AI Article Synopsis
- The brain can help sustain lower blood sugar levels in rats with type 2 diabetes after injecting a protein called FGF1 directly into the brain.
- This effect is linked to long-lasting activity in specific brain signaling pathways (ERK1/2) that last over 24 hours.
- Using a modified version of FGF1 that only has a short-lived effect on these pathways does not produce the same beneficial impact on blood sugar, highlighting the importance of sustained signaling for diabetes remission.
Article 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8368994 | PMC |
| http://dx.doi.org/10.1016/j.isci.2021.102944 | DOI Listing |
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