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Resistance metabolism

PPARy White adipose tissue, atherosclerotic lesions Insulin-sensitizing and glucoselowering re-directs TG from non-adipose tissues and visceral adipose depots for storage in subcutaneous adipose tissue slowed progression of atherosclerosis Fatty acids, eico-sanoids Th iazolid i ned iones pioglitazone (Actos ), rosiglita-zone (Avandia ) Type 2 diabetes, (insulin resistance, metabolic syndrome)... [Pg.945]

Etoposide (XV) is a semisynthetic gylcoside derivative of podophyllotoxin, which is one of the most extensively used anticancer drugs in the treatment of various types of tumors [64,65]. The anticancer activity of this drug is mainly due to its ability to inhibit an ubiquitous and essential enzyme human DNA topo II [66,67]. Despite its extensive use in the treatment of cancers, it has several limitations, such as poor water solubility, drug resistance, metabolic inactivation, myelosuppression, and toxicity [68]. In order to overcome these... [Pg.63]

To gain further insight into the mechanisms involved in defective insulin-stimulated glucose uptake in skeletal muscle of insulin-resistant subjects, the possible role of IMCL in the pathogenesis of skeletal muscle insulin resistance and type 2 diabetes mellitus was explored by comparing insulin sensitivity (GIR) and IMCL content of insulin-resistant and insulin-sensitive offsprings of patients with type 2 diabetes. Twenty-six healthy subjects were included in the first study, 13 of them classified as insulin-sensitive and further 13 as insulin-resistant. Metabolic and anthropometric data are given in Table 4. [Pg.50]

An alternative approach to preventing the formation of dihydroartemisinin by simple P450 metabolism is to replace the methyl function in artemether with an aryl function. Phenoxy analogues of DHA can easily be prepared in a one-step synthesis from dihydroartemisinin in a manner similar to the preparation of Ic and Id. In addition to having superior in vivo activity to artesunate and artemether, analogues substituted with a p-fluoro (71a) or trifluoromethyl group (71b), in the phenoxy ring, resist metabolism to DHA . ... [Pg.1314]

Ephedrine is a naturally occurring alkaloid that can cross the blood-brain barrier and thus exert a strong CNS-stim-ulating effect in addition to its peripheral actions. The latter effects are primarily due to its indirect actions and depend largely on the release of norepinephrine. However, ephedrine may cause some direct receptor stimulation, particularly in its bronchodilating effects. Because it resists metabolism by both COMT and MAO, its duration of action is longer than that of norepinephrine. As is the case with aU indirectly acting adrenomimetic amines,... [Pg.105]

C. Amphetamine is an indirectly acting adrenomimetic amine that depends on the release of norepinephrine from noradrenergic nerves for its action. Tlius, its effect depends on neuronal uptake (blocked by cocaine) to displace norepinephrine from the vesicles and the availability of norepinephrine (depleted by reserpine). The substitution on the a-carbon atom blocks oxidation by monoamine oxidase. With no substitution on its benzene ring, amphetamine resists metabolism by COMT. [Pg.107]

Metabolism of the antimalarial amodiaquine provides quinone-imine, which is an electrophilic metabolite responsible for hepatotoxicity and agranulocytosis. These side effects have severely restricted the clinical use of amodiaquine. Replacement of the phenolic hydroxyl by a fluorine prevents the oxidation process. Then Af-dealkylation becomes the major process. This has led to further refinements, with the preparation of the Af-fbutyl analogue, a compound that resists metabolic side chain cleavage and has an excellent in vitro and in vivo profile (Figure 3.16). ... [Pg.87]

Johansson JO, Fowelin J, Landin K, Lager I, Bengtsson BA. Growth hormone-deficient adults are insulin-resistant. Metabolism 1995 44(9) 1126-9. [Pg.516]

Finally a rare etiology of CL resistant metabolic alkalosis is a genetic (autosomal recessive) defect in CL reabsorption within the thick ascending limb of the loop of Henle, a condition known as Bartter s syndrome. ... [Pg.1773]

Glavinas, H. Krajcsi, P. Cserepes, J. Sarkadi, B. The role of ABC transporters in drug resistance, metabolism, and toxicity. Curr. Drug Deliv. 2004, 1, 27 2. [Pg.206]

