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Insulin-like growth factor-1 builds muscle (hypertrophy) and utilizes carbohydrates as fuel for energy.





[FONT=Minion W08 Regular_1167271]We characterized the metabolic profile of transgenic mice exhibiting enhanced muscle mass driven by increased mIGF-1 expression (MLC/mIGF-1). As expected, 6-month-old MLC/mIGF-1 mice were heavier than age-matched wild type (WT) mice (37.4 ± 0.3 versus 31.8 ± 0.6 g, resp.). MLC/mIGF-1 mice had higher respiratory quotient when compared to WT (0.9 ± 0.03 versus 0.74 ± 0.02, resp.) suggesting a preference for carbohydrate as the major fuel source.

MLC/mIGF-1 mice had a higher rate of glucose disposal when compared to WT (3.25 ± 0.14 versus 2.39 ± 0.03%/min, resp.). The higher disposal rate correlated to ∼2-fold higher GLUT4 content in the extensor digitorum longus (EDL) muscle. Analysis of mRNA content for the glycolysis-related gene PFK-1 showed ∼3-fold upregulation in MLC/mIGF-1 animals. We also found a 50% downregulation of PGC1α mRNA levels in MLC/mIGF-1 mouse EDL muscle, suggesting less abundant mitochondria in this tissue.

We found no difference in the expression of PPARα and PPARβ/δ, suggesting no modulation of key elements in oxidative metabolism. These data together suggest a shift in metabolism towards higher carbohydrate utilization, and that could explain the increased insulin sensitivity of hypertrophied skeletal muscle in MLC/mIGF-1 mice.

[/FONT]
1. Introduction

[FONT=Minion W08 Regular_1167271]One of the remarkable features of skeletal muscle is the capacity to adapt its metabolic and functional properties in response to a wide range of external factors, including physical and neuron activity, change in hormone levels, and oxygen and nutrient supply

However in several pathological conditions, skeletal muscle severely decreases this adaptive capacity, triggering alterations in its metabolic properties evolving to disease. In fact, insulin resistance (IR), obesity, high blood pressure, high fasting glucose or hyperglycemia, and lipid abnormalities are all conditions related to morphofunctional and metabolic changes in skeletal muscle

[/FONT]
[FONT=Minion W08 Regular_1167271]Recent evidences have shown that different therapeutic interventions can improve body composition and systemic metabolism

Among these, physical activity has been considered in the therapeutic effects of exercise for type II diabetes (T2DM) and other metabolic syndromes , although regular physical activity as a therapeutic tool can be seriously assumed in only a fraction of the population, mainly due to motivational and physical limitations.


From a metabolic point of view, however, it remains not well understood what molecular/cellular aspects of exercise should be mimicked and what type of muscle fiber is best targeted to improve metabolic dysfunction. Increased physical activity is usually achieved by exercise training, which can be divided into two major categories: endurance and resistance. It is well known that endurance training promotes metabolic alterations in skeletal muscle due to a shift in substrate preference as a consequence of fatty acid oxidative metabolism and muscle fiber type interconversion, resulting in a greater number of the slow twitch oxidative fibers

. In contrast, resistance training is known for its capacity to promote an increase in skeletal muscle mass (hypertrophy) and strength

. Nonetheless, the molecular factors linking skeletal muscle growth and metabolism still remain to be explored in detail. Among growth factors, the Insulin-like growth factor-1 (IGF-1) has been implicated in the control of both muscle mass and skeletal muscle homeostasis and its expression is significantly enhanced in response to exercise

.[/FONT]
[FONT=Minion W08 Regular_1167271]It has been previously reported that muscle restricted mIGF-1 transgene (MLC/mIGF-1) sustains muscle hypertrophy and regeneration in senescent skeletal muscle, enhances the recruitment of circulating stem cells in injured muscle and counteracts muscle wasting in mdx dystrophic mice , improving muscle mass and strength and elevating pathways associated with muscle survival and regeneration.

Although significant advances have been made with this genetic model, overall, the impact of manipulating skeletal muscle hypertrophic pathways upon whole body metabolism and glucose disposal is largely unknown.[/FONT]
[FONT=Minion W08 Regular_1167271]In the present study, we investigated metabolic features of MLC/mIGF-1 mice, revealing an unexpected higher respiratory quotient at rest, an index of higher carbohydrate utilization. These animals also showed higher insulin sensitivity, in line with a preference for carbohydrate as the primary energy source. In addition we have detected increased GLUT4 protein levels in skeletal muscle. These findings reinforce the potential of manipulating IGF-1 triggered intracellular pathways as therapeutic tools in the treatment of insulin resistance and type II diabetes.[/FONT]
 
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Insulin-like growth factor-1 builds muscle (hypertrophy) and utilizes carbohydrates as fuel for energy.





