Sustained inhibition of NPY/AgRP neuronal activity by FGF1

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

Standard

Sustained inhibition of NPY/AgRP neuronal activity by FGF1. / Hwang, Eunsang; Scarlett, Jarrad M.; Baquero, Arian F.; Bennett, Camdin M.; Dong, Yanbin; Chau, Dominic; Brown, Jenny M.; Mercer, Aaron J.; Meek, Thomas H.; Grove, Kevin L.; Phan, Bao Anh N.; Morton, Gregory J.; Williams, Kevin W.; Schwartz, Michael W.

In: JCI insight, Vol. 7, No. 17, e160891, 2022.

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

Harvard

Hwang, E, Scarlett, JM, Baquero, AF, Bennett, CM, Dong, Y, Chau, D, Brown, JM, Mercer, AJ, Meek, TH, Grove, KL, Phan, BAN, Morton, GJ, Williams, KW & Schwartz, MW 2022, 'Sustained inhibition of NPY/AgRP neuronal activity by FGF1', JCI insight, vol. 7, no. 17, e160891. https://doi.org/10.1172/jci.insight.160891

APA

Hwang, E., Scarlett, J. M., Baquero, A. F., Bennett, C. M., Dong, Y., Chau, D., Brown, J. M., Mercer, A. J., Meek, T. H., Grove, K. L., Phan, B. A. N., Morton, G. J., Williams, K. W., & Schwartz, M. W. (2022). Sustained inhibition of NPY/AgRP neuronal activity by FGF1. JCI insight, 7(17), [e160891]. https://doi.org/10.1172/jci.insight.160891

Vancouver

Hwang E, Scarlett JM, Baquero AF, Bennett CM, Dong Y, Chau D et al. Sustained inhibition of NPY/AgRP neuronal activity by FGF1. JCI insight. 2022;7(17). e160891. https://doi.org/10.1172/jci.insight.160891

Author

Hwang, Eunsang ; Scarlett, Jarrad M. ; Baquero, Arian F. ; Bennett, Camdin M. ; Dong, Yanbin ; Chau, Dominic ; Brown, Jenny M. ; Mercer, Aaron J. ; Meek, Thomas H. ; Grove, Kevin L. ; Phan, Bao Anh N. ; Morton, Gregory J. ; Williams, Kevin W. ; Schwartz, Michael W. / Sustained inhibition of NPY/AgRP neuronal activity by FGF1. In: JCI insight. 2022 ; Vol. 7, No. 17.

Bibtex

@article{2585c74c17d24791b9a32285afb84d28,
title = "Sustained inhibition of NPY/AgRP neuronal activity by FGF1",
abstract = "In rodent models of type 2 diabetes (T2D), central administration of FGF1 normalizes elevated blood glucose levels in a manner that is sustained for weeks or months. Increased activity of NPY/ AgRP neurons in the hypothalamic arcuate nucleus (ARC) is implicated in the pathogenesis of hyperglycemia in these animals, and the ARC is a key brain area for the antidiabetic action of FGF1. We therefore sought to determine whether FGF1 inhibits NPY/AgRP neurons and, if so, whether this inhibitory effect is sufficiently durable to offer a feasible explanation for sustained diabetes remission induced by central administration of FGF1. Here, we show that FGF1 inhibited ARC NPY/AgRP neuron activity, both after intracerebroventricular injection in vivo and when applied ex vivo in a slice preparation; we also showed that the underlying mechanism involved increased input from presynaptic GABAergic neurons. Following central administration, the inhibitory effect of FGF1 on NPY/AgRP neurons was also highly durable, lasting for at least 2 weeks. To our knowledge, no precedent for such a prolonged inhibitory effect exists. Future studies are warranted to determine whether NPY/AgRP neuron inhibition contributes to the sustained antidiabetic action elicited by intracerebroventricular FGF1 injection in rodent models of T2D.",
author = "Eunsang Hwang and Scarlett, {Jarrad M.} and Baquero, {Arian F.} and Bennett, {Camdin M.} and Yanbin Dong and Dominic Chau and Brown, {Jenny M.} and Mercer, {Aaron J.} and Meek, {Thomas H.} and Grove, {Kevin L.} and Phan, {Bao Anh N.} and Morton, {Gregory J.} and Williams, {Kevin W.} and Schwartz, {Michael W.}",
note = "Publisher Copyright: {\textcopyright} 2022, Hwang et al. This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License.",
year = "2022",
doi = "10.1172/jci.insight.160891",
language = "English",
volume = "7",
journal = "JCI Insight",
issn = "2379-3708",
publisher = "American Society for Clinical Investigation",
number = "17",

