Role of hypothalamic MAPK/ERK signaling and central action of FGF1 in diabetes remission

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Role of hypothalamic MAPK/ERK signaling and central action of FGF1 in diabetes remission. / Brown, Jenny M.; Bentsen, Marie A.; Rausch, Dylan M.; Phan, Bao Anh; Wieck, Danielle; Wasanwala, Huzaifa; Matsen, Miles E.; Acharya, Nikhil; Richardson, Nicole E.; Zhao, Xin; Zhai, Peng; Secher, Anna; Morton, Gregory J.; Pers, Tune H.; Schwartz, Michael W.; Scarlett, Jarrad M.

In: iScience, Vol. 24, No. 9, 102944, 2021.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Brown, JM, Bentsen, MA, Rausch, DM, Phan, BA, Wieck, D, Wasanwala, H, Matsen, ME, Acharya, N, Richardson, NE, Zhao, X, Zhai, P, Secher, A, Morton, GJ, Pers, TH, Schwartz, MW & Scarlett, JM 2021, 'Role of hypothalamic MAPK/ERK signaling and central action of FGF1 in diabetes remission', iScience, vol. 24, no. 9, 102944. https://doi.org/10.1016/j.isci.2021.102944

APA

Brown, J. M., Bentsen, M. A., Rausch, D. M., Phan, B. A., Wieck, D., Wasanwala, H., Matsen, M. E., Acharya, N., Richardson, N. E., Zhao, X., Zhai, P., Secher, A., Morton, G. J., Pers, T. H., Schwartz, M. W., & Scarlett, J. M. (2021). Role of hypothalamic MAPK/ERK signaling and central action of FGF1 in diabetes remission. iScience, 24(9), [102944]. https://doi.org/10.1016/j.isci.2021.102944

Vancouver

Brown JM, Bentsen MA, Rausch DM, Phan BA, Wieck D, Wasanwala H et al. Role of hypothalamic MAPK/ERK signaling and central action of FGF1 in diabetes remission. iScience. 2021;24(9). 102944. https://doi.org/10.1016/j.isci.2021.102944

Author

Brown, Jenny M. ; Bentsen, Marie A. ; Rausch, Dylan M. ; Phan, Bao Anh ; Wieck, Danielle ; Wasanwala, Huzaifa ; Matsen, Miles E. ; Acharya, Nikhil ; Richardson, Nicole E. ; Zhao, Xin ; Zhai, Peng ; Secher, Anna ; Morton, Gregory J. ; Pers, Tune H. ; Schwartz, Michael W. ; Scarlett, Jarrad M. / Role of hypothalamic MAPK/ERK signaling and central action of FGF1 in diabetes remission. In: iScience. 2021 ; Vol. 24, No. 9.

Bibtex

@article{3c486065be724b0eab5803788962ee99,

title = "Role of hypothalamic MAPK/ERK signaling and central action of FGF1 in diabetes remission",

abstract = "The capacity of the brain to elicit sustained remission of hyperglycemia in rodent models of type 2 diabetes following intracerebroventricular (icv) injection of fibroblast growth factor 1 (FGF1) is well established. Here, we show that following icv FGF1 injection, hypothalamic signaling by extracellular signal-regulated kinases 1 and 2 (ERK1/2), members of the mitogen-activated protein kinase (MAPK) family, is induced for at least 24 h. Further, we show that this prolonged response is required for the sustained antidiabetic action of FGF1 since it is abolished by sustained (but not acute) pharmacologic blockade of hypothalamic MAPK/ERK signaling. We also demonstrate that FGF1 R50E, a FGF1 mutant that activates FGF receptors but induces only transient hypothalamic MAPK/ERK signaling, fails to mimic the sustained glucose lowering induced by FGF1. These data identify sustained activation of hypothalamic MAPK/ERK signaling as playing an essential role in the mechanism underlying diabetes remission induced by icv FGF1 administration.",

