Would increased IGF and GH due to training affect both muscle cells as well as adipocyte cells?
Would insuline-like growth factor and growth hormon have affect on both types of cell after training? For instance stimulate mTOR in both tissues? OR would there be only effect in muscle, due to alterations (which ones?).
Thanks
All tissues that express the IGF and GH receptors could potentially be directly affected by increased levels of IGF and GH, not to mention all the secondary effects that might have.
Peter: On top of what Dr. Meister said about cells expressing receptors for IGF and GH that can be affected by the increased expression of the two hormones, I'd like to bring to your attention that another "hormone"-like protein simultaneously expressed along with IGF: Spp24 (aka "secreted phosphoprotein-24 kDa"). Both Spp24 and IGF are produced by the hepatocytes and other cells in response to GH, and are involved in bone metabolism and growth.
Thanks to both, the reason for my question is that training leads to increase of hormones or cytokines (myokines). They could go to receptors in all tissues, so if an adipocyte would have a receptor it would for instance promote AKT and mTOR in the adipocyte, which would see (I assume) different opposites effects. So how would GF go to muscle cells in stead of adipocytes? For instance would GH not affect also the hepatocytes, with different effects as would be in case of the muscle cells.
"They could go to receptors in all tissues,..."
- and they will go to the receptors in all the tissues. By definition, myokines are released from skeletal muscle cells, and once they are in the system (blood stream), they will reach all the peripheral tissues (and act on them) and the CNS, if they can penetrate the blood-brain barrier.
The effects that you will see, e.g. after exercise, are a total of autocrine, paracrine and endocrine actions of the released hormones across the body. You always have to assume, that there is an organ crosstalk.
The effect in the specific cell after receptor stimulation will depend on the pathway, that receptor regulate in this cell type (which depends on the function and 'equipment' of the cell type).
Because you mentioned mTOR, look at Figure 4 at this reviewArticle mTOR Signaling in Growth, Metabolism, and Disease
. It shows you the multiple effects that activation of mTORC has.Or look for some papers/reviews on myokines. I just came across this one Article Myokines in metabolic homeostasis and diabetes
, but there tons of them.Hope, that helps.
thanks, yes my point was that if mTOR activity is positive in one tissue, it can be negative in another, so perhaps positives from pysical activity might have opposites effects...so I would assume there is a kind of down-regulation of receptors or blockages (perhaps miRNA) that would prevent opposites effect. For instance if GH might have an effect on adipocytes to form more TG through mTOR that would not make sense as PA would led skeletal muscle to 'burn' TG. So you would lose TG but gain them also (not assuming it works like that, just as an example). So something must be preventing tissues from having or forming more receptors. For instance, glut 4 can be blocked to prevent glucose influx in cells, so perhaps that would be a way to communicate intra- and intercellular. Anyway much to read, so thanks again.
I would not necessarily call it "opposite effects", since the effects, you describe, might not happen at the same time. You have to consider the kinetic aspect as well. For example, lipogenesis will only happen if the pathway is stimulated AND there are enough 'substrates' for synthesis. Exercise uses a lot of energy. Evolutionary, the body wants to preserve and store energy for nutrition-wise 'bad times'. So actual lipogenesis might come later after exercise, since the pathway in the adipocytes might take longer...
Its important also to explain the role of insulin in this context. IGF-1 is significantly regulated by growth hormone, while insulin regulates IGF-I production from the liver modulating the GH receptor. Most IGF-1 is secreted by the liver and act as an endocrine hormone. IGF-1 take part in cell substrate metabolism besides an important role in regulating cell proliferation and apoptosis.
Insulin regulates cellular energy supply and macronutrient balance
and direct anabolic processes of the fed state. Insulin is essential for the
intracellular transport of glucose into insulin dependent tissues such as
skeletal muscle, adipose tissue and liver.
But IGF-1 can activate mTOR which will lead to adipocyte diff + genesis en lipid accumulation in adipocytes, through PPAR. So with IGF-1 in the blood it can be anabolic in the muscle, but also in adipocytes. So there might be hypertrophy in muscle and adipocytes. So training, increasing GH and IGF-1 with intention to increase muscle mass, can also increase fat mass. So how would that be regulated? As been said it can be time dependent...
Your answer is a straight one - increased exercise will increase GH levels and increase muscle mass (assuming you are not consuming excess calories that need to be converted to fat) but GH will also decrease fat deposition. It changes body composition. Look at transgenic pigs with extra GH - lean with virtually no fat. Look at cattle with GH administration - fat stores are preferentially tapped for energy and milk production. Sprague-Dawley rats (fed a moderately high fat diet diverge into 2 populations - obese and obesity resistant. The resistant (i.e. lean) rats have a higher GH production than the obese rats (this is before the diet was fed). So GH was actually protective in this model against obesity. There is lots out there. I had an NIH grant 20 years ago looking at this.
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