[FONT="]IGF 1 Study and Conclusion Below is pretty amazing, and puzzles the the scientists as to how its possible to add more muscle mass without adding anymore food intake, but rather just by adding in IGF 1 or IGF 1 lr3, and also greater utilization of carbs. Pretty awesome stuff man!
A main outcome of the present study was the surprising finding that although the MLC/mIGF-1 animals clearly have increased muscle mass, no proportional increase in food intake was observed. In fact these animals consume, in absolute numbers, similar amount of food. Intriguingly, these animals have higher insulin sensitivity and higher carbohydrate utilization without requiring additional food intake or altered blood total cholesterol or triglycerides. Currently it is not clear why and how MLC/mIGF-1 animals can build more lean mass without more food intake. Possibilities include more efficient substrate gut absorption and less energy expenditure. A recently described myokine called irisin has been associated with activation of brown fat and consequently more energy expenditure in form of heat [26]. In addition, it has been shown that irisin expression is increased by PGC-1 alpha. Interestingly our results show that PGC-1 alpha expression is strongly reduced in MLC/mIGF-1 animals as compared to WT, raising the possibility that decreased activity of the PGC-1-irisin axis might be responsible for sparing the necessary fuel to build increased skeletal muscle in MLC/mIGF-1 animals.[/FONT]
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It is currently not clear if the effects of IGF-1 increasing the use of carbohydrates observed in the present study are direct or rather a consequence of secondary changes in type II skeletal muscle fibers. It has been shown that exogenous administration of IGF1 to type 2 diabetes patients can improve insulin sensitivity [27]; therefore, a direct effect is possible. Another nonexclusive possibility involves secondary effects such as type II skeletal muscle fiber hypertrophy. In fact the MLC/mIGF1 animals have a consistent hypertrophy in those fibers and it has been shown that increased muscle mass can improve insulin sensitivity [28]. The metabolic consequence of increased insulin sensitivity in the MLC/mIGF1 animals could include resistance to the establishment of type II diabetes. Future studies submitting mIGF-1 hyperexpression animals to a long-term hypercaloric diet leading to increased body weight and also crossing these animals with ob/ob mice are warranted.[/FONT]
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To our knowledge no studies systematically have addressed the effects of IGF1 upon fiber type shift. In our model we found a consistent shift in EDL towards a glycolytic profile. This effect might be mediated by decreasing the levels of PGC-1. It is well described that PGC-1 is a strong fiber type I inducer [29]. Another fiber type I inducer, the calciuneurin-NFATc1 axis, might be modulated by IGF1 increased levels [30]. Accordingly modulation of myogenin levels also remain as a possible mechanism since it has been shown to shift enzyme activity from glycolytic to oxidative metabolism [31].[/FONT]
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Although in the present study we have, as expected, detected hypertrophy of type II fibers (IIa/IId and IIb) in EDL muscle, intriguingly we have also seen a decrease in cross-sectional area in fibers IIa in soleus muscle. This unexpected finding might reveal a conditional hypertrophic effect of IGF1. For instance one might envisage that the fiber type I, which is the predominant fiber in this muscle, secretes a factor that can interfere with IGF1 hypertrophic action.
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[FONT="]In conclusion, MLC/mIGF-1 mice have improved glucose homeostasis due to GLUT4-mediated higher insulin sensitivity. This improvement leads to a greater rate of carbohydrate utilization by the increased muscle, without interfering with other metabolic parameters.
[/FONT]
A main outcome of the present study was the surprising finding that although the MLC/mIGF-1 animals clearly have increased muscle mass, no proportional increase in food intake was observed. In fact these animals consume, in absolute numbers, similar amount of food. Intriguingly, these animals have higher insulin sensitivity and higher carbohydrate utilization without requiring additional food intake or altered blood total cholesterol or triglycerides. Currently it is not clear why and how MLC/mIGF-1 animals can build more lean mass without more food intake. Possibilities include more efficient substrate gut absorption and less energy expenditure. A recently described myokine called irisin has been associated with activation of brown fat and consequently more energy expenditure in form of heat [26]. In addition, it has been shown that irisin expression is increased by PGC-1 alpha. Interestingly our results show that PGC-1 alpha expression is strongly reduced in MLC/mIGF-1 animals as compared to WT, raising the possibility that decreased activity of the PGC-1-irisin axis might be responsible for sparing the necessary fuel to build increased skeletal muscle in MLC/mIGF-1 animals.[/FONT]
[FONT="]
It is currently not clear if the effects of IGF-1 increasing the use of carbohydrates observed in the present study are direct or rather a consequence of secondary changes in type II skeletal muscle fibers. It has been shown that exogenous administration of IGF1 to type 2 diabetes patients can improve insulin sensitivity [27]; therefore, a direct effect is possible. Another nonexclusive possibility involves secondary effects such as type II skeletal muscle fiber hypertrophy. In fact the MLC/mIGF1 animals have a consistent hypertrophy in those fibers and it has been shown that increased muscle mass can improve insulin sensitivity [28]. The metabolic consequence of increased insulin sensitivity in the MLC/mIGF1 animals could include resistance to the establishment of type II diabetes. Future studies submitting mIGF-1 hyperexpression animals to a long-term hypercaloric diet leading to increased body weight and also crossing these animals with ob/ob mice are warranted.[/FONT]
[FONT="]
To our knowledge no studies systematically have addressed the effects of IGF1 upon fiber type shift. In our model we found a consistent shift in EDL towards a glycolytic profile. This effect might be mediated by decreasing the levels of PGC-1. It is well described that PGC-1 is a strong fiber type I inducer [29]. Another fiber type I inducer, the calciuneurin-NFATc1 axis, might be modulated by IGF1 increased levels [30]. Accordingly modulation of myogenin levels also remain as a possible mechanism since it has been shown to shift enzyme activity from glycolytic to oxidative metabolism [31].[/FONT]
[FONT="]
Although in the present study we have, as expected, detected hypertrophy of type II fibers (IIa/IId and IIb) in EDL muscle, intriguingly we have also seen a decrease in cross-sectional area in fibers IIa in soleus muscle. This unexpected finding might reveal a conditional hypertrophic effect of IGF1. For instance one might envisage that the fiber type I, which is the predominant fiber in this muscle, secretes a factor that can interfere with IGF1 hypertrophic action.
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[FONT="]In conclusion, MLC/mIGF-1 mice have improved glucose homeostasis due to GLUT4-mediated higher insulin sensitivity. This improvement leads to a greater rate of carbohydrate utilization by the increased muscle, without interfering with other metabolic parameters.
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