[FONT=Minion W08 Regular_1167271]We characterized the metabolic profile of transgenic mice exhibiting enhanced muscle mass driven by increased mIGF-1 expression (MLC/mIGF-1). As expected, 6-month-old MLC/mIGF-1 mice were heavier than age-matched wild type (WT) mice (37.4 ± 0.3 versus 31.8 ± 0.6 g, resp.). MLC/mIGF-1 mice had higher respiratory quotient when compared to WT (0.9 ± 0.03 versus 0.74 ± 0.02, resp.) suggesting a preference for carbohydrate as the major fuel source.

MLC/mIGF-1 mice had a higher rate of glucose disposal when compared to WT (3.25 ± 0.14 versus 2.39 ± 0.03%/min, resp.). The higher disposal rate correlated to ∼2-fold higher GLUT4 content in the extensor digitorum longus (EDL) muscle. Analysis of mRNA content for the glycolysis-related gene PFK-1 showed ∼3-fold upregulation in MLC/mIGF-1 animals. We also found a 50% downregulation of PGC1α mRNA levels in MLC/mIGF-1 mouse EDL muscle, suggesting less abundant mitochondria in this tissue.

We found no difference in the expression of PPARα and PPARβ/δ, suggesting no modulation of key elements in oxidative metabolism. These data together suggest a shift in metabolism towards higher carbohydrate utilization, and that could explain the increased insulin sensitivity of hypertrophied skeletal muscle in MLC/mIGF-1 mice.

[/FONT]
1. Introduction

[FONT=Minion W08 Regular_1167271]One of the remarkable features of skeletal muscle is the capacity to adapt its metabolic and functional properties in response to a wide range of external factors, including physical and neuron activity, change in hormone levels, and oxygen and nutrient supply

However in several pathological conditions, skeletal muscle severely decreases this adaptive capacity, triggering alterations in its metabolic properties evolving to disease. In fact, insulin resistance (IR), obesity, high blood pressure, high fasting glucose or hyperglycemia, and lipid abnormalities are all conditions related to morphofunctional and metabolic changes in skeletal muscle

[/FONT]
[FONT=Minion W08 Regular_1167271]Recent evidences have shown that different therapeutic interventions can improve body composition and systemic metabolism

Among these, physical activity has been considered in the therapeutic effects of exercise for type II diabetes (T2DM) and other metabolic syndromes , although regular physical activity as a therapeutic tool can be seriously assumed in only a fraction of the population, mainly due to motivational and physical limitations.


From a metabolic point of view, however, it remains not well understood what molecular/cellular aspects of exercise should be mimicked and what type of muscle fiber is best targeted to improve metabolic dysfunction. Increased physical activity is usually achieved by exercise training, which can be divided into two major categories: endurance and resistance. It is well known that endurance training promotes metabolic alterations in skeletal muscle due to a shift in substrate preference as a consequence of fatty acid oxidative metabolism and muscle fiber type interconversion, resulting in a greater number of the slow twitch oxidative fibers

. In contrast, resistance training is known for its capacity to promote an increase in skeletal muscle mass (hypertrophy) and strength

. Nonetheless, the molecular factors linking skeletal muscle growth and metabolism still remain to be explored in detail. Among growth factors, the Insulin-like growth factor-1 (IGF-1) has been implicated in the control of both muscle mass and skeletal muscle homeostasis and its expression is significantly enhanced in response to exercise

.[/FONT]
[FONT=Minion W08 Regular_1167271]It has been previously reported that muscle restricted mIGF-1 transgene (MLC/mIGF-1) sustains muscle hypertrophy and regeneration in senescent skeletal muscle, enhances the recruitment of circulating stem cells in injured muscle and counteracts muscle wasting in mdx dystrophic mice , improving muscle mass and strength and elevating pathways associated with muscle survival and regeneration.

Although significant advances have been made with this genetic model, overall, the impact of manipulating skeletal muscle hypertrophic pathways upon whole body metabolism and glucose disposal is largely unknown.[/FONT]
[FONT=Minion W08 Regular_1167271]In the present study, we investigated metabolic features of MLC/mIGF-1 mice, revealing an unexpected higher respiratory quotient at rest, an index of higher carbohydrate utilization. These animals also showed higher insulin sensitivity, in line with a preference for carbohydrate as the primary energy source. In addition we have detected increased GLUT4 protein levels in skeletal muscle. These findings reinforce the potential of manipulating IGF-1 triggered intracellular pathways as therapeutic tools in the treatment of insulin resistance and type II diabetes.[/FONT]
Can you help me understand the very end of the write-up? What I'm taking from it is that a GF helps people who have or are pre-diabetic to type 2 diabetes? If that is the case that is great because my good friend who has the problem with his lower back we talked about is pre-diabetic for type 2.

from BM
 
Therapeutic potential of insulin-like growth factor-1 in patients with diabetes mellitus.

