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Irisin -- Is it a myth?

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http://www.medpagetoday.com/Endocrinology/Obesity/50500

 

http://www.nature.com/srep/2015/150309/srep08889/full/srep08889.html#close

 

 

It's beginning to look like the initial hype was based on misinterpreted results.

Shit, did I say "beginning"? There was some indication of this a couple of years ago: https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0033-1336630

 

Question is: Despite the fact that humans don't seem to produce functional Irisin, would it serve any role in humans? That is to say: Would exogenous administration prove beneficial?

 

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It still has some interesting data stuff, though also some conflicting.

 

Brain Plast. 2015;1(1):55-61. doi: 10.3233/BPL-150019.

FNDC5/irisin - their role in the nervous system and as a mediator for beneficial 
effects of exercise on the brain.

Wrann CD(1).

Author information: 
(1)Dana-Farber Cancer Institute and Department of Cell Biology, Harvard Medical
School, 44 Binney Street, Boston, MA 02115, USA.

Exercise can improve cognitive function and the outcome of neurodegenerative
diseases, like Alzheimer's disease. This effect has been linked to the increased 
expression of brain-derived neurotrophic factor (BDNF). However, the underlying
molecular mechanisms driving the elevation of this neurotrophin remain unknown.
Recently, we have reported a PGC-1α-FNDC5/irisin pathway, which is activated by
exercise in the hippocampus in mice and induces a neuroprotective gene program,
including Bdnf. This review will focus on FNDC5 and its secreted form "irisin", a
newly discovered myokine, and their role in the nervous system and its
therapeutic potential. In addition, we will briefly discuss the role of other
exercise-induced myokines on positive brain effects.

DOI: 10.3233/BPL-150019 
PMCID: PMC5419585
PMID: 28480165

 

Med Hypotheses. 2016 May;90:23-8. doi: 10.1016/j.mehy.2016.02.020. Epub 2016 Mar 
2.

FNDC5/irisin, a molecular target for boosting reward-related learning and
motivation.

Zsuga J(1), Tajti G(2), Papp C(2), Juhasz B(3), Gesztelyi R(4).

Interventions focusing on the prevention and treatment of chronic
non-communicable diseases are on rise. In the current article, we propose that
dysfunction of the mesocortico-limbic reward system contributes to the emergence 
of the WHO-identified risk behaviors (tobacco use, unhealthy diet, physical
inactivity and harmful use of alcohol), behaviors that underlie the evolution of 
major non-communicable diseases (e.g. cardiovascular diseases, cancer, diabetes
and chronic respiratory diseases). Given that dopaminergic neurons of the
mesocortico-limbic system are tightly associated with reward-related processes
and motivation, their dysfunction may fundamentally influence behavior. While
nicotine and alcohol alter dopamine neuron function by influencing some
receptors, mesocortico-limbic system dysfunction was associated with elevation of
metabolic set-point leading to hedonic over-eating. Although there is some
empirical evidence, precise molecular mechanism for linking physical inactivity
and mesocortico-limbic dysfunction per se seems to be missing; identification of 
which may contribute to higher success rates for interventions targeting
lifestyle changes pertaining to physical activity. In the current article, we
compile evidence in support of a link between exercise and the mesocortico-limbic
system by elucidating interactions on the axis of muscle - irisin - brain derived
neurotrophic factor (BDNF) - and dopaminergic function of the midbrain. Irisin is
a contraction-regulated myokine formed primarily in skeletal muscle but also in
the brain. Irisin stirred considerable interest, when its ability to induce
browning of white adipose tissue parallel to increasing thermogenesis was
discovered. Furthermore, it may also play a role in the regulation of behavior
given it readily enters the central nervous system, where it induces BDNF
expression in several brain areas linked to reward processing, e.g. the ventral
tegmental area and the hippocampus. BDNF is a neurotropic factor that increases
neuronal dopamine content, modulates dopamine release relevant for neuronal
plasticity and increased neuronal survival as well as learning and memory.
Further linking BDNF to dopaminergic function is BDNF's ability to activate
tropomyosin-related kinase B receptor that shares signalization with presynaptic 
dopamine-3 receptors in the ventral tegmental area. Summarizing, we propose that 
the skeletal muscle derived irisin may be the link between physical activity and 
reward-related processes and motivation. Moreover alteration of this axis may
contribute to sedentary lifestyle and subsequent non-communicable diseases.
Preclinical and clinical experimental models to test this hypothesis are also
proposed.

Copyright © 2016 Elsevier Ltd. All rights reserved.

DOI: 10.1016/j.mehy.2016.02.020 
PMID: 27063080  [Indexed for MEDLINE]

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