scholarly journals The Hypothalamic Arcuate Nucleus–Median Eminence Is a Target for Sustained Diabetes Remission Induced by Fibroblast Growth Factor 1

Diabetes ◽  
2019 ◽  
Vol 68 (5) ◽  
pp. 1054-1061 ◽  
Author(s):  
Jenny M. Brown ◽  
Jarrad M. Scarlett ◽  
Miles E. Matsen ◽  
Hong T. Nguyen ◽  
Anna L. Secher ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Median Eminence ◽  
Arcuate Nucleus ◽  
Diabetes Remission ◽  
Fibroblast Growth ◽  
Hypothalamic Arcuate Nucleus

A Single-Cell Transcriptomics Roadmap to Investigate Diabetes Remission Induced by the Central Action of Fibroblast Growth Factor-1 (FGF-1)

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 375-OR
Author(s):  
MARIE A. BENTSEN ◽  
DYLAN RAUSCH ◽  
JARRAD SCARLETT ◽  
KIMBERLY M. ALONGE ◽  
PASCAL N. TIMSHEL ◽  
...  
Keyword(s):  
Growth Factor ◽  
Single Cell ◽  
Fibroblast Growth Factor ◽  
Diabetes Remission ◽  
Central Action ◽  
Fibroblast Growth

1800-P: Transcriptomic Evidence of a Role for Neuron-Glia Interactions in Diabetes Remission Induced by the Central Action of Fibroblast Growth Factor 1 (FGF-1)

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1800-P
Author(s):  
MARIE A. BENTSEN ◽  
DYLAN RAUSCH ◽  
ZAMAN MIRZADEH ◽  
JARRAD SCARLETT ◽  
JENNY M. BROWN ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Diabetes Remission ◽  
Central Action ◽  
Fibroblast Growth

scholarly journals Role of Hypothalamic MAPK/ERK Signaling in Diabetes Remission Induced by the Central Action of Fibroblast Growth Factor 1

2021 ◽  
Author(s):  
Jenny M. Brown ◽  
Marie A. Bentsen ◽  
Dylan M. Rausch ◽  
Bao Anh Phan ◽  
Danielle Wieck ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Diabetes Remission ◽  
Erk Signaling ◽  
Central Action ◽  
Fibroblast Growth

scholarly journals Hypothalamic perineuronal net assembly is required for sustained diabetes remission induced by fibroblast growth factor 1 in rats

2020 ◽  
Vol 2 (10) ◽  
pp. 1025-1033 ◽  
Author(s):  
Kimberly M. Alonge ◽  
Zaman Mirzadeh ◽  
Jarrad M. Scarlett ◽  
Aric F. Logsdon ◽  
Jenny M. Brown ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Diabetes Remission ◽  
Fibroblast Growth ◽  
Perineuronal Net

Sustained Diabetes Remission Induced by the Central Action of Fibroblast Growth Factor-1 (FGF-1) Requires Activation of Integrin Receptor aνß3

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 373-OR
Author(s):  
JARRAD SCARLETT ◽  
JENNY M. BROWN ◽  
BAO ANH N. PHAN ◽  
EDDIE L. KHAV ◽  
MILES E. MATSEN ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Diabetes Remission ◽  
Central Action ◽  
Fibroblast Growth ◽  
Integrin Receptor

scholarly journals Fibroblast Growth Factor-1 Activates Neurons in the Arcuate Nucleus and Dorsal Vagal Complex

2021 ◽  
Vol 12 ◽  
Author(s):  
Brandon L. Roberts ◽  
Eric J. Kim ◽  
Sarah R. Lindsley ◽  
Katherine G. Tennant ◽  
Paul Kievit
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Arcuate Nucleus ◽  
Area Postrema ◽  
Physiological Role ◽  
Brain Regions ◽  
Dorsal Vagal Complex ◽  
Fibroblast Growth ◽  
Central Administration ◽  
Fgf Receptor

