Browsing by Subject "Lipid metabolism"
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- PublicationOpen AccessAmeliorative Effect of Spinach on Non-Alcoholic Fatty Liver Disease Induced in Rats by a High-Fat Diet(MDPI, 2019-04-03) Periago-Castón, Mª Jesús; Elvira-Torales, Laura Inés; Navarro-González, Inmaculada; Pallarés, Francisco José; Santaella, Marina; García-Alonso, Javier; Sevilla, Ángel; González-Barrio, Rocío; Tecnología de Alimentos, Nutrición y BromatologíaThe purpose of this work was to evaluate the effect of dietary carotenoids from spinach on the inflammation and oxidative stress biomarkers, liver lipid profile, and liver transcriptomic and metabolomics profiles in Sprague–Dawley rats with steatosis induced by a high-fat diet. Two concentrations of spinach powder (2.5 and 5%) were used in two types of diet: high-fat (H) and standard (N). Although rats fed diet H showed an accumulation of fat in hepatocytes, they did not show differences in the values of adiponectin, tumor necrosis factor alpha (TNF- ), and oxygen radical absorption (ORAC) in plasma or of isoprostanes in urine compared with animals fed diet N. The consumption of spinach and the accumulation of and carotenes and lutein in the liver was inversely correlated with serum total cholesterol and glucose and the content of hepatic cholesterol, increasing monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA) and reducing cholesterol in the livers of rats fed diet H and spinach. In addition, changes in the expression of genes related to the fatty liver condition occurred, and the expression of genes involved in the metabolism of fatty acids and cholesterol increased, mainly through the overexpression of peroxisome proliferator activated receptors (PPARs). Related to liver metabolites, animals fed with diet H showed hypoaminoacidemia, mainly for the glucogenic aminoacids. Although no changes were observed in inflammation and oxidative stress biomarkers, the consumption of spinach modulated the lipid metabolism in liver, which must be taken into consideration during the dietary treatment of steatosis.
- PublicationOpen AccessChitooligosaccharide promotes immune organ development in broiler chickens and reduces serum lipid levels(Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Shenghe, Li; Erhui, Jin; Enmei, Qiao; Guozhong, Wu; Kui, LiThis study investigated the effects of chitooligosaccharide on lipid metabolism, immune organ development, and lymphocyte apoptosis in broiler chickens. A total of 480 one-day-old broiler chickens (Arbor Acres) were randomly and evenly assigned to control group and experimental groups I, II, and III. The control group was given a basic diet, while experimental groups I, II, and III were given basic diets for 42 days, supplemented with 50 mg/kg chlortetracycline, 20, and 40 mg/kg chitooligosaccharide, respectively. We found levels of serum triglycerides (TG) and low density lipoprotein cholesterol (LDL-C) to be significantly reduced in experimental group II after 21 days, while the periarterial lymphatic sheath area of the spleens and the average number of bursa of Fabricius nodes were markedly increased. The serum total protein (TP) and high density lipoprotein cholesterol (HDL-C) levels, bursa of Fabricius index, and bursa of Fabricius lobule areas were additionally increased in experimental group III. After 42 days, the serum TP content had also increased and the bursa of Fabricius lobule area was augmented as well in experimental group II. Moreover, the splenic periarterial lymphatic sheath areas and the average numbers of bursa of Fabricius nodes were significantly increased in experimental group III. At both 21 and 42 days, numbers of Caspase-3 positive cells in spleen and bursa of Fabricius were significantly decreased in experimental groups II and III. Our results show that appropriate supplementation of chitooligosaccharide may improve lipid metabolism, promote immune organ development, and inhibit lymphocyte apoptosis in broilers.
