Introduction
The skeletal muscle glucose metabolism is an extremely important process which means the exchanging of the elements. This process enables the organism to take in the needed nutrients in order to function properly and to utilize those which are harmful or needless for humans’ viability. And inefficiency of this kind of metabolism is usually associated with different disorders, such as diabetes, hyperglycemia, and obesity. Different factors, such as nutrition and environment, may be dangerous for the normal skeletal muscle mass and strength. Thus, it can be very helpful to define the factors which can improve the process of glucose metabolism to prevent different disorder and loss of skeletal muscle mass. The other tasks of these pathways are to prevent the DNA from being synthesed, and the genetic phone from being distorted. The transcriptional factors are aimed at achieving the balance of different elements in humans’ muscle tissue.
Description of different pathways
There are different signal transcription mechanisms which may contribute to this process and therefore should not be underestimated. The main among them are considered to be carbohydrate responsive element-binding protein (ChREBP) and sterol regulatory element binding protein-1c (SREBP-1c) together with the peroxisome proliferator-sctivated receptors (PPARs) and peroxisome proliferator-activated receptor-coactivator (PGC-1α). These pathways all have been studied and proved to play the key role in the skeletal muscle glucose metabolism. There are also many other transcriptional factors such as, for example, the upstream stimulatory factor (USF). All the pathways are practically based on insulin and carbohydrates production in order to recycle the glucose. Glucagon can also be useful while stimulating cells to react to the nutrients. If glucose will be uptaken in the muscle, it can lead to the development of diabetes.
ChREBP is a very significant signaling pathway in the process of glucose metabolism. It increases the participation of the genes which are responsible for this process. This pathway is rather controversial, as it is aimed at recycling carbohydrates with the help of a high level of carbohydrates. ChREBP is responsible for activating the lipogenic enzyme genes according to the hormones and nutrition and for preventing various disorders such as obesity, diabetes, and hypertension. This transcription factor has also proved to improve the insulin resistance.
SREBP-1c has the functions similar to those of ChREBP. It also tends to activate and regulate the fatty acid synthesis (FAS).
Peroxisome proliferator-activated receptors (PPARs) are the nuclear receptor supergenes which regulate the storage and metabolism of dietary fats with comparatively little loss of the amino acids. It is also involved in oxidation of fatty acids in the liver with the receptor activation. This helps to controll the activity of genes involved in the transportation and metabolism.
Another pathway, the PGC-1α is a transcription factor which is responsible for the energy metabolism in cells. It is strongly connected to the environmental changes and can be caused essentially by low temperatures. The fubctioning of the PGC-1α is represented in the fact that it rebuilds the tissue of muscles into a more oxidative one. It also stimulates mitochondrial biogenesis and is involved in carbohydrate and lipid metabolism.
PGC is a transcriptional factor which promotes the activation of gluconeogenesis and also oxidates the fatty acid.
Impact of fast and underfeeding
As it was mentioned before, nutrition plays a key role in the process of the skeletal muscle glucose metabolism. Therefore lack or too great quantity of some important chemical elements can influence this process, either helping or preventing it. A multitude of experiments with rats was held in order to investigate the connection between the nutrition and the functioning of different molecular signaling pathways. It was established by the scientists that consuming too much fat can repress the ChREBP activation, because in that case the quantity of AMP in liver cells increases. This proves an impediment to the blocks glucose induction of ChREBP. On the other hand, undernutrition and fast can also be harmful for the process. The study has shown that the cells become insensitive to insulin because of fast and this ability cannot be returned even after refeeding. In addition, the refeeding period may be marked with the disposal of glucose which is unable to be oxidated. The mistake of undernutrition is usually made by those who are trying to fight their obesity. In case of extra weight a special diet should be composed, and it should not exclude fat as it is one of the elements which are needed for the skeletal muscle glucose metabolism.
For some of the transcription factors underfeeding might be a positive phenomenon. It can fasten some of the processes and their effectiveness. For instance, in case with PPARs fasting can activate the fatty acid oxidation which will help the process of the skeletal muscle glucose metabolism. This proves that sometimes the organism needs to be less supplied with the food in order to be able to manage its processes on a molecular level.
Conclusion
In conclusion it must be said that the skeletal muscle glucose metabolism can be regulated with a set of molecular signaling pathways. They usually have some necessary conditions in order to function properly. Another important fact is that underfeeding and fast are predominantly negative for the process. The human organism needs the whole range of elements to function properly and it should be especially considered while dealing with the molecular level.