Central administration of fibroblast growth factor-1 (FGF1) results in long-lasting resolution of hyperglycemia in various rodent models, but the pre- and postsynaptic mechanisms mediating the central effects of FGF1 are unknown. Here we utilize electrophysiology recordings from neuronal populations in the arcuate nucleus of the hypothalamus (ARH), nucleus of the solitary tract (NTS), and area postrema (AP) to investigate the mechanisms underlying FGF1 actions. While FGF1 did not alter membrane potential in ARH-NPY-GFP neurons, it reversibly depolarized 83% of ARH-POMC-EGFP neurons and decreased the frequency of inhibitory inputs onto ARH-POMC-EGFP neurons. This depolarizing effect persisted in the presence of FGF receptor (R) blocker FIIN1, but was blocked by pretreatment with the voltage-gated sodium channel (VGSC) blocker tetrodotoxin (TTX). Non-FGF1 subfamilies can activate vascular endothelial growth factor receptors (VEGFR). Surprisingly, the VEGFR inhibitors axitinib and BMS605541 blocked FGF1 effects on ARH-POMC-EGFP neurons. We also demonstrate that FGF1 induces c-Fos in the dorsal vagal complex, activates NTS-NPY-GFP neurons through a FGFR mediated pathway, and requires VGSCs to activate AP neurons. We conclude that FGF1 acts in multiple brain regions independent of FGFRs. These studies present anatomical and mechanistic pathways for the future investigation of the pharmacological and physiological role of FGF1 in metabolic processes.

scholarly journals A Role for Fibroblast Growth Factor 19 and Bile Acids in Diabetes Remission After Roux-en-Y Gastric Bypass

Diabetes Care ◽  
2013 ◽  
Vol 36 (7) ◽  
pp. 1859-1864 ◽  
Author(s):  
G. S. Gerhard ◽  
A. M. Styer ◽  
G. C. Wood ◽  
S. L. Roesch ◽  
A. T. Petrick ◽  
...  
Keyword(s):  
Gastric Bypass ◽  
Growth Factor ◽  
Bile Acids ◽  
Fibroblast Growth Factor ◽  
Diabetes Remission ◽  
Fibroblast Growth ◽  
Fibroblast Growth Factor 19

scholarly journals Transcriptomic analysis links diverse hypothalamic cell types to fibroblast growth factor 1-induced sustained diabetes remission

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Marie A. Bentsen ◽  
Dylan M. Rausch ◽  
Zaman Mirzadeh ◽  
Kenjiro Muta ◽  
Jarrad M. Scarlett ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Cell Types ◽  
Diabetes Remission ◽  
Ependymal Cells ◽  
Sustained Remission ◽  
Fibroblast Growth ◽  
Transcriptional Responses ◽  
Wide Range ◽  
Melanocortin Signaling

Abstract In rodent models of type 2 diabetes (T2D), sustained remission of hyperglycemia can be induced by a single intracerebroventricular (icv) injection of fibroblast growth factor 1 (FGF1), and the mediobasal hypothalamus (MBH) was recently implicated as the brain area responsible for this effect. To better understand the cellular response to FGF1 in the MBH, we sequenced >79,000 single-cell transcriptomes from the hypothalamus of diabetic Lepob/ob mice obtained on Days 1 and 5 after icv injection of either FGF1 or vehicle. A wide range of transcriptional responses to FGF1 was observed across diverse hypothalamic cell types, with glial cell types responding much more robustly than neurons at both time points. Tanycytes and ependymal cells were the most FGF1-responsive cell type at Day 1, but astrocytes and oligodendrocyte lineage cells subsequently became more responsive. Based on histochemical and ultrastructural evidence of enhanced cell-cell interactions between astrocytes and Agrp neurons (key components of the melanocortin system), we performed a series of studies showing that intact melanocortin signaling is required for the sustained antidiabetic action of FGF1. These data collectively suggest that hypothalamic glial cells are leading targets for the effects of FGF1 and that sustained diabetes remission is dependent on intact melanocortin signaling.

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