Type 1 DM results from the pancreas's failure to produce enough insulin. This form was previously referred to as "insulin-dependent diabetes mellitus" (IDDM) or "juvenile diabetes". The cause is unknown. Type 2 DM begins with insulin resistance, a condition in which cells fail to respond to insulin properly.
Mohamed-Ali V1, Pinkney J.
Author information



Abstract

<abstracttext></abstracttext>
<abstracttext></abstracttext><abstracttext>Insulin-like growth factor-1 (IGF-1) and its receptors share considerable homology with insulin and insulin receptors, and their respective signaling pathways interact at the post receptor level.</abstracttext><abstracttext></abstracttext><abstracttext></abstracttext><abstracttext> While the growth hormone (GH)-IGF-1 axis principally regulates tissue growth and differentiation, insulin exerts it primary effects on fuel metabolism. However, these two endocrine systems interact at multiple levels and in diabetes mellitus the GH-IGF-1 axis is grossly disturbed, with increased secretion of GH, reduced plasma levels of IGF-1, and complex tissue-specific changes in IGF binding proteins (IGFBPs). These observations have given rise to the view that GH-IGF-1 axis dysfunction, particularly low plasma levels of circulating IGF-1, probably play a significant role in several aspects of the pathophysiology of diabetes mellitus, including insulin resistance and poor glycemic control, and may also influence the development of microvascular complications.

The availability of recombinant human IGF-1 (rhIGF-1; mecasermin), used either alone or in combination with insulin, has led to experimental studies and clinical trials in humans testing these hypotheses. These studies have examined the impact of subcutaneous rhIGF-1 injections on sensitivity and metabolic parameters.
</abstracttext>
<abstracttext> In patients with type 1 and 2 diabetes mellitus, insulin sensitivity is significantly improved, insulin requirements are reduced, and glycemic control of dyslipidemia is generally improved in short-term studies.</abstracttext><abstracttext></abstracttext><abstracttext></abstracttext><abstracttext> rhIGF-1 is a particularly attractive possibility in patients with type 2 diabetes mellitus, where insulin resistance is the fundamental problem.

</abstracttext>
<abstracttext> Some patients with genetic syndromes of severe insulin resistance also benefit from treatment with rhIGF-1, which can bypass blocks in the insulin signaling pathway.</abstracttext><abstracttext></abstracttext><abstracttext></abstracttext><abstracttext>

The common adverse effects reported for rhIGF-1 are dose-related and include edema, jaw pain, arthralgia, myalgia, hypotension, injection site pain, and less commonly, Bell's palsy and raised intracranial pressure. Although disturbance of the GH-IGF-1 axis participates in the development of diabetic complications, the functional consequences of the complex changes in IGFBP expression at the tissue level are uncertain, and it is not known whether systemic IGF-1 therapy or other manipulations of the GH-IGF-1 axis would be helpful or harmful.
</abstracttext>
<abstracttext> Experimentally, IGF-1 has a protective effect on neuropathy, and could find an application in the healing of neuropathic ulcers. </abstracttext><abstracttext>The potential benefits of IGF-1 therapy in diabetes mellitus have yet to be realised.</abstracttext><abstracttext></abstracttext><abstracttext></abstracttext><abstracttext></abstracttext><abstracttext>
</abstracttext>

 
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For those of you looking for actual medical documentation, studies, and publications on IGF-1 lr3 instead of Broscience! lol. Although, I would listen to some bioscience over those with a PHD in some cases lmao
 
Bumping IGF 1 info. It always better when you understand how and why it works before using it!
 
This is great info, being type 2 diabetic I can tell you that taking my Igf before I train has a significate impact on my pumps and keeping my BS level stable after I workout.
 
we could use a lot more information regarding diabetics and how insulin-like Growth Factor impacts them. I know I’ve been asked about it quite a few times and it would make a great sticky thread to refer them to.
 
When my BS gets high, I get very bad headaches and I can attest that when I take my MC igf-lr3 in the morning I don't have any issues throughout the day. I still get awesome pumps when I train and walk around with a pump most of the day prior to workout out.
 
we could use a lot more information regarding diabetics and how insulin-like Growth Factor impacts them. I know I’ve been asked about it quite a few times and it would make a great sticky thread to refer them to.
I think it is different for people who have type 1 or type 2 diabetes. It is also different for people who are predisposed to type 2 diabetes I read some information a day or two ago on that and will post what I seen.

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I think it is different for people who have type 1 or type 2 diabetes. It is also different for people who are predisposed to type 2 diabetes I read some information a day or two ago on that and will post what I seen.

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IGF-1 May Help Insulin Resistance

Human growth hormone exerts most of its effects through the powerful growth factor called IGF-1.

