About this Research Topic

Manuscript Submission Deadline 12 December 2022

It is widely accepted and well-documented that Fibroblast growth factor 21 (FGF21) is induced physiologically under a wide range of stressful conditions and seems to be the key signal which communicates and coordinates, the physiologic response to restore the metabolic homeostasis in different tissues. On the ...

It is widely accepted and well-documented that Fibroblast growth factor 21 (FGF21) is induced physiologically under a wide range of stressful conditions and seems to be the key signal which communicates and coordinates, the physiologic response to restore the metabolic homeostasis in different tissues. On the other hand, FGF21 is elevated in pathological conditions such as obesity, insulin resistance, or liver diseases where an impairment in its signalling has been described.

Many questions are still open regarding the metabolic role of FGF21 in humans, especially under nonpathological conditions. Some divergent data between mice and humans have been observed regarding the mechanisms that induce FGF21 expression, but also on its metabolic effects. While in mice short-term fasting and ketogenic diets increase FGF21 serum levels, in humans this induction was observed only after a very prolonged period of fasting (7–10 days). Furthermore, in humans, it seems that FGF21 is secreted under carbohydrate intake as a postprandial hormone produced under the insulin signal, after protein intake, or stimulated by exercise. Genetic studies in humans have associated some SNPs in and around the FGF21 gene with carbohydrates, protein, fat, and alcohol preferences. These differences also affect beta-Klotho (KLB) expression, a co-receptor for FGF21. Beyond the liver and adipose tissue, in humans, KLB is also detected in the breast, bone marrow, and pancreas and these differences may explain, at least in part, the differential metabolic effects of FGF21 in humans.

FGF21 analogues tested in overweight/obese patients with T2D can reduce dyslipidaemia and steatosis, but improvements in glycaemia or body weight were not globally obtained. Studies in humans show the involvement of FGF21 in dietary preferences, appetite, and lipid profile, and also described beta-Klotho (KLB), a co-receptor for FGF21, as a potential regulator of FGF21 action, and fibroblast activation protein (FAP) as a putative target to control FGF21 activity. As FGF21 is considered an attractive therapeutic target for obesity and obesity-related disorders, this Research Topic is interested in deepening our knowledge about the true potential of FGF21 either as a pharmacological target, or a therapeutic molecule, for treating obesity and insulin resistance in humans. Studies using animal and cellular models to explore FGF21 signalling in central and peripheral tissues will be also considered. This will give the opportunity for researchers to publish their most recent advances related to the molecular mechanisms upstream and downstream of the metabolic effects of FGF21, including its receptors and regulating proteins.

Obesity is a global pandemic that requires the urgent development of therapies and prevention strategies. To define new pharmacological or nutritional therapeutic approaches it is mandatory to find new targets. FGF21 is considered a potential target to treat obesity not just by directly impacting on it but also on its signalling pathways and regulatory mechanisms.

It is the scope of this Topic to publish the new advances involving FGF21, its signalling pathway and its regulatory mechanisms in the onset and development of obesity. We are looking for molecular data from animal and cellular models but also for human approaches that shed light to the real potential of FGF21 as a target for obesity treatment.

Results from the basic research, preclinical, or clinical fields, are all welcome, as well as reviews that comprehensively highlight new findings in the subject.

Keywords: FGF21; obesity; insulin resistance; human therapy; adipose tissue; signal transduction; metabolism


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