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The use of ethanolic extract of cogongrass roots to reduce triglyceride absorption in male mice
Published in Ade Gafar Abdullah, Isma Widiaty, Cep Ubad Abdullah, Medical Technology and Environmental Health, 2020
M.R.A.A. Syamsunarno, G.R. Mukarromah, A. Achadiyani, D.D. Djunaedi, M. Putri
The second possibly mechanism is by reducing triglyceride formation in enterocyte. Lipid absorption affected by three main components; absorption of hydrolyzed lipid into the enterocyte, intracellular processing, and exocytosis into the mesenteric lymph and vein (Mansbach & Gorelick 2007). A study using 3T3-L1 cell culture showed that flavonoids inhibit the activity of glycerol-3-phosphate dehydrogenase (GPDH), a cytosolic enzyme to convert glycerol into triglyceride (Hsu & Yen 2007). Flavonoids also regulate the activity of sterol regulatory element-binding proteins SREBP-1, and SREBP-2 and other relevant enzymes in lipid metabolism (Horton et al. 2002).
Natural Polyketides to Prevent Cardiovascular Disease
Published in Catherina Caballero-George, Natural Products and Cardiovascular Health, 2018
An additional key characteristic of the statins’ mechanism of action is the systemic cellular response to the reduction of endogenously produced cholesterol circulating in the blood. The decrease in circulating cholesterol triggers the activation of a proteolytic mechanism that releases Sterol Regulatory Element-Binding Proteins (SREBPs). The release of these membrane-bound transcription factors allows their translocation into the nucleus. Once there, SREBPs bind to specific DNA sequences that initiate the transcription of genes that code for LDL receptors. Thus, in addition to the decrease in the production of cholesterol by inhibiting the mevalonate pathway, a transcriptional response results in the increase in uptake of circulating cholesterol and lowering plasma LDL levels even further (Sehayek et al., 1994).
Inhibiting Insulin Resistance and Accumulation of Triglycerides and Cholesterol in the Liver
Published in Christophe Wiart, Medicinal Plants in Asia for Metabolic Syndrome, 2017
Extract of shoots of Sechium edule (Jacq.) Sw. at a concentration of 1 mg/mL inhibited in vitro the accumulation of triglycerides in HepG2 cells cultured with oleic acid.205 This treatment reduced the expression of sterol regulatory element-binding protein-1 and its targets fatty acid synthetase and glycerol-3-phosphate-acyltransferase.205 Cholesterol synthesis was decreased as evidenced by a decreased 3-hydroxy-3-methylglutaryl-coenzyme A reductase and low-density lipoprotein receptor.205 Carnitine palmitoyltransferase I and peroxisome proliferator-activated receptor-α expression were increased as well as phosphorylated adenosine monophosphate-activated protein kinase.205 In physiological conditions, activation of farnesoid X receptor by agonist in the liver result in decrease in sterol regulatory element-binding protein-1c and downstream fatty acid synthetase and glycerol-3-phosphate-acyltransferase and activates peroxisome proliferator-activated receptor-α.49 Simultaneously, activation of farnesoid X receptor by agonist lowers low-density lipoprotein receptor expression as well as 3-hydroxy-3-methylglutaryl-coenzyme A reductase lowering thus hepatic cholesterol.49 In this experiment, sterol regulatory element-binding protein-2 was decreased on probable account of reduced cytosolic concentration of cholesterol.206 The active principles here are unknown. Consumption of Sechium edule (Jacq.) Sw. could be of value in metabolic syndrome.
Ellagic acid protects against non-alcoholic fatty liver disease in streptozotocin-diabetic rats by activating AMPK
Published in Pharmaceutical Biology, 2022
Jozaa Z. ALTamimi, Ghedeir M. Alshammari, Nora A. AlFaris, Reham I. Alagal, Dalal H. Aljabryn, Norah A. Albekairi, Mahmoud Ahmad Alkhateeb, Mohammed Abdo Yahya
Yet, the pathogenesis of mechanisms of NAFLD in T1DM is still unclear. Available experimental suggest that hepatic oxidative stress due to increased production of reactive oxygen species (ROS) and concomitant reduction in antioxidants in response to an increasing influx of glucose and free fatty acids (FFAs) is the major mechanism responsible for hepatic inflammation, ischemia/reperfusion (I/R), fibrosis, necrosis, and apoptosis (Ucar et al. 2013; Mohamed et al. 2016; Kitade et al. 2017; Masarone et al. 2018). Besides, independent of oxidative stress, T1DM is associated with several independent pathological mechanisms that stimulate hepatic lipid synthesis steatosis. These include impaired VLDL-c secretion, increased glucose uptake and conversion to fats, abnormally upregulated transcription factors including the carbohydrate-responsive element-binding protein (ChREBP), and the sterol regulatory element-binding protein 1 (SREBP1c) (Bhatt and Smith 2015).
Liver X receptor: a potential target in the treatment of atherosclerosis
Published in Expert Opinion on Therapeutic Targets, 2022
Shreya R. Savla, Kedar S Prabhavalkar, Lokesh K Bhatt
As a response to cholesterol derivatives’ binding, LXRs carry out regulation of gene expression and subsequent encoding of proteins, like the ATP-binding cassette (ABC) transporters (ABCA1, ABCG5 and ABCG8), which are responsible for mediating cholesterol transport out of the peripheral cells (also known as cholesterol efflux), into the liver, and out of the body. The ability of cholesterol derivatives to increase LXR’s transcriptional activity suggests the function of LXRs as cholesterol sensors, thus maintaining cholesterol homeostasis in the whole body [7,13]. A complementary relationship exists between the positively regulated cholesterol efflux and the negatively regulated cholesterol biosynthesis, which is mediated partly by inhibition of transcription and translation of the sterol regulatory element binding proteins (SREBPs). Therefore, upon rise in intracellular levels of cholesterol, its synthesis is inhibited followed by a stimulation of its efflux [5].
Mechanism of tumor cells escaping from immune surveillance of NK cells
Published in Immunopharmacology and Immunotoxicology, 2020
Zhe Ge, Shan Wu, Zhe Zhang, Shuzhe Ding
Tumors suppress the function of NK cells through many mechanisms, such as the secretion of TGF-β, PGE2, and activin-A, but in addition to the influence of tumor cells, many other factors are still regulating the NK cell cytotoxicity (Table 1). Sterol regulatory element-binding protein (Srebp) is a transcription factor involved in the expression of genes involved in fatty acid synthesis and cholesterol synthesis. In cytokine-activated NK cells, Srebp induces glucose to be metabolized to cytosolic citrate via the citrate-malate shuttle, so that NK cells maintain a high level of glycolysis and oxidative phosphorylation, thus providing sufficient energy for the growth, proliferation, function of NK cells, and maintaining the anti-tumor activity of NK cells. However, Srebp activity is negatively regulated by cholesterol and oxysterol. For example, when 25-hydroxycholesterol (25HC) is utilized to block the function of Srebp, the anti-tumor activity of NK cells decreases significantly [106]. In fact, glioblastoma (GBM) cells can produce and secrete 25HC [107], indicating that tumor cells may suppress NK cell activity by secreting 25HC. Moreover, obesity is associated with increased plasma cholesterol and leptin levels compared to normal weight individuals, and increased leptin levels are similarly associated with decreased NK cell cytotoxicity, which may be the cause for the reduced NK cell cytotoxicity in obese individuals [108].