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Plesiomonas
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Gabriel Forn-Cuní, Zoha Tavakkoliamol, Juan M. Tomás
It is common for P. shigelloides strains to contain plasmids, which may be involved in its pathogenicity, assisting cell invasion [79] or antibiotic resistance [80], although further studies are needed. Some Plesiomonas strains also produce triacylglycerol lipase, a virulence factor found in other bacteria [81]. Several exoenzymes such as gelatinase [81], DNAse [82], and elastolytic activity have also been described [83].
Biochemical Adaptations to Early Extrauterine Life
Published in Emilio Herrera, Robert H. Knopp, Perinatal Biochemistry, 2020
José M. Medina, Carlos Vicario, María C. Juanes, Emilio Fernández
BAT accumulates a high amount of triacylglycerol as a consequence of the increase in lipogenic activity during late gestation. This process is very active around birth in order to accomplish the necessary fat reserves to support postnatal nonshivering thermogenesis. BAT thermogenesis is triggered by the sympathetic nervous system which stimulates adrenergic receptors through the release of noradrenaline in situ.18 The binding of noradrenaline to the receptor stimulates adenylate cyclase by the G-protein system, resulting in an increase of cAMP concentrations in brown adipocytes. Phosphorylation of triacylglycerol lipase brought about by an activated cAMP-dependent protein kinase finally stimulates lipolysis. Fatty acids from triacylglycerol breakdown are oxidized in mitochondria, yielding the necessary energy for thermogenesis. Since energy has to be used for heat generation, BAT mitochondria are uncoupled by the presence of a unique protein: the uncoupling protein (UCP). This protein provides a system for continuous heat production by channeling protons across the inner mitochondrial membrane which dissipates the membrane potential. Although UCP gene expression is initiated during late gestation, UCP synthesis continues during the early postnatal period.20,21 UCP synthesis is stimulated by noradrenaline, although insulin and thyroid hormones potentiate the adrenergic effect.22,23 The increase in UCP synthesis is followed by a parallel increase in UCP affinity for GDP, modulating the uncoupling properties of the protein, and by an increase in the ability of protons to permeate the inner mitochondrial membrane. However, thermogenesis mechanisms in rat BAT are not fully developed until the last day of gestation since preterm newborns are unable to respond to a cold environment.20
Nature, Function, and Biosynthesis of Surfactant Lipids
Published in Jacques R. Bourbon, Pulmonary Surfactant: Biochemical, Functional, Regulatory, and Clinical Concepts, 2019
PC biosynthesis in the lung can be summarized as the two pathways which generate the immediate precursors of PC: diacylglycerol and CDP-choline (Figure 3). The first pathway proceeds from either dihydroxyacetone phosphate (DHAP) or glycerol-3-phosphate, two substrates of the glycolytic pathway. Fatty acids are activated as acyl-CoAs and are condensed either with DHAP to form acylhydroxy-acetone phosphate or with glycerol-3-phosphate to form a 1-acylglycerol-3-phosphate (steps 1 and 2 on Figure 3). Acylhydroxyacetone phosphate is in turn converted into 1-acylglycerol-3-phosphate (step 4). The relative proportion of each route leading to l-acylglycerol-3-phosphate formation is not precisely known. It has been suggested114that the DHAP pathway could account for up to 60% of phosphatidic acid production in type II cells. In most tissues, by contrast, this pathway appears to operate primarily for ether-lipid synthesis115 and the alternative pathway is predominant for phospholipid production. Subsequently, a second acylation step generates phosphatidic acid (PA) from two l-acylglycerol-3-phosphate molecules (step 5). This second acylation seems to proceed much faster than the first one in type II cells.116 Phosphatidic acid occupies a central position in phospholipid anabolism since it represents the common precursor of PC, PE, PS, PI, and PG. For PC synthesis, PA is converted into diacylglycerols by phosphatidic acid phosphatase (or phosphatidic acid phosphohydrolase or PAPase, step 6). Rat lung also contains considerable triacylglycerol lipase activity and it has been recently suggested that diacylglycerol generation could alternatively proceed through hydrolysis of triacylglycerols.117In parallel, choline is phosphorylated by choline kinase, then choline phosphate and CTP are converted into CDP-choline by cholinephosphate cytidylyltransferase (steps 7 and 8). Finally, choline phosphotransferase catalyzes the formation of PC from CDP-choline and diacylglycerol (step 9).
The challenges of oral drug delivery via nanocarriers
Published in Drug Delivery, 2018
Jonas Reinholz, Katharina Landfester, Volker Mailänder
However, the oral dosage form also has several drawbacks. Before the orally applied drug is able to reach its target, in most instances it needs to overcome multiple compartments of the human body, which is challenging for a broad spectrum of pharmaceuticals, especially for protein- or peptide-based ones. In general, the first major challenge for the drug after ingestion is surviving the harsh acidic pH value in the stomach. In addition, the proteases pepsin and cathepsin start to digest proteins into peptides. Once the drug surpasses the stomach and enters the small intestine via the duodenum, it faces the major enzymatic digestion machinery of the human body. Oligosaccharides and maltose are degraded into glucose, fructose, galactose, and mannose via sucrase, maltase, and lactase. Lipids are cleaved into glycerol and fatty acids via the pancreatic triacylglycerol lipase and carboxyl ester lipase. Peptides are digested into amino acids via trypsin, chymotrypsin, carboxypeptidase, dipeptidase, and aminopeptidase.
Recent trends and perspectives in enzyme based biosensor development for the screening of triglycerides: a comprehensive review
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Vinita Hooda, Anjum Gahlaut, Ashish Gothwal, Vikas Hooda
Triglycerides (TGs, triacylglycerols), also acknowledged as natural fats, an ester composed of one glycerol molecule attached to three fatty acid molecules (Unsaturated/saturated or both). The ester bond is formed between the hydroxyl groups of glycerol and the carboxyl groups of the fatty acids. Triacylglycerols are the chief components of very-low-density lipoprotein (VLDL) and chylomicrons, which are a lead source of energy in metabolism besides transporting dietary fat throughout the bloodstream [1]. In the digestive tract, triglycerides are broken into monoacylglycerol and free unsaturated fats, in a procedure called lipolysis, with the discharge of bile and lipases, which in turn move to absorptive enterocytes, cells coating the digestive tract. Abnormally high rate of lipoprotein synthesis and low rate of catabolism results in accumulation of TGs. One more reason for triglyceride accumulation may be reduced activity of triacylglycerol lipase, which catalyzes the hydrolysis reaction of TG into free fatty acids and glycerol. Quantification of triglycerides (TGs) in human serum is crucial for health care diagnostics since its high levels in the bloodstream could result in hyperlipidemia. In human body, the level of TGs less than 150 mg/dl is considered to be normal. The condition is known as hyperlipoprotenemias when the level lies between 150–199 mg/dl and high risk of pancreatitis is associated with TGs level above 500 mg/dl. The reference range of triglycerides level in blood has been shown in Figure 1. The presence of excessive triglycerides (above 500 mg/dl) in the blood is one of the leading causes of diabetes mellitus, liver obstruction, hypertension, atherosclerosis, Alzheimer disease [2] and various cardiovascular diseases [3]. In addition, the elevated amount of TGs causes reduction in nitric oxide level and raising the sum of many inflammatory compounds, which are partly responsible for vascular injury and endothelial dysfunction [4]. Consequently, the determination of total triglycerides level in serum has attracted clinical significance as a marker of deviation from the normal range, which could affect the lipid metabolism in our body and early diagnosis of a range of diseases associated with it.