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

Pyrrhus

Senior Member
Messages
4,172
Location
U.S., Earth
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

Senior Member
Messages
302
Location
New Zealand
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

Senior Member
Messages
302
Location
New Zealand
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.