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Pharmaceutical Applications of Gum Arabic
Published in Amit Kumar Nayak, Md Saquib Hasnain, Dilipkumar Pal, Natural Polymers for Pharmaceutical Applications, 2019
It was demonstrated that GA could decrease 6% and 10.4% total serum cholesterol when orally administrated at either 25 g/day or 30 g/day for periods of 21 or 30 days respectively (Ross et al., 1983) and it was confirmed that only the decrease of cholesterol, very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) were observed but not for high-density lipoprotein (HDL) and triglycerides. GA did not affect the plasma cholesterol concentration, but a significant lower of plasma triacylglycerol was observed (Annison et al., 1995). However, the effect of GA on the metabolism of lipid is quite variable. GA was revealed to have no significant effect on cholesterol concentration either in plasma or in the liver, and the concentration of triacylglycerol in plasma was, however, higher when fed with GA (Jensen et al., 1993). The most accepted mechanism of the cholesterol-lowering effect was related to the fecal bile acid increase and the excretion of neutral sterol as well as modification of absorption and lipid digestion (Eastwood, 1992; Moundras et al., 1994). Generally, the bile acids could be bonded or sequestered by dietary fibers, and their active reabsorption in the ileum could be diminished, resulting in excretion in feces. Consequently, the plasma cholesterol concentration decreased (Pasquier et al., 1996). Although there are various mechanisms to demonstrate the GA’s effect on lipid metabolism, no clear mechanism is available, especially for the unaffected plasma cholesterol by GA, and the deep mechanism should be further explored.
Toxicity of Nanomaterial-Based Systems in Drug Delivery
Published in Jince Thomas, Sabu Thomas, Nandakumar Kalarikkal, Jiya Jose, Nanoparticles in Polymer Systems for Biomedical Applications, 2019
The liver is the largest internal human organ weighing about 1.5 kg in an adult, with many essential roles in metabolism and clearance. Bile acids are formed by the liver, which are of critical importance for the maintenance of cholesterol metabolism and intestinal lipid absorption.63 The liver is a critical target tissue for drug delivery because many fatal conditions including chronic hepatitis, enzyme deficiency, and hepatoma occur in hepatocytes.64 Biodegradable NPs are effective drug delivery devices. Various polymers have been used in drug delivery research as they can effectively deliver the drug to a target site and thus increase the therapeutic benefit, while minimizing side effects.65 Nanomaterial-based drugs may overcome many of the hurdles of traditional non-nano drugs, because they bear the advantage of enabling a cell-type specific drug delivery based on binding to a specific surface structure. High toxicity and poor specificity of the therapeutic agents may lead to systemic toxicity and adverse effects that are harmful for the patient.
Thin-Layer Chromatography in Clinical Chemistry
Published in Bernard Fried, Joseph Sherma, Practical Thin-Layer Chromatography, 2017
Bile acids are 24-carbon steroid derivatives. They are formed by the conversion of cholesterol to cholic and chenodeoxy cholic acids (primary bile acids). These are then conjugated with glycine or taurine via amide linkage in the liver. After conjugation they are eliminated together with the bile. Most of the bile acids entering the gut are reabsorbed in the terminal ileum, while some of them undergo bacterial deconjugation. In this process, secondary bile acids (deoxy cholic, lithocholic, and ursodeoxycholic acids) and a number of keto-bile acids occurring in feces are formed. The investigation of bile acids has clinical importance in the diagnosis of certain liver or intestinal disorders. In biomedicine, concentrations of bile acids in human feces are used for diagnosis of bile acid malabsorption and chologenic diarrhea. In liver disorders, serum levels of bile acids are elevated and their measurement is a sensitive index of liver disease. Bile acids are not found in urine owing to efficient uptake by the liver and excretion into the intestine. In hepatocellular disease and obstructive jaundice, however, their urinary excretion increases.