}

RIS

TY - JOUR

T1 - Sustained inhibition of NPY/AgRP neuronal activity by FGF1

AU - Hwang, Eunsang

AU - Scarlett, Jarrad M.

AU - Baquero, Arian F.

AU - Bennett, Camdin M.

AU - Dong, Yanbin

AU - Chau, Dominic

AU - Brown, Jenny M.

AU - Mercer, Aaron J.

AU - Meek, Thomas H.

AU - Grove, Kevin L.

AU - Phan, Bao Anh N.

AU - Morton, Gregory J.

AU - Williams, Kevin W.

AU - Schwartz, Michael W.

N1 - Publisher Copyright: © 2022, Hwang et al. This is an open access article published under the terms of the Creative Commons Attribution 4.0 International License.

PY - 2022

Y1 - 2022

N2 - In rodent models of type 2 diabetes (T2D), central administration of FGF1 normalizes elevated blood glucose levels in a manner that is sustained for weeks or months. Increased activity of NPY/ AgRP neurons in the hypothalamic arcuate nucleus (ARC) is implicated in the pathogenesis of hyperglycemia in these animals, and the ARC is a key brain area for the antidiabetic action of FGF1. We therefore sought to determine whether FGF1 inhibits NPY/AgRP neurons and, if so, whether this inhibitory effect is sufficiently durable to offer a feasible explanation for sustained diabetes remission induced by central administration of FGF1. Here, we show that FGF1 inhibited ARC NPY/AgRP neuron activity, both after intracerebroventricular injection in vivo and when applied ex vivo in a slice preparation; we also showed that the underlying mechanism involved increased input from presynaptic GABAergic neurons. Following central administration, the inhibitory effect of FGF1 on NPY/AgRP neurons was also highly durable, lasting for at least 2 weeks. To our knowledge, no precedent for such a prolonged inhibitory effect exists. Future studies are warranted to determine whether NPY/AgRP neuron inhibition contributes to the sustained antidiabetic action elicited by intracerebroventricular FGF1 injection in rodent models of T2D.

AB - In rodent models of type 2 diabetes (T2D), central administration of FGF1 normalizes elevated blood glucose levels in a manner that is sustained for weeks or months. Increased activity of NPY/ AgRP neurons in the hypothalamic arcuate nucleus (ARC) is implicated in the pathogenesis of hyperglycemia in these animals, and the ARC is a key brain area for the antidiabetic action of FGF1. We therefore sought to determine whether FGF1 inhibits NPY/AgRP neurons and, if so, whether this inhibitory effect is sufficiently durable to offer a feasible explanation for sustained diabetes remission induced by central administration of FGF1. Here, we show that FGF1 inhibited ARC NPY/AgRP neuron activity, both after intracerebroventricular injection in vivo and when applied ex vivo in a slice preparation; we also showed that the underlying mechanism involved increased input from presynaptic GABAergic neurons. Following central administration, the inhibitory effect of FGF1 on NPY/AgRP neurons was also highly durable, lasting for at least 2 weeks. To our knowledge, no precedent for such a prolonged inhibitory effect exists. Future studies are warranted to determine whether NPY/AgRP neuron inhibition contributes to the sustained antidiabetic action elicited by intracerebroventricular FGF1 injection in rodent models of T2D.

U2 - 10.1172/jci.insight.160891

DO - 10.1172/jci.insight.160891

M3 - Journal article

C2 - 35917179

AN - SCOPUS:85137664478

VL - 7

JO - JCI Insight

JF - JCI Insight

SN - 2379-3708

IS - 17

M1 - e160891

ER -

ID: 320649792