Dr. Michael Bade Wheeler M.D.
Hematologist-Oncologist | Hematology & Oncology
28391 Essential Road Merton WI, 53056About
Dr. Michael Wheeler is a hematologist oncologist practicing in Merton, WI. Dr. Wheeler specializes in the diagnosis, treatment and prevention of blood diseases such as anemia, hemophilia, sickle-cell disease, leukemia and lymphoma. Hematologist Oncologists are also trained in the study of cancer and its attack on other organs.
Education and Training
St Louis Univ Sch of Med, St Louis Mo 1978
Board Certification
Internal MedicineAmerican Board of Internal MedicineABIM- Medical Oncology
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Glucagon-like peptide-1 inhibits pancreatic ATP-sensitive potassium channels via a protein kinase A- and ADP-dependent mechanism.
- Inhibition of Kv2.1 voltage-dependent K+ channels in pancreatic beta-cells enhances glucose-dependent insulin secretion.
- Abnormal expression of pancreatic islet exocytotic soluble N-ethylmaleimide-sensitive factor attachment protein receptors in Goto-Kakizaki rats is partially restored by phlorizin treatment and accentuated by high glucose treatment.
- Uncoupling protein 2 knockout mice have enhanced insulin secretory capacity after a high-fat diet.
- Synaptosome-associated protein of 25 kilodaltons modulates Kv2.1 voltage-dependent K(+) channels in neuroendocrine islet beta-cells through an interaction with the channel N terminus.
- Exogenous nitric oxide and endogenous glucose-stimulated beta-cell nitric oxide augment insulin release.
- The multiple actions of GLP-1 on the process of glucose-stimulated insulin secretion.
- Glucagon-like peptide-1 receptor activation antagonizes voltage-dependent repolarizing K(+) currents in beta-cells: a possible glucose-dependent insulinotropic mechanism.
- Epac-selective cAMP analog 8-pCPT-2'-O-Me-cAMP as a stimulus for Ca2+-induced Ca2+ release and exocytosis in pancreatic beta-cells.
- Temperature and redox state dependence of native Kv2.1 currents in rat pancreatic beta-cells.
- The phosphatidylinositol 3-kinase inhibitor LY294002 potently blocks K(V) currents via a direct mechanism.
- Mitochondrial functional state in clonal pancreatic beta-cells exposed to free fatty acids.
- Peroxisome proliferator-activated receptor-alpha agonist treatment in a transgenic model of type 2 diabetes reverses the lipotoxic state and improves glucose homeostasis.
- Antagonism of rat beta-cell voltage-dependent K+ currents by exendin 4 requires dual activation of the cAMP/protein kinase A and phosphatidylinositol 3-kinase signaling pathways.
- Gene and protein kinase expression profiling of reactive oxygen species-associated lipotoxicity in the pancreatic beta-cell line MIN6.
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