Evaluation of antioxidation, regulation of glycolipid metabolism and potential as food additives of exopolysaccharide from Sporidiobolus pararoseus PFY-Z1
Published in Preparative Biochemistry & Biotechnology, 2023
Di Xue, Fangyi Pei, Henan Liu, Zhenyan Liu, Yuchao Liu, Lei Qin, Yinzhuo Xie, Changli Wang
Bile acid binding in vitro was analyzed via the reported method, with modifications.[37–40] In brief, 1 mL of SPZ at different concentrations (0.05, 0.1, 0.2, 0.4, 0.6, 0.8, 1.0 mg/mL) was combined with 1 mL of HCl (0.01 mol/L) and 3 mL of pepsin (10 mg/mL), respectively, and the reaction was performed at 120 rpm at 37 °C for 1 h. NaOH (0.1 mol/L) was used to adjust the pH to 6.3, and 4 mL of trypsin (10 mg/mL) was added at 37 °C and 120 rpm for 1 h. In total, 4 mL each of cholic acid (CA, 0.5 mg/mL), taurochenocholic acid (TA, 0.5 mg/mL) and glycocholic acid (GA, 0.5 mg/mL) were added to the reaction system, respectively. Subsequently, the reaction was performed at 120 rpm at 37 °C for 1 h. After centrifugation at 4000 rpm for 20 min, 1 mL of supernatant was taken and 3 mL of 60% sulfuric acid (v/v) was added to the reaction system at 70 °C for 20 min, before being placed in an ice bath for 5 min. The absorbance was measured at 387 nm using a microplate reader, with phosphate buffer without bile acid used as the blank. The ability of bile acid binding was calculated according to the formula: where C1 is the initial concentration of cholate solution, and C2 is the residual concentration of the cholate solution.
Process optimization in ginseng fermentation by Monascus ruber and study on bile acid-binding ability of fermentation products in vitro
Published in Preparative Biochemistry & Biotechnology, 2021
Chongyan Zhao, Fang Yang, Feng Lin, Qingsong Qu, Zhixun Li, Xing Liu, Lu Han, Xinyuan Shi
Cholesterol is a precursor to the synthesis of bile acids. About 80% of the cholesterol is metabolized by liver tissue and converted to bile acid, which is involved in the enterohepatic circulation. Finally, part of bile acid is reabsorbed by the body.[36,37] de Aguiar Vallim[38] reported that bile acids can bind some food ingredients and then excrete with the digestion of food. Therefore, Cholesterol will be continuously converted to bile acids to maintain the homeostasis of the bile acid pool, thereby reducing the cholesterol content in the blood. In the human body, bile acids are classified into free bile acids (cholic acid, deoxycholic acid, etc.) and conjugated bile acid (cholic acid, deoxycholic acid, etc. combined with glycine and taurine).[39] The conjugated bile acids are generally present in the form of sodium salts, which is more common in the human body. Therefore, in this study, it is applicable that sodium taurocholate and sodium cholate were selected as representative of the conjugated bile acids.
Regulation of cytochrome P450 expression by microRNAs and long noncoding RNAs: Epigenetic mechanisms in environmental toxicology and carcinogenesis
Published in Journal of Environmental Science and Health, Part C, 2019
Dongying Li, William H. Tolleson, Dianke Yu, Si Chen, Lei Guo, Wenming Xiao, Weida Tong, Baitang Ning
Li et al.47 described a systemic lipid metabolic pathway in mice involving CYP8B1, an important enzyme in bile acid synthesis, and lncLSTR, a liver-specific lncRNA. Identified using the Affymetrix Mouse Genome 430 2.0 Array gene chip, the expression of lncLSTR fluctuated in response to fasting and refeeding, suggesting a role for this lncRNA in energy metabolism. Predominantly expressed in the nucleus, lncLSTR interacts with TDP-43, a transcriptional repressor, to reduce the occupancy of TDP-43 on the Cyp8b1 promoter and abolish TDP-43-dependent CYP8B1 inhibition. In a lncLSTR-knockdown mouse line, depletion of lncLSTR decreased the expression of CYB8B1 and altered the ratio of muricholic acid (MCA)/cholic acid (CA), two major bile acids in mice. This change in the bile acid composition activated the FXR pathway and its downstream gene apoC2, a potent activator of lipoprotein lipase (LPL), which in turn enhanced triglyceride clearance in the plasma. This study depicts a cascade of multi-player molecular events involving lncRNA modulation of CYP expression, which ultimately led to a physiological change in lipid metabolism.