S. Reynisdottir, K. Ellerfeldt, H. Wahrenberg, H. Lithell, and P. Arner, Multiple lipolysis defects in the insulin resistance (metabolic) syndrome, J. ain. Invest., 1994, 93, 2590-2599. [Pg.305]

Urea, the end product of nitrogen metabolism, accumulates rapidly in ARF. Most patients with ARF have a primary stressful illness that results in ureagenesis, and thus protein breakdown is markedly accelerated. Protein catabolism in ARF may be stimulated as the result of insulin resistance, metabolic acidosis, circulating proteases and inflammatory mediators, and the effects of uremic toxins. The mechanism may be direct, via modulation of protein synthesis, or indirect, by inhibiting the action of anabolic hormones. ... [Pg.2636]

Genetic engineering of transgenic plants (pest resistance, metabolic pathways)... [Pg.59]

Metflurazon inhibits photosynthesis and prevents the development of chloro-plastids in sensitive plants (Hilton et al., 1969). The authors also report on their investigation of the mode of action of 4 pyridazinone herbicides on barley. Metflurazon and its phenyl- and unsubstituted amino analogues, structurally similar to pyrazon, also inhibited the Hill reaction and photosynthesis, but showed two further biological features they resisted metabolic oxidation and inhibited chloroplast formation. The latter effect is similar to that of amitrol and dichlormate, but 100-1000 times stronger. [Pg.740]

Wareham NJ, Ness EM, Byrne CD, Cox BD, Day NE, Hales CN. Cigarette smoking is not associated with hyperinsulinemia evidence against a causal relationship between smoking and insulin resistance. Metabolism (1996) 45, 1551-6. [Pg.510]

Our interest in GOase came from a need to find an efficient process for making 5-C-hydroxymethyl-L-arabino-hexopyranose derivatives 1 (Equation 1). These compounds have been developed as candidates for nonnutritive sugar substitutes in foods because they resist metabolism and have sucrose-like functional properties (7). These materials would be too expensive if made using the techniques of traditional chemical synthesis, so we developed a simple "one-pot" process (Equation 1) using GOase. [Pg.99]

Enzyme Cells Microorganisms Body cells/cellular networks Biocatalytic Catalyzed decrease of substrate or increase of product concentration Release of enzymes, biocatalytic reactions Cell-cell interaction (resistance) Metabolic products Direct electric response (e.g. neurons, heart muscle) Amperometric, conductometric potentiometric, FETs Amperometric, potentiometric Conductometric, impedimetric Amperometric, potentiometric IS FETs, FETs... [Pg.357]

Liao, J., Qian, F., Tchabo, N. et al (2014) Ovarian cancer spheroid cells with stem cell-like properties contribute to tumor generation, metastasis and chemotherapy resistance through hypoxia-resistant metabolism. PLOS One, 9 (1), e84941. [Pg.89]

Elmslie JL, Porter RJ, Joyce PR, Hunt PJ, Shand BI. Scott RS Comparison of insulin resistance, metabolic s5mdrome and adipo-nectin in overweight bipolar patients taking sodium valproate and controls. Aust N Z J Psychiatry 2009 43(1) 53-60. [Pg.200]


See other pages where Resistance metabolism is mentioned: [Pg.28]    [Pg.98]    [Pg.455]    [Pg.14]    [Pg.1140]    [Pg.89]    [Pg.1140]    [Pg.1314]    [Pg.30]    [Pg.123]    [Pg.866]    [Pg.681]    [Pg.1773]    [Pg.50]    [Pg.382]    [Pg.412]    [Pg.777]    [Pg.508]    [Pg.40]    [Pg.358]    [Pg.181]    [Pg.2362]    [Pg.67]    [Pg.156]    [Pg.213]   


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Carbamates metabolic resistance

Glucose metabolism insulin resistance

Insulin resistance metabolic syndrome

Insulin resistance triglycerides metabolism

Metabolic resistance

Metabolic resistance

Metabolic resistance mechanisms

Metabolism PCBs resistance

Metabolism based resistance

Metabolism insulin resistance, growth hormone

Metabolism resistance mechanisms

Resistance enhanced herbicide metabolism

Resistance metabolic detoxification

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