Explore chapters and articles related to this topic
Allopathic Medicines
Published in Varma H. Rambaran, Nalini K. Singh, Alternative Medicines for Diabetes Management, 2023
Varma H. Rambaran, Nalini K. Singh
Alpha-glucosidase inhibitors (AGIs), such as acarbose (Glucobay) (Figure 2.9a), miglitol (Figure 2.9b), and voglibose (Figure 2.9c), form a new class of “suppressing-based” therapy that target the enzyme, α-glucosidase (AG). AG is an exo-type carbohydrase that is responsible for breaking down complex carbohydrates to glucose in the upper gastrointestinal tract (Kumar, Narwal et al. 2011, Lebovitz 1998). As such, the inhibition of the AG enzyme results in a decrease in complex carbohydrate catabolism, which as a consequence, retards the rise in postprandial BG levels (Lebovitz 1998).Structural formulae of α-glucosidase inhibitors: (a) acarbose, (b) miglitol, and (c) voglibose.
Resuscitation Physiology
Published in Kenneth D Boffard, Manual of Definitive Surgical Trauma Care: Incorporating Definitive Anaesthetic Trauma Care, 2019
The hypovolaemia will stimulate release of catecholamines, which in turn trigger the neuroendocrine response. This plays an important role in volume and electrolyte conservation and protein, fat, and carbohydrate catabolism.
Biology of microbes
Published in Philip A. Geis, Cosmetic Microbiology, 2006
Amino acid synthesis. Simply put, the amino acids come from the digested polymers ingested by the cells. They can come from protein catabolism or from the intermediates of carbohydrate catabolism that are diverted from the catabolic process into the anabolic process of making amino acids. The production of amino acids requires energy in the form of ATP. Thus, these synthetic processes only occur when plenty of ATP is available from catabolism and the intermediates can be diverted away from the process of energy generation.
Profiling plasma levels of thiamine and histamine in Jordanian children with autism spectrum disorder (ASD): potential biomarkers for evaluation of ASD therapies and diet
Published in Nutritional Neuroscience, 2023
Ayat Hussein B. Rashaid, Mazin Taha Alqhazo, Shreen Deeb Nusair, James B. Adams, Mahmoud Ahmad Bashtawi, O’la Al-Fawares
Neurotransmitters have important effects on brain growth, motor skills, memory, and behavior [9]. Abnormal levels of neurotransmitters could disturb brain development, nerve cell migration, differentiation, and synaptogenesis [10,11]. Thiamine (vitamin B1) is required for all tissues and is concentrated in the liver, heart, kidneys, skeletal muscles and brain [12]. The active form of thiamine is thiamine diphosphate that serves as a cofactor for several enzymes which act primarily in carbohydrate catabolism, and in the biosynthesis of the neurotransmitter acetylcholine [13]. These enzymes are also involved in the antioxidant defense system [12]. Major thiamine uptake occurs by the small intestine via the saturable high transport system [12]. Thiamine deficiency in humans mainly affects the cardiovascular and the nervous system, resulting in a number of pathological conditions such as Wernicke-Korsakoff syndrome, peripheral vasodilation, biventricular myocardial failure, and cerebellar degeneration [12]. Other neuropathology includes bilateral hemorrhagic and necrotic lesions brainstem, diencephalon and cerebellum [12]. Thiamine supplementation can reverse some of these signs but not the severe defects in memory and cognition [12]. In a previous study, thiamine tetrahydrofurfuryl disulfide (TTFD) was found to have a beneficial clinical effect in children with ASD, since 8 out of 10 children involved in the study were clinically improved following TTFD intake [14]. However, thiamine levels were found to be similar in ASD vs. controls in children in the US [15].
Effect of wheat bran derived prebiotic supplementation on gastrointestinal transit, gut microbiota, and metabolic health: a randomized controlled trial in healthy adults with a slow gut transit
Published in Gut Microbes, 2020
Mattea Müller, Gerben D. A. Hermes, Canfora Emanuel E., Jens J. Holst, Erwin G. Zoetendal, Hauke Smidt, Freddy Troost, Frank G. Schaap, Steven Olde Damink, Johan W. E. Jocken, Kaatje Lenaerts, Ad A. M. Masclee, Ellen E. Blaak
Colonic SCFA may affect gastrointestinal motility via stimulation of enterochromaffin cells amongst other mechanisms.58 Despite the increase of acetate-producing Bifidobacterium, plasma and fecal SCFA concentrations were not affected by AXOS intervention. Of note, we observed a time-dependent decrease in plasma acetate and butyrate in both groups reflecting a high temporal variability in SCFA metabolism. Circulating acetate and butyrate have several sources: 1) direct exogenous ingestion via food sources, 2) indirect exogenous production by colonic bacterial fermentation of non-digested food components, and 3) endogenous production from protein, lipid, and carbohydrate catabolism in mainly the liver.4 Plasma SCFA concentrations are thus the net result of SCFA production, absorption and splanchnic extraction/hepatic metabolism, and are therefore difficult to interpret. Since rate of appearance from endogenous or exogenous sources can only be acquired by using stable isotope tracer techniques, we cannot provide this information for the present study.
Proteomics of Pseudomonas aeruginosa: the increasing role of post-translational modifications
Published in Expert Review of Proteomics, 2018
Charlotte Gaviard, Thierry Jouenne, Julie Hardouin
Proteomics has advanced our knowledge in bacterial virulence, in resistance mechanisms, in host–pathogen interactions, and so on.Various PTMs have been described in P. aeruginosa but we are only at the beginning of this characterization. Many other modifications have to be investigated to obtain a global map of PTMs in this bacterium.Some PTMs remain to be discovered, in particular those specific to bacteria.Modified proteins are involved in a wide range of biological processes as central carbohydrate catabolism, amino acid metabolism, transcription/translation, and in bacterial pathogenicity, virulence, or drug resistance.Chemical and enzymatic mechanisms involved in the addition/removal of PTMs are still largely unknown. The identification of these enzymes and their substrates constitutes a great challenge for the future since they might constitute new therapeutic targets.