keywords = "Diabetology, Molecular biology, Molecular neuroscience",

author = "Brown, {Jenny M.} and Bentsen, {Marie A.} and Rausch, {Dylan M.} and Phan, {Bao Anh} and Danielle Wieck and Huzaifa Wasanwala and Matsen, {Miles E.} and Nikhil Acharya and Richardson, {Nicole E.} and Xin Zhao and Peng Zhai and Anna Secher and Morton, {Gregory J.} and Pers, {Tune H.} and Schwartz, {Michael W.} and Scarlett, {Jarrad M.}",

note = "Publisher Copyright: {\textcopyright} 2021 The Authors",

year = "2021",

doi = "10.1016/j.isci.2021.102944",

language = "English",

volume = "24",

journal = "iScience",

issn = "2589-0042",

publisher = "Elsevier",

number = "9",

}

RIS

TY - JOUR

T1 - Role of hypothalamic MAPK/ERK signaling and central action of FGF1 in diabetes remission

AU - Brown, Jenny M.

AU - Bentsen, Marie A.

AU - Rausch, Dylan M.

AU - Phan, Bao Anh

AU - Wieck, Danielle

AU - Wasanwala, Huzaifa

AU - Matsen, Miles E.

AU - Acharya, Nikhil

AU - Richardson, Nicole E.

AU - Zhao, Xin

AU - Zhai, Peng

AU - Secher, Anna

AU - Morton, Gregory J.

AU - Pers, Tune H.

AU - Schwartz, Michael W.

AU - Scarlett, Jarrad M.

PY - 2021

Y1 - 2021

N2 - The capacity of the brain to elicit sustained remission of hyperglycemia in rodent models of type 2 diabetes following intracerebroventricular (icv) injection of fibroblast growth factor 1 (FGF1) is well established. Here, we show that following icv FGF1 injection, hypothalamic signaling by extracellular signal-regulated kinases 1 and 2 (ERK1/2), members of the mitogen-activated protein kinase (MAPK) family, is induced for at least 24 h. Further, we show that this prolonged response is required for the sustained antidiabetic action of FGF1 since it is abolished by sustained (but not acute) pharmacologic blockade of hypothalamic MAPK/ERK signaling. We also demonstrate that FGF1 R50E, a FGF1 mutant that activates FGF receptors but induces only transient hypothalamic MAPK/ERK signaling, fails to mimic the sustained glucose lowering induced by FGF1. These data identify sustained activation of hypothalamic MAPK/ERK signaling as playing an essential role in the mechanism underlying diabetes remission induced by icv FGF1 administration.

AB - The capacity of the brain to elicit sustained remission of hyperglycemia in rodent models of type 2 diabetes following intracerebroventricular (icv) injection of fibroblast growth factor 1 (FGF1) is well established. Here, we show that following icv FGF1 injection, hypothalamic signaling by extracellular signal-regulated kinases 1 and 2 (ERK1/2), members of the mitogen-activated protein kinase (MAPK) family, is induced for at least 24 h. Further, we show that this prolonged response is required for the sustained antidiabetic action of FGF1 since it is abolished by sustained (but not acute) pharmacologic blockade of hypothalamic MAPK/ERK signaling. We also demonstrate that FGF1 R50E, a FGF1 mutant that activates FGF receptors but induces only transient hypothalamic MAPK/ERK signaling, fails to mimic the sustained glucose lowering induced by FGF1. These data identify sustained activation of hypothalamic MAPK/ERK signaling as playing an essential role in the mechanism underlying diabetes remission induced by icv FGF1 administration.

KW - Diabetology

KW - Molecular biology

KW - Molecular neuroscience

U2 - 10.1016/j.isci.2021.102944

DO - 10.1016/j.isci.2021.102944

M3 - Journal article

C2 - 34430821

AN - SCOPUS:85112585566

VL - 24

JO - iScience

JF - iScience

SN - 2589-0042

IS - 9

M1 - 102944

ER -

ID: 280176642