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TZDs, Thiazolidinediones

PAOP pulmonary artery occlusion pressure P-gp P-glycoprotein RAA renin-angiotensin-aldosterone RVF right ventricular failure SDC serum digoxin concentration S VR systemic vascular resistance TNF-a tumor necrosis factor-a TZD thiazolidinedione VAD ventricular assist device... [Pg.257]

A few cases of hepatotoxicity have been reported with rosiglitazone and pioglitazone, but no serious complications have been reported, and symptoms typically reverse within several weeks of discontinuing therapy. Therefore, periodic liver function tests should be performed at baseline and during thiazolidinedione therapy. Patients with a baseline alanine aminotransferase (ALT) level greater than 2.5 times the upper limit of normal should not receive a TZD. If ALT levels rise to greater than 3 times the upper limit of normal in patients receiving a TZD, the medication should be discontinued. [Pg.657]

Analysis Pioglitazone, the active ingredient in Actos, is a member of the thiazolidinedione (TZD) molecular class and has the structure (1) ... [Pg.461]

Thiazolidinediones (TZDs) are potent synthetic agonists of PPARy and medicine for type 2 diabetes. TZDs were shown to induce neuroprotection after cerebral ischemia by blocking inflammation (Culman et al., 2007). Spinal cord injury (SCI), another type of neurodegenerative disease, also induces massive inflammation that precipitates secondary neuronal death. Park et al. (2007) analyzed the therapeutic efficacy of TZDs, pioglitazone, and rosiglitazone, after SCI... [Pg.171]

TRPV1 receptors and PKRs, 152 True Lavender (Lavandula angustifolia), 241 Tumor necrosis factor-a (TNF—a), 180 TZDs. See Thiazolidinediones... [Pg.436]

Fig. 19 Primary structural requirements of thiazolidinediones (TZDs) for PPARy agonistic activity... Fig. 19 Primary structural requirements of thiazolidinediones (TZDs) for PPARy agonistic activity...
Pharmacology. Thiazohdinediones are also referred to as TZDs or glitazones. Pioglitazone and rosiglitazone are the two currently approved thiazolidinediones for the treatment of type 2 DM (see Table 72-11). Thiazolidinediones work by binding to the peroxisome pro-liferator activator receptor-y (PPAR-y), which are primarily located on fat cells and vascular cells. The concentration of these receptors in the muscle is very low thus this is unlikely to be the main site of action. Thiazolidinediones enhance insulin sensitivity at muscle, hver, and fat tissues indirectly. Thiazohdinediones cause preadipocytes to differentiate into mature fat cells in subcutaneous fat stores. Small fat cells are more sensitive to insulin and more able to store free fatty acids. The result is a flux of free fatty acids out of the plasma, visceral fat, and liver into subcutaneous fat, a less insulin-resistant storage tissue. Muscle intracellular fat products, which contribute to insulin resistance, also decline. [Pg.1351]

F. 3 General ehemieal stmctuies of PPARy agonists 1 and 2 that contain a thiazolidinedione (TZD) ot an oxazolidindione (OZD) ring system, respectively. The TZD moiety is prone to bioactivation via P450-mediated oxidation of the sulfur atom, while the OZD ring system is devoid of such liability... [Pg.523]


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See also in sourсe #XX -- [ Pg.902 ]




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Thiazolidinedione

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