The role of @entity12721 (currently @entity6170 and @entity12098 ) in the treatment of @entity164 2 @entity6 is firmly established. The mechanism of action involves binding to the @entity6864 , a transcription factor that regulates the expression of specific genes especially in fat cells but also other cell types such as endothelial cells, macrophages and monocytes, vascular smooth muscle cells and colonic epithelium. @entity12721 have been shown to interfere with expression and release of mediators of insulin resistance originating in adipose tissue (e.g., increased free @entity1718 , decreased @entity1254 ) in a way that results in net improvement of insulin sensitivity (i.e., in muscle and liver). A direct or indirect effect on @entity860 -dependent protein kinase may also be involved. Prevention of lipid accumulation in tissues critical to glycaemia such as visceral adipocytes, liver, muscle and beta-cells at the expense of lipids accumulating at the less harmful subcutaneous site may be central to their net metabolic effect. The sustained beneficial effect of @entity4506 on beta-cell function in @entity1 with previous gestational @entity6 in addition to the insulin-sensitising properties point to an important role of this class of drugs in the prevention of @entity164 2 @entity6 . Original safety concerns based on animal and in vitro studies (e.g., fatty @entity236 , @entity694 , adipogenic transdifferentiation of blood cells) remain theoretical issues but become less pressing practically with prolonged uneventful clinical use. Hepatotoxicity for @entity4506 and fluid retention, which can aggravate pre-existing @entity712 , are the most important side effects. In summary, with the @entity12721 , a novel concept for the treatment of insulin resistance and possibly preservation of beta-cell function is available that could become effective in the prevention of @entity164 2 @entity6 . Moreover, their anti-inflammatory properties also make them interesting in the prevention and treatment of @entity731 and possibly other inflammatory conditions (e.g., @entity29 ). Long-term data will be necessary for a final risk-benefit assessment of these substances.

XXXX -- some recent developments.

@entity1 :: ('9606', 'Species') :: ['women'] @entity712 :: ('MESH:D006333', 'Disease') :: ['heart failure'] @entity6 :: ('MESH:D003920', 'Disease') :: ['diabetes'] @entity731 :: ('MESH:D050197', 'Disease') :: ['atherosclerosis'] @entity4506 :: ('MESH:C057693', 'Chemical') :: ['troglitazone'] @entity12098 :: ('MESH:C060836', 'Chemical') :: ['pioglitazone'] @entity694 :: ('MESH:D003110', 'Disease') :: ['colonic cancer'] @entity29 :: ('MESH:D015212', 'Disease') :: ['inflammatory bowel disease'] @entity236 :: ('MESH:D001855', 'Disease') :: ['bone marrow transformation'] @entity12721 :: ('MESH:D045162', 'Chemical') :: ['Thiazolidinediones', 'thiazolidinediones'] @entity1254 :: ('9370', 'Gene') :: ['adiponectin'] @entity164 :: ('MESH:D017827', 'Disease') :: ['Type'] @entity860 :: ('MESH:D000249', 'Chemical') :: ['AMP'] @entity1718 :: ('MESH:D005227', 'Chemical') :: ['fatty acids'] @entity6170 :: ('MESH:C089730', 'Chemical') :: ['rosiglitazone'] @entity6864 :: ('5468', 'Gene') :: ['peroxisome proliferator-activated receptor-gamma']
@entity12721 :: (MESH:D045162,Chemical) :: ['Thiazolidinediones']
