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Glycogenolysis is the process by which glycogen, the primary carbohydrate stored in the liver and muscle cells of animals, is broken down into glucose to provide immediate energy and to maintain blood glucose levels. In the muscles, glycogenolysis begins due to the binding of cAMP to phosphorylase kinase, converting it to its active form. This then converts phosphorylase b to phosphorylase a, which catalyses the breakdown of glycogen. The breakdown of glycogen into glucose-1-phosphate is catalysed by the enzyme glycogen phosphorylase. Glucose-1-phosphate is then converted to glucose-6-phosphate, which often enters glycolysis. Glycogenolysis is inhibited by glycogenesis, the synthesis of glycogen, and various rare inherited diseases of glycogen storage produce abnormalities in glycogenolysis.
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What You'll Learn
Glucagon and epinephrine signalling
Glucagon and epinephrine are hormones that regulate glycogenolysis, the breakdown of glycogen into glucose-1-phosphate and free glucose. In the liver, glucagon increases glycogenolysis, while epinephrine decreases glycogen synthesis and increases glycogenolysis and gluconeogenesis. However, in skeletal muscle, glucagon has no effect due to the lack of glucagon receptors, while epinephrine increases the rate of glycogenolysis by promoting glycogen degradation.
Glucagon is a peptide hormone secreted by the pancreas's alpha cells when blood glucose levels are low, indicating hypoglycemia. Glucagon signalling begins when the hormone binds to receptors on liver cells, leading to the activation of a series of intracellular events that stimulate glycogenolysis. This process is highly controlled, as only the liver can release glucose back into the bloodstream to maintain homeostasis.
Epinephrine, also known as adrenaline, plays a crucial role in increasing glycogenolysis in both the liver and skeletal muscle. In the liver, epinephrine decreases glycogen synthesis by inactivating glycogen synthase while increasing glycogenolysis and gluconeogenesis through glycogen breakdown. In skeletal muscle, epinephrine enhances glycogenolysis by increasing glycogen degradation.
The process of glycogenolysis in skeletal muscle involves the enzyme adenyl cyclase and cyclic adenosine monophosphate (cAMP). cAMP binds to phosphorylase kinase, converting it to its active form. This active form then converts phosphorylase b to phosphorylase a, which catalyses the breakdown of glycogen. The overall reaction results in the conversion of glycogen to glucose-1-phosphate, which is further converted to glucose-6-phosphate and directed into glycolysis or other metabolic pathways.
In summary, glucagon and epinephrine signalling play important roles in regulating glycogen metabolism, particularly in the liver and skeletal muscle. While glucagon primarily acts on the liver to increase glycogenolysis, epinephrine influences both the liver and skeletal muscle by modulating glycogen synthesis, glycogenolysis, and gluconeogenesis. These hormonal signals help maintain energy homeostasis and ensure a sufficient supply of glucose for bodily functions.
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Enzyme defects
Firstly, the enzyme glycogen phosphorylase plays a crucial role in glycogenolysis, the breakdown of glycogen to glucose-1-phosphate. Defects in this enzyme, such as in glycogen storage disease type V (McArdle disease), can impair glycogen breakdown and prevent muscles from meeting their energy demands during exercise. This results in a lack of glycogen phosphorylase activity, hindering the conversion of glycogen to glucose-1-phosphate.
Secondly, the debranching enzyme is essential for completing the breakdown of glycogen by targeting its branching points. Glycogen storage disease type III (Cori or Forbes disease) is caused by mutations affecting the production of this enzyme. Consequently, abnormal, partially broken-down glycogen molecules accumulate in cells, leading to tissue damage, particularly in the liver and muscles.
Additionally, defects in the enzyme glucose-6-phosphatase can impact muscle glycogen glycolysis. This enzyme is responsible for removing the phosphate group from glucose-6-phosphate, converting it to free glucose that can be utilised by the body. Defects in this enzyme can disrupt the normal glycolytic pathway and affect glucose homeostasis in the body.
Moreover, lysosomal α-1,4-glucosidase (acid α-glucosidase) is another enzyme that, when defective, can lead to glycogen storage disease type II (Pompe disease). This disorder results in lysosomal accumulation of glycogen, primarily affecting cardiac and skeletal muscles. The deficiency of this enzyme hinders the breakdown of glycogen within lysosomes, leading to a build-up of glycogen in various tissues.
In summary, enzyme defects in glycogen phosphorylase, debranching enzyme, glucose-6-phosphatase, and lysosomal α-1,4-glucosidase can all contribute to disruptions in muscle glycogen glycolysis. These defects lead to a range of glycogen storage diseases and impact the body's ability to utilise glycogen as an energy source during exercise and muscle contraction.
