Glucose is the primary source of energy for most cells.
The liver can convert non-carbohydrate sources into glucose through gluconeogenesis, which occurs when blood glucose levels are low or insulin levels are high.
Liver stores about 100 grams of glycogen at any given time.
Liver stores about 10% of total body carbohydrates as glycogen.
Muscle tissue also contains glycogen, but it accounts for only 2% of total body carbohydrates.
Glycogenolysis is the breakdown of stored glycogen to release glucose molecules.
Pyruvic acid is converted into acetyl CoA by oxidative decarboxylation.
Acetyl CoA enters the citric acid cycle (Krebs cycle) and produces ATP.
Gluconeogenesis involves converting pyruvate from lactate, amino acids, and fatty acids into glucose.
In gluconeogenesis, pyruvate is first converted into oxaloacetic acid using carbon dioxide.
Gluconeogenesis occurs when blood glucose levels are low due to fasting, exercise, or stress.
In the absence of dietary carbohydrates, the liver uses gluconeogenesis to maintain normal blood glucose concentrations.
During fasting, the liver breaks down fats and proteins to generate energy and synthesize glucose via gluconeogenesis.
Oxaloacetic acid is then reduced to malic acid through NADH-dependent reduction.
Malic acid is converted back to pyruvic acid via dehydrogenation with FAD as an electron acceptor.
The resulting pyruvic acid can be used for gluconeogenesis or enter the Krebs cycle.
Muscle cells can also use gluconeogenesis to produce glucose for energy production.
The liver uses gluconeogenesis to maintain normal blood sugar levels during periods of low carbohydrate intake.
The process of glycogenolysis releases glucose-1-phosphate, which can be further processed through phosphoglucomutase to form glucose-6-phosphate.
Glucose-6-phosphatase catalyzes the conversion of glucose-6-phosphate to free glucose, allowing it to enter the bloodstream.
Galactose is metabolized similarly to glucose, with galactokinase adding a phosphate group to convert galactose to galactose-1-phosphate.
The process of glycogenolysis releases glucose molecules stored as glycogen in the liver and muscles.
Pyruvate is produced during glycolysis and can be further metabolized through aerobic respiration if sufficient oxygen is available.
Malic acid is decarboxylated by Malic Enzyme (ME) to produce Pyruvate and CO2.
Pyruvate is transported out of mitochondria and converted back to PEP by Pyruvate Kinase (PK).
PEP is phosphorylated by Phosphoenolpyruvate Carboxykinase (PEPCK) to form Oxaloacetate.
Pyruvic acid is decarboxylated by pyruvate carboxylase to form acetyl CoA.
Pyruvate carboxylase catalyzes the conversion of pyruvate into oxaloacetate using biotin as a cofactor.
Phosphoenolpyruvate (PEP) is produced from pyruvate through decarboxylation and phosphorylation reactions.
Gluconeogenesis occurs primarily in the liver but can occur in other tissues such as muscle cells during prolonged exercise.
Noncarbohydrate precursors include lactate, glycerol, amino acids (alanine), and fatty acids.
Gluconeogenesis occurs primarily in the liver but can occur in other tissues such as muscle cells under certain conditions.
In the absence of insulin, glycogenolysis predominates over gluconeogenesis.
Insulin stimulates glucose uptake by target organs (muscles) and inhibits hepatic glucose release.
Glucose-6-phosphatase catalyzes the removal of the phosphate group from glucose-6-phosphate, producing free glucose that enters the bloodstream.
Glycolysis occurs in the cytoplasm of all cells except red blood cells (RBC), while gluconeogenesis takes place only in the liver and kidneys.
In RBCs, there are no mitochondria, so they cannot perform oxidative metabolism.
Pyruvate produced by glycolysis enters the mitochondria and undergoes oxidative decarboxylation to become acetyl CoA.
Acetyl CoA enters the citric acid cycle (Krebs cycle) and generates more ATP.
Uridine diphospho (UDP) galactose transfers its galactose moiety from UDP to glucose-1-phosphate, forming uridine diphosphate (UDP).