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Visa fullständig version : Ökad muskelmassa med injektioner av nanopartiklar


King Grub
2018-12-18, 12:02
Det här blir nästa stora dopningsmetod. Det finns ingen anledning till varför det inte skulle fungera på människan. Kraftig muskeltillväxt och förhindrade fettökningar, även utan träning, genom att manipulera mRNA. Det här är första gången man utför det i praktiken, och det fungerade.

Muscle atrophy occurs during chronic diseases, resulting in diminished quality of life and compromised treatment outcomes. There is a high demand for therapeutics that increase muscle mass while abrogating the need for special dietary and exercise requirements. Therefore, we developed an efficient nanomedicine approach capable of increasing muscle mass.

Methods:

The therapy is based on nanoparticle-mediated delivery of follistatin messenger RNA (mRNA) to the liver after subcutaneous administration. The delivered mRNA directs hepatic cellular machinery to produce follistatin, a glycoprotein that increases lean mass through inhibition of negative regulators of muscle mass (myostatin and activin A). These factors are elevated in numerous disease states, thereby providing a target for therapeutic intervention.

Results:

Animal studies validated that mRNA-loaded nanoparticles enter systemic circulation following subcutaneous injection, accumulate and internalize in the liver, where the mRNA is translated into follistatin. Follistatin serum levels were elevated for 72 h post injection and efficiently reduced activin A and myostatin serum concentrations. After eight weeks of repeated injections, the lean mass of mice in the treatment group was ~10% higher when compared to that of the controls.

Conclusion:

Based on the obtained results demonstrating an increased muscle mass as well as restricted fat accumulation, this nanoplatform might be a milestone in the development of mRNA technologies and the treatment of muscle wasting disorders.

Theranostics. 2018 Oct 22;8(19):5276-5288. Increasing lean muscle mass in mice via nanoparticle-mediated hepatic delivery of follistatin mRNA.

Lucipha
2018-12-18, 12:41
Coolt! När det är testat i 10 år utan feta bieffekter vill jag prova

Xtreme-G
2018-12-18, 12:44
Wow, detta är ju inte minst ett medicinskt genombrott!

Diomedea exulans
2018-12-18, 12:45
https://media.balls.ie/uploads/2014/12/6a0133ec991857970b01901ddb1a17970b.jpg

exevision
2018-12-18, 12:46
Min första tanke är "Cancer?"

Diomedea exulans
2018-12-18, 12:48
Min första tanke är "Cancer?"

Och hur blir det med hjärtat, musklerna i innerörat, tungan osv?

King Grub
2018-12-18, 12:51
Att minska myostatinnivåerna förhindrar kakeksi och tumörtillväxt.

http://cancerres.aacrjournals.org/content/74/24/7344

Anders The Peak
2018-12-18, 13:35
Antagligen redan beprövat inom cirkusen.

Context: Follistatin is a plasma protein recently reported to increase under conditions with negative energy balance such as exercise and fasting in humans. Currently, the perception is that circulating follistatin is a result of para/autocrine actions from various tissues. The large and acute increase in circulating follistatin in response to exercise suggests that it may function as an endocrine signal. Objective: Here, we assessed origin and regulation of circulating follistatin in humans. Design /interventions: First, we assessed arterial-to-venous difference of follistatin over the splanchnic bed at rest and during exercise in healthy humans. To evaluate the regulation of plasma follistatin we manipulated glucagon-to-insulin ratio in humans at rest, as well as in cultured hepatocytes. Finally, the impact of follistatin on human islets of Langerhans was assessed. Results: We demonstrate that in humans the liver is a major contributor to circulating follistatin both at rest and during exercise. Glucagon increases and insulin inhibits follistatin secretion both in vivo and in vitro mediated via the secondary messenger cAMP in the hepatocyte. Short-term follistatin treatment reduced glucagon secretion from islets of Langerhans, whereas long-term follistatin treatment prevented apoptosis and induced proliferation of rat β-cells. Conclusions: In conclusion, in humans, the liver secretes follistatin at rest and during exercise and the glucagon-to-insulin ratio is a key determinant of circulating follistatin levels. Circulating follistatin may be a marker of the glucagon-to-insulin tone on the liver.