Obesity is a major inducer of type II diabetes and it is estimated by the World Health Organization that over 500 million people worldwide suffer from either of these disorders, with the incidence increasing dramatically over the last 10 years. At present there is no definite treatment for either disease and complications include severe cardiovascular problems, high blood pressure, kidney failure, blindness and even loss of limbs and death in the later stages of the disorders. Insulin is an important regulator in energy homeostasis but insulin signaling is normally severely impaired in these disorders. There is thus great interest in identifying functional insulin-independent mechanisms that stimulate energy transport in peripheral tissues in order to find novel ways to cure these diseases.

We have found that activation of the sympathetic nerves and the release of norepinephrine and activation of adrenergic receptors lead to an insulin-independent mechanisms that increases glucose uptake in brown fat and skeletal muscle. Our aim is to understand these novel mechanisms and if these mechanisms can be utilized to combat obesity and type II diabetes.

 

Adrenergic receptors, second messenger signaling, atypical signaling, glucose homeostasis, obesity, type 2 diabetes. A) L6 skeletal muscle cells. F-actin (green) and nuclei (blue) are visualized with fluoresence microscopy. B) L6 skeletal muscle in our 2-DMS system for stimulation of formation of separated myotubes. F-actin (green), nuclei (blue) and GLUT4 (yellow) are visualized with fluoresence microscopy

 

 

Keywords

Adrenergic receptors, second messenger signaling, atypical signaling, glucose homeostasis, obesity, type 2 diabetes

Selected publications

Kupferschmidt, N., Csikasz, R., Naeem Iqbal, M., Atluri, R., Ballell, L., Bengtsson, T., & Garcia-Bennett, A.E. (2013). Large pore mesoporous silica induced weight loss in obese mice Nanomedicine (Accepted for publication)

Dehvari, N., Hutchinson, D.S., Nevzorova, J., Dallner, O., Sato, M., Kocan, M.,
Merlin, J., Evans, B.A., Summers, R.J., & Bengtsson, T. (2012). β2-Adrenoceptors increase translocation of GLUT4 via G protein-coupled receptor kinase sites in the receptor C-terminal tail. British Journal of Pharmacology. 165:1442-56

Dehvari, N.,Tapan, M., Persson, J., Bengtsson, T., Graff, C., Winblad, B., Rönnbäck, A., & Behbahani, H. (2012). Amyloid precursor protein accumulates in aggresomes in response to proteasome inhibitor. Neurochemistry Int. 60:533-42

Sato, M., Hutchinson, D.S., Furness, F., Bengtsson, T., Evans, B.A., & Summers, R.J. (2012). Interaction with caveolin-1 modulates G protein coupling of the mouse β3-adrenoceptor. Journal of Biological Chemistry. 287:20674-88

Mattsson, C.L., Csikasz, R.I., Chernogubova, E., Yamamoto, D.L., Hogberg, H.,
Amri, E.Z., Hutchinson, D.S., & Bengtsson, T. (2011). β1-Adrenergic receptors increase UCP1 in human MADS brown adipocytes and rescue cold-acclimated β3-adrenergic receptor KO mice via nonshivering thermogenesis. American Journal of Physiology. 301:E1108-111