Effects of sulfonylurea drugs on adiponectin production from 3T3-L1 adipocytes: implication of different mechanism from pioglitazone
Y Kanda, M Matsuda, K Tawaramoto… - Diabetes research and …, 2008 - Elsevier
Y Kanda, M Matsuda, K Tawaramoto, F Kawasaki, M Hashiramoto, M Matsuki, K Kaku
Diabetes research and clinical practice, 2008•ElsevierAdiponectin is a fat-derived cytokine with anti-diabetic and anti-atherogenic properties. In
this study, effects of sulfonylureas (SUs) on adiponectin production and the action
mechanism were evaluated using 3T3-L1 adipocytes. The cells were incubated with
glimepiride, glibenclamide, gliclazide, pioglitazone, metformin and the medium only as the
control. In the control, the adiponectin level evaluated as the production rate per 24h was not
changed, while pioglitazone significantly increased the adiponectin level. SUs also …
this study, effects of sulfonylureas (SUs) on adiponectin production and the action
mechanism were evaluated using 3T3-L1 adipocytes. The cells were incubated with
glimepiride, glibenclamide, gliclazide, pioglitazone, metformin and the medium only as the
control. In the control, the adiponectin level evaluated as the production rate per 24h was not
changed, while pioglitazone significantly increased the adiponectin level. SUs also …
Adiponectin is a fat-derived cytokine with anti-diabetic and anti-atherogenic properties. In this study, effects of sulfonylureas (SUs) on adiponectin production and the action mechanism were evaluated using 3T3-L1 adipocytes. The cells were incubated with glimepiride, glibenclamide, gliclazide, pioglitazone, metformin and the medium only as the control. In the control, the adiponectin level evaluated as the production rate per 24h was not changed, while pioglitazone significantly increased the adiponectin level. SUs also increased the adiponectin level, but metformin failed to show any increase in adiponectin production. SUs induced adiponectin gene expression as well as pioglitazone. Pioglitazone significantly increased adipogenesis, but glimepiride did not. The aP2 gene expression was increased by pioglitazone, but not by glimepiride. Forskolin, a protein kinase A stimulator, reduced the adiponectin production stimulated by glimepiride but not by pioglitazone. These observations strongly suggest that SUs stimulate the adiponectin production through a different mechanism from pioglitazone, namely an interaction with protein kinase A activity. The significance of the extrapancreatic action of SUs observed in this study should be further evaluated in the clinical field.
Elsevier
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