pgc-1 alpha

PGC-1 alpha- The Secret Metabolism Controlling Molecule

What is PGC-1 alpha? 

Peroxisome proliferator-activated receptor gamma coactivator-1 alpha also known as PGC-1 alpha (PGC-1a, PGC-1α) is a lesser known, but very important molecule that affects many biological processes within the body, including the process of fat loss and energy metabolism in humans. 

PGC-1 alpha is a transcription coactivator.  Transcription coactivators help to “activate” transcription factors in cells. Transcription factors can up-regulate or down-regulate the production of certain genes in cells. PGC-1a also regulates the expression of genes located in the mitochondria. Specifically, PGC-1 alpha regulates the genes that control mitochondrial biogenesis and mitochondrial respiration.  

PGC-1α has effects on many transcription factors in the cells.  These transcription factors go on to affect many biological processes such as mitochondrial biogenesis, the remodeling of muscle tissue to a fiber composition that is metabolically more oxidative and less glycolytic, and also the regulation of carbohydrate and lipid metabolism.  All of these effects lead to a stronger metabolism and better fat burning ability. 

Because PGC-1α has such an effect on the “power plants” (the mitochondria) of the cells , it is a key molecule of interest when it comes to energy balance and fat loss.  

If you are unfamiliar with what mitochondria are, be sure to check out our other article that goes into depth about mitochondria and mitochondrial health. 

Where in the Body is PGC-1 alpha the Most Concentrated?

PGC-1α is found in energetically demanding tissues such as skeletal muscle, the heart, and brown adipose tissue or BAT.  Brown fat is the type of fat that is responsible for thermoregulation when you are cold. When you shiver from being cold, brown fat helps to keep you warm. Its primary function is thermoregulation, where white adipose tissue’s (WAT or normal body fat) main purpose is for energy storage.

High PGC-1 alpha levels are also found in the brain and kidneys. Low levels of PGC-1 alpha are located in the liver and WAT.

PGC-1 alpha’s Mechanism of Action

PGC-1α triggers fat loss by affecting lipid metabolism in the body.  It does this by binding to target proteins which signal to the mitochondria in the cell to transport and utilize fatty acids more readily. In essence, the more PGC-1 alpha you have binding to these signaling proteins, the more your body is going to burn fat.  

In addition, PGC-1 alpha has been shown to increase the expression of the GLUT4 in cultured muscle cells and skeletal muscle. GLUT4 is a glucose transporter located on the surface of muscle cells. An increase in GLUT4 leads to better insulin sensitivity and sugar is more readily stored in muscle rather than fat.  In fact, according to one study, PGC-1 alpha was able to increase the transportation of glucose into the muscle cells 3-fold! 

3 Ways to Increase PGC-1 alpha Levels

Cold exposure

When mammals (including humans) are exposed to the cold, PGC-1 alpha levels rise.  This starts a cascade of different transcription factors to signal for an increase in mitochondrial biogenesis, brown fat production, heat production, and overall energy metabolism.  This results in more fat being burned, and overall better body composition. 

Exercise

After bouts of endurance exercise, the total PGC-1a levels and its activity in skeletal muscle become elevated [1]. Just another reason why exercise is good for you.

Fasting

Fasting causes a large increase of PGC-1α expression, which results in hepatic gluconeogenesis and fatty acid oxidative metabolism [2]. Fasting has been shown to increase the amount of PGC-1a in cardiac muscle as well.

Conclusion

PGC-1 alpha is another molecule that has been proven to improve metabolism, mitochondrial biogenesis, fat loss, and body composition. By focusing on exercising often, getting occasional cold exposure, and fasting, anyone can keep their PGC-1a levels high.

References:

  1. https://pubmed.ncbi.nlm.nih.gov/21501593/
  2. https://pubmed.ncbi.nlm.nih.gov/11557984/

Leave a Comment

Your email address will not be published. Required fields are marked *