Are Circulating Fibroblast Growth Factor 21 & N-Terminal Prohormone of Brain Natriuretic Peptide Promising Biomarkers in ME/CFS? (Domingo et al, 2021)

Pyrrhus

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A new paper looking at blood markers of oxidative stress and inflammation in ME:

Are Circulating Fibroblast Growth Factor 21 and N-Terminal Prohormone of Brain Natriuretic Peptide Promising Novel Biomarkers in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome? (Domingo et al., 2021)
https://pubmed.ncbi.nlm.nih.gov/33353469/

Excerpt:
Domingo et al 2021 said:
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic, disabling, and complex multisystem illness of unknown etiology. The protein fibroblast growth factor 21 (FGF21) regulates glucose homeostasis and lipid metabolism, and the protein N-terminal prohormone of brain natriuretic peptide (NT-proBNP) is strongly associated with an elevated cardiovascular risk; however, little is known about their role in ME/CFS patients.

To address this gap, we explored the association between FGF21 and NT-proBNP and oxidative stress and inflammatory markers in ME/CFS. Twenty-one ME/CFS patients and 20 matched healthy controls were included in the study. Participants filled out validated self-reported questionnaires on their current health status covering demographic and clinical characteristics.

Plasma showed significantly decreased total antioxidant capacity and increased lipoperoxide levels (p = 0.009 and p = 0.021, respectively) in ME/CFS. These ME/CFS patients also had significantly increased levels of inflammatory cytokines (interleukin [IL]-1β, IL-6, IL-10, TNF-α, and C-reactive protein) (p < 0.05 for all) but not for IL-8 (p = 0.833), indicating low-grade systemic inflammation status.

Circulating FGF21 and NT-proBNP levels were significantly higher (p < 0.0001 and p = 0.005, respectively) in ME/CFS patients than in healthy controls. Significantly positive correlations were found between NT-proBNP levels and IL-1β and IL-6 (p = 0.04 and p = 0.01) in ME/CFS patients but not between FGF21 and these cytokines. In contrast, no significant correlations were found for either FGF21 or NT-proBNP in controls.

These findings lead to the hypothesis that elevated FGF21 and NT-proBNP levels and the association between NT-proBNP and inflammation may be promising novel diagnostic and therapeutic targets in ME/CFS.
(spacing and emphasis added for readability)
 

SNT Gatchaman

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I had my FGF21 checked and sadly it was in range.
There are two types of assay: total and bioactive. FGF21 can be rendered inactive by proteolysis of its N- and C- terminals (which are needed to bind to the FGFR co-receptor β-Klotho). FAP (fibroblast activation protein) is responsible for deactivating FGF21.

Total assays detect the mid-portion of the protein. Bioactive assays detect the N- or C- terminals. So I assume that depending on the assay used, you can look normal (or even high) but be functionally low.
 

SNT Gatchaman

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FGF21 physiology is complicated and incompletely characterised. It is a hormone related to starvation and overnutrition and has varying effects in multiple tissues depending on metabolic state.

Effector organs include liver, gut, pancreas, adipose tissue - and, importantly, brain including hypothalamus and brainstem/dorsal vagal complex.

I've posted some core papers under the fgf21 tag.