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Exenatide binds to the intact human Glucagon-like peptide-1 receptor (GLP-1R) in a similar way to the human peptide glucagon-like peptide-1 (GLP-1); exenatide bears a 50% amino acid homology to GLP-1 and it has a longer half-life in vivo. [22] Exenatide is believed to facilitate glucose control in at least five ways:
δ-Aminolevulinic acid (also dALA, δ-ALA, 5ALA or 5-aminolevulinic acid), an endogenous non-proteinogenic amino acid, is the first compound in the porphyrin synthesis pathway, the pathway that leads to heme [3] in mammals, as well as chlorophyll [4] in plants. 5ALA is used in photodynamic detection and surgery of cancer. [5] [6] [7] [8]
Micrograph of fatty liver, as may be seen due to long-term prednisone use. Trichrome stain.. Short-term side effects, as with all glucocorticoids, include high blood glucose levels (especially in patients with diabetes mellitus or on other medications that increase blood glucose, such as tacrolimus) and mineralocorticoid effects such as fluid retention. [24]
Insulin-treated athletes are perceived to have lean body mass because physiological hyperinsulinemia in human skeletal muscle improves the activity of amino acid transport, which in turn promotes protein synthesis. [78] Insulin stimulates the transport of amino acids into cells and also controls glucose metabolism.
Similar considerations apply to other amino acids with ionizable side-chains, including not only glutamate (similar to aspartate), but also cysteine, histidine, lysine, tyrosine and arginine with positive side chains. Amino acids have zero mobility in electrophoresis at their isoelectric point, although this behaviour is more usually exploited ...
Endocrine: By increasing the production of glucose from amino-acid breakdown and opposing the action of insulin, corticosteroids can cause hyperglycemia, [26] insulin resistance and diabetes mellitus. [27] Skeletal: Steroid-induced osteoporosis may be a side-effect of long-term corticosteroid use.
Administration can prevent common side-effects, such as nausea and vomiting, as a result of interaction with D 2 receptors in the vomiting center (or cheomoreceptor trigger zone) located outside the blood–brain barrier. [2] Examples of extracerebral decarboxylase inhibitors include carbidopa and benserazide.
Aminoguanidine is a colorless solid that is soluble in water and ethanol. It is basic, producing salts when reacted with organic acids. As established by many crystallographic studies, protonation of aminoguanidine occurs at the imino nitrogen. [16] With formic acid, condensation occurs, leading to cyclization to give 3-amino-1,2,4-triazole. [14]