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Insulin resistance
In the liver, DAG-mediated activation of PKCε impairs hepatic insulin signalling, constraining insulin-stimulated hepatic glycogen synthesis. In skeletal muscle, DAG-mediated activation of PKCθ impairs muscle insulin signalling, impeding insulin-stimulated muscle glucose uptake and causing increased glucose delivery to the liver. This diversion of ingested glucose to the liver results in increased hepatic de novo lipogenesis and hyperlipidemia.
Exercise improves insulin sensitivity in both healthy subjects and insulin-resistant people. While the improved insulin sensitivity after a single bout of exercise is short-lived, repeated bouts of endurance training improve insulin sensitivity beyond the acute effect of the last training session. Importantly, the risk for the development of type 2 diabetes is reduced by year-long training.
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Glycogen storage diseases
Glycogen is a branched, glucose polymer and is the storage form of glucose in cells. It is a key source of energy for the body. Glycogenolysis is the breakdown of glycogen to glucose-1-phosphate and glycogen. Glycogen storage diseases (GSDs) are a group of inherited genetic disorders that cause glycogen to be improperly stored in the body. GSDs are rare conditions that change the way the body uses and stores glycogen. They are passed down from parents to children (hereditary). GSDs are caused by a genetic enzyme defect that is inherited from both parents.
There are at least nine known types of GSD, and each has its own symptoms and treatment. The types of GSD are categorized by number and name. The main types of GSD in children are types I, III, IV, and VI, which affect the liver, and types V and VII, which affect the muscles. Type I, or Von Gierke disease, is the most common type of GSD, accounting for 90% of all cases. It can cause arthritis, dental problems, inflammatory bowel disease, benign liver tumours, and recurring infections. Type II, or Pompe's disease, affects nearly all organs, including the heart and skeletal muscles. Type III can cause benign liver tumours, slow growth, and muscle weakness. Type IV can lead to liver cirrhosis and heart failure. Type V and VII affect the muscles and are treated by regulating or limiting strenuous exercise to avoid fatigue.
GSDs are diagnosed through clinical evaluation, biochemical testing, and genetic identification of mutations in specific enzymes. Imaging studies may also be used to assess organ involvement. Management focuses on addressing the underlying enzyme deficiency and preventing complications. There is currently no way to prevent GSDs, but early treatment can help control symptoms.
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Glycogenesis
The first step in glycogenesis is the phosphorylation of glucose into glucose-6-phosphate, which is achieved through the action of glucokinase or hexokinase. This molecule can then enter the glycogenesis pathway, where it is converted into glucose-1-phosphate by the enzyme phosphoglucomutase. This molecule then combines with uridine triphosphate (UTP) to form a uridine diphosphate (UDP)-glucose molecule, which is the basic building block for glycogen.
The transfer of glucose molecules from UDP-glucose to glycogen is facilitated by glycogen synthase (GS). The enzyme glycogenin is needed to create the initial short glycogen chains, which are then lengthened and branched by other enzymes of glycogenesis. GS is responsible for elongating the glycogen main chain by forming α(1→4) glycosidic bonds using UDP-glucose as the activated donor.
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Frequently asked questions
Glycolysis is the set of reactions that break down glucose to capture and store energy in the form of adenosine triphosphate (ATP). Glycogen is a branched, glucose polymer and the storage form of glucose in cells. Muscle glycogen glycolysis is, therefore, the breakdown of muscle glycogen to meet the energy demands of exercise.
Various factors can inhibit muscle glycogen glycolysis, including:
- Enzyme defects, such as those affecting glucose-6-phosphatase, lysosomal x-1,4-glucosidase, and the glycogen debranching enzyme.
- Inherited diseases of glycogen storage, such as glycogen storage disease type V (McArdle's disease) and type III (Cori or Forbes disease).
- Insulin resistance or type 2 diabetes, which impair insulin signaling and insulin-stimulated glucose transport.
Glycogenolysis is the breakdown of glycogen to glucose-1-phosphate, which is then converted to glucose-6-phosphate. This process occurs in the muscles and is catalysed by the enzyme glycogen phosphorylase. Glucose-6-phosphate then enters glycolysis to meet immediate energy demands. Therefore, glycogenolysis is a prerequisite for muscle glycogen glycolysis.
Glycogenesis is the synthesis of glycogen from glucose. Glycogen is the storage form of glucose in cells, so glycogenesis can be seen as the opposite of glycogenolysis and glycolysis. Insulin signaling activates glycogenesis, while glucagon signaling inhibits it and activates glycogenolysis. Therefore, glycogenesis and glycolysis are inversely related, and high levels of glycogenesis can inhibit glycolysis.
