Glimepiride and Phosphoinositolglycans

Both events induce the redistribution of hpid-modified signahng protein, which are known to reside within DIGs on basis of their acylation/glypiation and/ or direct binding to caveolin (for reviews see Refs. [477, 488, 489]). In particular, 

DifTerences in Regulation of TAC Storage and Mobilization between Visceral and Subcutaneous Adipocytes 

In detail, adipocytes from visceral adipose tissue are more resistant to insuhn-induced anti-lipolysis and re-esterification of NEFA than those from leg and non-visceral body fat both in vitro [503, 504] and in vivo [505]. Various functional differences in these ceUs have been identified at the level of the insuhn receptor and the post-receptor insulin signahng cascade [503, 504]. PDE3B involved in hpolysis regulation by insuhn (see above. Fig. 11.7) and protein tyrosine phosphatases de-phosphorylating fhe insuhn receptor, such as PTPlb, could be affected in differen- 

Insulin receptor expression (exon 11 deleted) vAT scAT 

Insulin-induced insulin receptor tyrosine phosphorylation scAT vAT 

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G. Muller, N. Hanekop, S. Wied, and W. Frick, Cholesterol depletion blocks redistribution of lipid raft components and insulin-mimetic signaling by glimepiride and phosphoinositolglycans in rat adipocytes. Mol. Med., 2002, 8, 120-136. 

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