As the name indicates IGF-1 (insulin-like growth factor-1) has properties similar to insulin and it has been shown to improve blood sugar profiles in type 2 diabetics. High doses of HGH have been shown to increase insulin resistance, but IGF-1 administration has actually normalized the insulin resistance in a group of volunteers.

Nelly Mauras and Bernard Beaufrere of the Nemours Children's Clinic in Jacksonville, Florida conducted a study where they looked at several areas. They studied the effect of IGF-1 on protein metabolism, IGF-1's ability to stop the protein-wasting caused by glucocorticosteroid drugs like prednisone, and the effect IGF-1 has on insulin and glucose metabolism. They divided the volunteers into three groups, one group received IGF-1 alone, one group received IGF-1 and prednisone, and one group received prednisone alone.

The study found that IGF-1 at 100 mcg per kilogram of body weight given twice daily enhanced the body's protein metabolism in the same way as human growth hormone did.

Like human growth hormone IGF-1 markedly decreased the protein breakdown in the volunteers who were taking prednisone but IGF-1 did not cause the diabetes-like effects of carbohydrate intolerance and insulin resistance as human growth hormone had done when given in combination with prednisone in an earlier study.

Instead, the test subjects who received IGF-1 and prednisone had normal glucose metabolism. The researchers saw this as remarkable because glucocorticoids are known to decrease insulin sensitivity and suppress the circulating insulin in the body. These researchers believe IGF-1 offers much promise in the treatment of protein catabolic states.

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IGF-1 May Help Insulin Resistance

Human growth hormone exerts most of its effects through the powerful growth factor called IGF-1.

As the name indicates IGF-1 (insulin-like growth factor-1) has properties similar to insulin and it has been shown to improve blood sugar profiles in type 2 diabetics. High doses of HGH have been shown to increase insulin resistance, but IGF-1 administration has actually normalized the insulin resistance in a group of volunteers.

Nelly Mauras and Bernard Beaufrere of the Nemours Children's Clinic in Jacksonville, Florida conducted a study where they looked at several areas. They studied the effect of IGF-1 on protein metabolism, IGF-1's ability to stop the protein-wasting caused by glucocorticosteroid drugs like prednisone, and the effect IGF-1 has on insulin and glucose metabolism. They divided the volunteers into three groups, one group received IGF-1 alone, one group received IGF-1 and prednisone, and one group received prednisone alone.

The study found that IGF-1 at 100 mcg per kilogram of body weight given twice daily enhanced the body's protein metabolism in the same way as human growth hormone did.

Like human growth hormone IGF-1 markedly decreased the protein breakdown in the volunteers who were taking prednisone but IGF-1 did not cause the diabetes-like effects of carbohydrate intolerance and insulin resistance as human growth hormone had done when given in combination with prednisone in an earlier study.

Instead, the test subjects who received IGF-1 and prednisone had normal glucose metabolism. The researchers saw this as remarkable because glucocorticoids are known to decrease insulin sensitivity and suppress the circulating insulin in the body. These researchers believe IGF-1 offers much promise in the treatment of protein catabolic states.

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The Effects IGF-1 Has on Diabetes

Two 1997 double-blind clinical studies showed that recombinant IGF-1 injections can reduce the need for insulin in patients with insulin-dependent diabetes by up to 45%. One study involved 8 adults aged 24 to 49 years and 43 children and teenagers aged 8 to 17 years.

While these trials lasted 19 days and 4 weeks and were short term trials, the fact that these test subjects saw such a drop in their insulin requirement and they had no serious side effects make IGF-1 a promising treatment of diabetes.

While in these short term studies IGF-1 therapy did not completely do away with the need for insulin it did improve the control of blood sugar and so may help prevent the complications of diabetes.

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Thank you brother I appreciate the compliment..

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I have had a few people say that they almost go into diabetic shock rubbing on high doses such as 100 to 120 MCG.
Personally I have never had a problem but I also apply it by laterally and only at 30 to 40 MCG bilaterally. However I am also one of those guys who can take 10 IU's of insulin and be just fine. Now that could be because I am smart about it and I make sure for every IU I have at least 10 grams of carbohydrates in my body both fast and slow acting.. starting July 1st I am going to go with GH igf and insulin. I was thinking about running the insulin at 7 Iu's in the morning along with 1.5iu's of GH, and 40 MCG of igf bilaterally on the muscles I train that day, one hour after my workout, then another 1.5iu's of GH either pre-workout or post workout? if I could get some suggestions on that too I would appreciate it. this is where I need some veterans opinions. The reason I say one hour post workout is because of all the stuff I hear about igf blunting the release of MGF which I don't know if it is true or not and I'm asking for some veterans opinions on what they think about that? As everyone knows I appreciate everybody's feedback as we are all here long to learn and nobody knows everything. Thanks Brothers..

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