Post-doc (funded by Nordic Center of Excellence in disease Genetics)
My project focuses on the roll of epigenetics in the pathogenesis of type 2 Diabetes. Currently, I am looking into changes in global DNA methylation patterns in skeletal muscle after an exercise intervention study in men. DNA methylation, which occurs on CpG dinucleotides, generally reduces the likelihood of gene transcription. Therefore, DNA methylation can be a mechanism for regulation gene expression. It is not yet clear to whcih extent DNA methylation is altered in type 2 Diabetes.
We are also looking into changes in epigenetic patterns in human islets of Langerhans since they are central players in type 2 Diabetes.
Fex, M, Haemmerle, G., Wierup, N., Dekker Nitert, M., Rehn, M., Ristow, M., Zechner, R., Sundler, F., Holm, C., Eliasson, L., Mulder, H. (2009). A beta-cell-specific knock-out of hormone-sensitive lipase results in hyperglycemia and disruption of exocytosis. Diabetologia 52: 271-280
Dekker Nitert, M., Nagorny, C.L.F, Wendt, A., Eliasson, L., and Mulder, H. (2008) CaV1.2 rather than CaV1.3 is coupled to glucose-stimulated insulin secretion in INS-1 832/13 cells. Journal of Molecular Endocrinology 41: 1-11
Fex, M., Wierup, N., Dekker Nitert, M., Ristow, M., Mulder, H. (2007) Rat insulin promoter 2-Cre recombinase mice bred onto a pure C57BL/6J background exhibit unaltered glucose tolerance. Journal of Endocrinology 194, 551-555
Fex, M., Dekker Nitert, M., Wierup, N., Sundler, F., Ling, C., and Mulder, H. (2007) Enhanced mitochondrial metabolism may account for the adaptation to insulin resistance in islets from C57BL/6J mice fed a high-fat diet. Diabetologia 50(1): 74-83
Last updated: April 4, 2011
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