Four years later, the study to treat type 2 diabetes finally had a sequel.

Back in 2016, researchers at the University of Washington in the United States published a study in Nature Medicine that showed that in rodent models with type 2 diabetes, a single injection of fibroblast growth factor 1 (FGF1) in the brain continued to relieve hyperglycemia (the blood sugar level of 200 mg/dl was maintained for 17 weeks).
anti-diabetes effect is not a secondary effect of weight loss, nor does it increase the risk of hypoglycemia, but increases the ability to remove glucose from the blood.
, however, the mechanisms for such a role are not yet clear.
when it comes to fibroblast growth factors, we should be no strangers.
modern surgery and cosmetic surgery, you cut the double eyelids after the face repair may have its credit.
if an injection of FGF1 allows the body to remove glucose on its own and continues to function, it is bound to alleviate the pain of the patient's inseating medication and avoid the side effects of taking it.
four years after the study, the research finally made new progress and was re-published in nature Communications, a sub-issue of Nature.
previous study, the team found that the inner base base (MBH) of the hypothyclycermic brain is the brain region responsible for the continuous relief of high blood sugar in FGF1 in the brain.
In this way, after an in-depth study of MBE's response to FGF1 cells, they found that hypothycline nerve glial cells were the main target of FGF1's action, and that continuous diabetes relief depended on complete black cortical signaling.
specifically, the researchers combined the discovery of transcriptomic methods with tissue chemistry, electron microscopes, and pharmacological and physiological studies in the body to explore why the brains of diabetic animals have the ability to continuously improve high blood sugar.
results were surprising, with transcription and morphological changes in both monocytes and astrocytes in the days after FGF1 injections in the brain. the expression of
elongation cell modules mapped to the spatial distribution of the third brain chamber Changes in the response of astrological glial cells to injection of FGF1 in the brain at the ultra-microstructure level, an increase in astrocyte coverage of synhapus buttons was detected in the dexterous ratchets of ARC neurons, including Agrp neurons.
injection of FGF1 in the brain, the transcriptional group of Agrp neurons also undergone strong changes, including continued inhibition of gene expression in Agrp and Npy.
the relationship between these neurons may be unfamiliar, explained here.
brain contains a variety of specific neurons that perform different functions to regulate the body's behavior and metabolic balance.
the bow nucleus (ARC) of the hypothyroids contains two main types of neurons that regulate metabolism: those that suppress appetite, such as those of ahexinogen (POMC), and those that promote appetite, including neuropeptide Y (Npy) and agrp neurons.
and FGF1's suppression of appetite-promoting neurons in the brain will cause patients to eat less.
the effects of intra-brain injection of FGF1 on Agrp neurons Several studies have shown that the decrease in the conduction of black cortical signaling is associated with the pathogenesis of diabetes in rodents and humans, while Agrp neurons are endogenous inhibitors of black cortical signaling.
, the researchers looked at whether FGF1's continued anti-diabetic effects depended on complete black cortical signaling.
found that although initial anorexia and blood sugar reduction did not require complete black cortical signaling, it was necessary for the persistent anti-diabetic effect induced by intra-brain injections of FGF1.
FGF1-induced persistent diabetes relief is black cortical dependence These observations suggest that the effects of FGF1 on glial cells may alter the function of Agrp neurons, so additional work is needed to assess this possibility.
If the above inference is true, then the continuous sugar-lowering effect of central FGF1 may regulate one or more types of glial cells in the healing brain, which in turn alters the function of the sugar-regulated neural circuit in a highly persistent way.
, this is a substantial therapeutic finding, and understanding the relationship between different cell responses to FGF1 and associated blood sugar normalization may reveal new strategies for sustained diabetes relief.
: [1] [2] #Ack1 [3] [4]