- PublicationOpen AccessConsumption of spinach and tomato modifies lipid metabolism, reducing Hepatic Steatosis in rats(MDPI, 2020-10-24) Elvira Torales, Laura Inés; Navarro González, Inmaculada; Rodrigo García, Joaquín; Seva Alcaraz, Juan; García Alonso, Javier; Periago Castón, María Jesús; Anatomía y Anatomía Patológica ComparadasNon-alcoholic fatty liver disease (NAFLD) is currently a serious and growing clinical problem in developed and developing countries and is considered one of the most frequent chronic liver diseases in the world. The aim of this study was to evaluate the functionality of dietary carotenoids provided by tomato and spinach in the dietary treatment of steatosis. Twenty-two Sprague-Dawley rats with induced steatosis were grouped into three groups and fed standard diet (CD group) and two experimental diets supplemented with 12.75% (LC12.75 group) and 25.5% (HC25.5 group) of a mixture of spinach and tomato powder. Rats fed carotenoid-rich feeds showed an improvement in the plasma biomarkers of steatosis, with lower levels of glucose, total cholesterol, VLDL, TG, proteins, ALT and AST. Likewise, a decrease in oxidative stress was observed, with a significant reduction of malondialdehyde (MDA) in plasma (up to 54%), liver (up to 51.42%) and urine (up to 78.89%) (p < 0.05) and an increase in plasma antioxidant capacity (ORAC) (up to 73.41%) (p < 0.05). Furthermore, carotenoid-rich diets led to an accumulation of carotenoids in the liver and were inversely correlated with the content of total cholesterol and hepatic triglycerides, increasing the concentrations of MUFA and PUFA (up to 32.6% and 48%, respectively) (p < 0.05). The accumulation of carotenoids in the liver caused the modulation of genes involved in lipid metabolism, and we particularly observed an overexpression of ACOX1, APOA1 and NRIH2 (LXR) and the synthesis of the proteins. This study suggests that dietary carotenoids from spinach and tomato aid in the dietary management of steatosis by reversing steatosis biomarkers.
- PublicationEmbargoEffects of total replacement of fish oil by vegetable oils on n-3 and n-6 polyunsaturated fatty acid desaturation and elongation in sharpsnout seabream (Diplodus puntazzo) hepatocytes and enterocytes(Elsevier, 2007-11-26) Almaida Pagán, Pedro Francisco; Hernandez, M. D.; García García, B.; Madrid, Juan A.; Costa, J. de; Mendiola, P.; FisiologíaThe main aim of this work was to determine the impact of total dietary fish oil replacement by vegetable oils on the fatty acid metabolism of sharpsnout seabream hepatocytes and digestive tract enterocytes. Three isonitrogenous (48% crude protein) and isoenergetic (23 MJ/kg) experimental diets were formulated using three different lipid sources: fish oil (FO), rich in n-3 HUFAs; soybean oil (SO), rich in linoleic acid (LA), and linseed oil (LO), especially rich in linolenic acid (LNA). These diets were fed, three times a day to apparent satiation, to triplicate groups of 30 sharpsnout seabream (with an initial average weight of 14.9 g) for nine months at 23.5±1.2 °C. Inclusion of vegetable oils in sharpsnout seabream diet did not have any quantitative nutritional effects on desaturation/elongation of [1-14C] LNA and [1-14C] LA in isolated hepatocytes and total digestive tract enterocytes. Most of the radioactivity found in tissue lipid extracts (94% and 86% for hepatocytes and enterocytes, respectively) using silver nitrate thin-layer chromatography was recovered as [1-14C] C18 PUFA, clearly showing the lack of any significant desaturase/elongase activity in these cells. Only the high levels of HUFA in fish tissues pointed to the existence of some kind of regulatory mechanism, presumably based on HUFA bioaccumulation and C18 PUFA oxidation. Moreover, direct measurements of β-oxidation rates yielded very low values in all cases, the only significant difference being a higher oxidation rate in hepatocytes from fish fed LO versus FO diet.
