 polyunsaturated FAs (n-6 PUFAs) and had more intense lipid deposition of monounsaturated FAs (MUFAs), n-3 PUFAs, and total FAs. The C group also showed higher ACC1 expression. Moreover, on day 56, the C group showed higher expressions of the inflammatory genes F4/80, TNF-α, IL-1ß, and IL-6, as well as the anti-inflammatory IL-10. In conclusion, a diet containing canola oil as a lipid source does not prevent the fatty acid accumulation and inflammation induced by a HCD.

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Coconut oil has properties that are beneficial to human health. It assists in reducing total cholesterol, triacylglycerol (TAG), phospholipids, low-density lipoprotein (LDL) cholesterol, and very low-density lipoprotein (VLDL) cholesterol in serum and tissues. So its production, and consequently consumption, have increased in recent years. However, it has been a target for intentional adulteration with lower priced oils and fats, such as soybean oil and palm kernel oil (PKO). Coconut oil (CO) and PKO have similar chemical and physical characteristics that make it difficult to verify adulteration of CO with PKO. This study demonstrates a simple, sensitive, and fast technique that uses direct infusion electrospray ionisation mass spectrometry (ESI-MS) in conjunction with principal component analysis (PCA), in order to detect CO adulterated with PKO. Among the seven commercial coconut oil samples analysed, three were adulterated with PKO. Therefore, the suggested direct infusion ESI-MS method can be used in routine analysis to guarantee the quality of coconut oil.

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