A possible role for mitochondrial-derived peptides humanin and MOTS-c in patients with Q fever fatigue syndrome and CFS (Raijmakers et al 2019)

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J Transl Med. 2019 May 14;17(1):157. doi: 10.1186/s12967-019-1906-3.
A possible role for mitochondrial-derived peptides humanin and MOTS-c in patients with Q fever fatigue syndrome and chronic fatigue syndrome.
Raijmakers RPH1,2, Jansen AFM3,4, Keijmel SP3,4, Ter Horst R4, Roerink ME4, Novakovic B5,6, Joosten LAB3,4,7, van der Meer JWM3,4, Netea MG3,4,7, Bleeker-Rovers CP3,4,7.
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Abstract
BACKGROUND:
Q fever fatigue syndrome (QFS) is a well-documented state of prolonged fatigue following around 20% of acute Q fever infections. It has been hypothesized that low grade inflammation plays a role in its aetiology. In this study, we aimed to identify transcriptome profiles that could aid to better understand the pathophysiology of QFS.
METHODS:
RNA of monocytes was collected from QFS patients (n = 10), chronic fatigue syndrome patients (CFS, n = 10), Q fever seropositive controls (n = 10), and healthy controls (n = 10) who were age- (± 5 years) and sex-matched. Transcriptome analysis was performed using RNA sequencing.
RESULTS:
Mitochondrial-derived peptide (MDP)-coding genes MT-RNR2 (humanin) and MT-RNR1 (MOTS-c) were differentially expressed when comparing QFS (- 4.8 log2-fold-change P = 2.19 × 10-9 and - 4.9 log2-fold-change P = 4.69 × 10-8), CFS (- 5.2 log2-fold-change, P = 3.49 × 10-11 - 4.4 log2-fold-change, P = 2.71 × 10-9), and Q fever seropositive control (- 3.7 log2-fold-change P = 1.78 × 10-6 and - 3.2 log2-fold-change P = 1.12 × 10-5) groups with healthy controls, resulting in a decreased median production of humanin in QFS patients (371 pg/mL; Interquartile range, IQR, 325-384), CFS patients (364 pg/mL; IQR 316-387), and asymptomatic Q fever seropositive controls (354 pg/mL; 292-393).
CONCLUSIONS:
Expression of MDP-coding genes MT-RNR1 (MOTS-c) and MT-RNR2 (humanin) is decreased in CFS, QFS, and, to a lesser extent, in Q fever seropositive controls, resulting in a decreased production of humanin. These novel peptides might indeed be important in the pathophysiology of both QFS and CFS.
 

ljimbo423

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I've definitely not felt like a humanin much since I got ME. Does anyone know what this substance does?
Research
Experiments using cultured cells have demonstrated that humanin has both neuroprotective as well as cytoprotective effects and experiments in rodents have found that it has protective effects in Alzheimer's disease models, Huntington's disease models and stroke models.[13]

Humanin is proposed to have myriad neuroprotective and cytoprotective effects. Both studies in cells and rodents have both found that administration of humanin or humanin derivatives increases survival and/or physiological parameters in Alzheimer's disease models.[14][15]

In addition to Alzheimer's disease, humanin has other neuroprotective effects against models of Huntington's disease, prion disease, and stroke.[16][17][18] Beyond the possible neuroprotective effects, humanin protects against oxidative stress, atherosclerotic plaque formation, and heart attack.[19][20][21][22]

Metabolic effects have also been demonstrated and humanin helps improve survival of pancreatic beta-cells, which may help with type 1 diabetes,[23] and increases insulin sensitivity, which may help with type 2 diabetes.[24] In rats, the humanin analog appears to normalize glucose levels and reduce diabetes symptoms.[25]

Rattin shows the same ability as humanin to defend neurons from the toxicity of beta-amyloid, the cause of degeneration in Alzheimer's Disease.[6]

Small humanin-like peptides are a group of peptides found in the mitochondrial 16S rRNA, and also possess retrograde signaling functions.
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