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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Anabolic Steroids: Effect on Muscle, Metabolism and the Heart
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<blockquote data-quote="madman" data-source="post: 191815" data-attributes="member: 13851"><p><strong>Fig. 1 <span style="color: rgb(184, 49, 47)">Genomic and non-genomic mechanisms of AAS induced skeletal muscle hypertrophy and mechanisms of insulin signalling and resistance. </span><span style="color: rgb(26, 188, 156)">Genomic pathway:</span> Androgen binding of the AR complex causes translocation to the nucleus following dissociation of heat shock proteins <span style="color: rgb(184, 49, 47)">(HSP)</span>. The androgen/AR complex regulates gene transcription on the androgen response element <span style="color: rgb(184, 49, 47)">(ARE)</span> of DNA. <span style="color: rgb(26, 188, 156)">Non-genomic pathway:</span> In addition to the AR, androgens can activate other membrane-bound receptors such as EGFR and SHBGR. This causes an increase in intracellular calcium <span style="color: rgb(184, 49, 47)">(Ca2+)</span>, activation of several second messengers signalling such as extracellular regulated kinases 1/2 <span style="color: rgb(184, 49, 47)">(ERK 1/2)</span>, protein kinase A <span style="color: rgb(184, 49, 47)">(PKA)</span>, calmodulin <span style="color: rgb(184, 49, 47)">(CaM)</span> and phosphatidylinositol-3- phosphate kinase <span style="color: rgb(184, 49, 47)">(PI3K)/</span><span style="color: rgb(0, 0, 0)">Akt/mTORc1</span> pathways and deactivation of myostatin pathway. Activation of these genomic and non-genomic pathways leads to skeletal muscle hypertrophy via upregulating gene transcription of anabolic genes, nutrient sensing, storage and transporting. While also upregulating satellite cell proliferation, differentiation, MPS and inhibiting muscle protein breakdown <span style="color: rgb(184, 49, 47)">(MPB)</span>. <span style="color: rgb(26, 188, 156)">Insulin/IGF-1 signalling pathway:</span> Insulin/IGF-1 bind to the insulin/IGF-1 receptor on the cell membrane inflicting tyrosine phosphorylation. The now activated receptor causes phosphorylation of insulin receptor substrate-1/2 <span style="color: rgb(184, 49, 47)">(IRS-1/2)</span> activating the PI3K/Akt signalling cascade leading to satellite cell proliferation; MPS via mTORc1, 4E-binding protein 1<span style="color: rgb(184, 49, 47)"> (4E BP1)</span> and p70 S6 kinase 1 <span style="color: rgb(184, 49, 47)">(S6K1)</span> activation; glucose uptake via GLUT4 translocation and inhibition of forkhead O transcription factor<span style="color: rgb(184, 49, 47)"> (FOXO)</span> leading to reduced MPB. Abnormal levels of circulating fatty acids and inflammatory cytokines result in serine/threonine phosphorylation of IRS-1 causing insulin resistance. </strong></p><p>[ATTACH=full]11934[/ATTACH]</p></blockquote><p></p>
[QUOTE="madman, post: 191815, member: 13851"] [B]Fig. 1 [COLOR=rgb(184, 49, 47)]Genomic and non-genomic mechanisms of AAS induced skeletal muscle hypertrophy and mechanisms of insulin signalling and resistance. [/COLOR][COLOR=rgb(26, 188, 156)]Genomic pathway:[/COLOR] Androgen binding of the AR complex causes translocation to the nucleus following dissociation of heat shock proteins [COLOR=rgb(184, 49, 47)](HSP)[/COLOR]. The androgen/AR complex regulates gene transcription on the androgen response element [COLOR=rgb(184, 49, 47)](ARE)[/COLOR] of DNA. [COLOR=rgb(26, 188, 156)]Non-genomic pathway:[/COLOR] In addition to the AR, androgens can activate other membrane-bound receptors such as EGFR and SHBGR. This causes an increase in intracellular calcium [COLOR=rgb(184, 49, 47)](Ca2+)[/COLOR], activation of several second messengers signalling such as extracellular regulated kinases 1/2 [COLOR=rgb(184, 49, 47)](ERK 1/2)[/COLOR], protein kinase A [COLOR=rgb(184, 49, 47)](PKA)[/COLOR], calmodulin [COLOR=rgb(184, 49, 47)](CaM)[/COLOR] and phosphatidylinositol-3- phosphate kinase [COLOR=rgb(184, 49, 47)](PI3K)/[/COLOR][COLOR=rgb(0, 0, 0)]Akt/mTORc1[/COLOR] pathways and deactivation of myostatin pathway. Activation of these genomic and non-genomic pathways leads to skeletal muscle hypertrophy via upregulating gene transcription of anabolic genes, nutrient sensing, storage and transporting. While also upregulating satellite cell proliferation, differentiation, MPS and inhibiting muscle protein breakdown [COLOR=rgb(184, 49, 47)](MPB)[/COLOR]. [COLOR=rgb(26, 188, 156)]Insulin/IGF-1 signalling pathway:[/COLOR] Insulin/IGF-1 bind to the insulin/IGF-1 receptor on the cell membrane inflicting tyrosine phosphorylation. The now activated receptor causes phosphorylation of insulin receptor substrate-1/2 [COLOR=rgb(184, 49, 47)](IRS-1/2)[/COLOR] activating the PI3K/Akt signalling cascade leading to satellite cell proliferation; MPS via mTORc1, 4E-binding protein 1[COLOR=rgb(184, 49, 47)] (4E BP1)[/COLOR] and p70 S6 kinase 1 [COLOR=rgb(184, 49, 47)](S6K1)[/COLOR] activation; glucose uptake via GLUT4 translocation and inhibition of forkhead O transcription factor[COLOR=rgb(184, 49, 47)] (FOXO)[/COLOR] leading to reduced MPB. Abnormal levels of circulating fatty acids and inflammatory cytokines result in serine/threonine phosphorylation of IRS-1 causing insulin resistance. [/B] [ATTACH type="full"]11934[/ATTACH] [/QUOTE]
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Clinical Use of Anabolics and Hormones
Clinical Use of Anabolics and Hormones
Anabolic Steroids: Effect on Muscle, Metabolism and the Heart
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