Metformin and insulin meet in a most atypical way.
A recent Cell paper by He et al. (2009) shows how metformin circumvents a block between insulin and atypical protein kinase C in obese and diabetic mice to inhibit gluconeogenesis by stimulating the phosphorylation of CBP and the disassembly of the CREB transcriptional complex.
White
Morris F
MF
Howard Hughes Medical Institute, Division of Endocrinology, Children's Hospital Boston, Harvard Medical School, Boston, MA 02115, USA. morris.white@childrens.harvard.edu
D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy; D005943:Gluconeogenesis; D007004:Hypoglycemic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D007328:Insulin / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D008565:Membrane Proteins / Q000378:metabolism; D008687:Metformin / Q000494:pharmacology* / Q000627:therapeutic use; D051379:Mice; D010750:Phosphoproteins / Q000378:metabolism; D011493:Protein Kinase C / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism
D007004:Hypoglycemic Agents; D007328:Insulin; D008565:Membrane Proteins; C498709:Pag1 protein, mouse; D010750:Phosphoproteins; D014157:Transcription Factors; D008687:Metformin; C115015:PKC-3 protein; D011493:Protein Kinase C