- PublicationOpen AccessHigh FITM2 expression promotes cell migration ability of hepatocellular carcinoma by regulating the formation of caveolae and indicates poor patient survival(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2021) Chen, Yan; Ji, Li-juan; Wang, Yan; Guo, Xiang-FengBackground. Hepatocellular carcinoma (HCC) is among the most malignant tumors with high recurrence and low 5-year survival rate. Lipid metabolism is essential in tumor metastasis, although how altered lipid metabolism promotes HCC progression has not been well elucidated. Fat Storage Inducing Transmembrane Protein 2 (FITM2) is a gene involved in lipid homeostasis and cytoskeletal organization; however, its role in regulating tumor biological behavior has not been evaluated. Methods. In this study, immunohistochemistry was performed to evaluate the expression of FITM2 in HCC. Univariate and multivariate analysis was performed to identify the prognostic factors. RNA interference wound healing and transwell experiments were performed to analyze the biological role of FITM2. Western blot analysis was performed to investigate the potential downstream signaling. Results. The results revealed that FITM2 was highly expressed in the intratumoral tissues of HCC. Expression of intratumoral FITM2 was associated with microvascular invasion. FITM2 is an independent risk factor of HCC disease-free survival and overall survival. In vitro studies revealed that knockdown of FITM2 significantly inhibited the migration ability of HCC cells. FITM2 promotes HCC cell migration by regulating the expression of caveolin-1 and promoting the formation of caveolae. These results indicate that high intratumoral expression of FITM2 is associated with poor HCC prognosis, which may be applied to develop a new adjuvant therapy
- PublicationOpen AccessTetrahydropalmatine promotes macrophage autophagy by inhibiting the AMPK/mTOR pathway to attenuate atherosclerosis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Wang, Hui; Ding, Ke; He, Jiaqi; Wang, JiahongBackground. Atherosclerosis (AS) is a chronic progressive arterial disease that is associated with macrophage autophagy and AMP-activated protein kinase (AMPK)/mechanistic target of the rapamycin (mTOR) pathway. Tetrahydropalmatine (THP) can activate AMPK-dependent autophagy. We aim to study the mechanism of macrophage autophagy mediated by THP in the treatment of AS via the AMPK/mTOR pathway. Methods. High-fat diet apolipoprotein E-deficient mice and ox-LDL-induced RAW264.7 cells were used to mimic the AS model, then THP was administered. Cell viability was detected by MTT. Pathological aorta lesions were detected using Hematoxylin and Eosin, Masson, and oil red staining. Lipid metabolism indices and inflammatory factors were measured using ELISA. A transmission electron microscope was used to observe autophagosomes. Autophagy and AMPK/mTOR pathway protein expression was detected by immunofluorescence and Western blot. The AMPK inhibitor 9-β-d-Arabinofuranosyl Adenine (Ara-A) was used to validate the effect of THP. The mRNA expression of Beclin-1 and MCP-1 was detected by q-PCR. Results. THP administration regulated lipid metabolism by lowering total cholesterol, triacy-lglycerol, low-density lipoprotein, and high-density lipoprotein levels, and suppressed aortic damage. THP suppressed aortic damage and regulated lipid metabolism by altering serum lipid levels. THP reduced inflammation and macrophage CD68 expression. Twenty μg/mL THP reduced cell viability. THP decreased cholesterol uptake and increased efflux, promoting autophagy. THP increased autophagosome number, LC3B expression, and autophagy markers p-AMPK/AMPK and LC3-II/LC3-I. THP also decreased p-mTOR/mTOR and P62. THP increased Beclin-1 mRNA expression and decreased MCP-1 mRNA expression. Ara-A reversed THP's effects. Conclusion. THP promotes macrophage autophagy by inhibiting the AMPK/mTOR pathway to attenuate AS.
- PublicationOpen AccessThe role of endothelial lipase in lipid metabolism, inflammation and cancer(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Yu, Justine E; Han, Shu Yan; Wolfson, Benjamin; Zhou, QunEndothelial lipase (LIPG) plays a critical role in lipoprotein metabolism, cytokine expression, and the lipid composition of cells. Thus far, the extensive investigations of LIPG have focused on its mechanisms and involvement in metabolic syndromes such as atherosclerosis. However, recent developments have found that LIPG plays a role in cancer. This review summarizes the field of LIPG study. We focus on the role of LIPG in lipid metabolism and the inflammatory response, and highlight the recent insights in its involvement in tumor progression. Finally, we discuss the potential of targeting LIPG in therapeutic strategies.