The breakdown of glycogen to glucose-1-phosphate is catalyzed by phosphorylase. Glycogen synthesis involves a different pathway via uridine diphosphate glucose and glycogen synthase .

The relationships between gluconeogenesis and the glycolytic pathway are shown in Figure 1. After transamination or deamination, glucogenic amino acids yield either pyruvate or intermediates of the citric acid cycle. Therefore, the reactions described earlier can account for the conversion of both lactate and glucogenic amino acids to glucose or glycogen.

Fig1. Major pathways and regulation of gluconeogenesis and glycolysis in the liver. Entry points of glucogenic amino acids after transamination are indicated by arrows extended from circles. The key gluconeogenic enzymes are shown in double bordered boxes. The ATP required for gluconeogenesis is supplied by the oxidation of fatty acids. Propionate is important only in ruminants. Arrows with wavy shafts signify allosteric effects; dash-shafted arrows, covalent modification by reversible phosphorylation. High concentrations of alanine act as a “gluconeogenic signal” by inhibiting glycolysis at the pyruvate kinase step.

Propionate is a major precursor of glucose in ruminants; it enters gluconeogenesis via the citric acid cycle. After esterification with CoA, propionyl-CoA is carboxylated to d-methylmalonyl-CoA, catalyzed bypropionyl-CoA carboxylase, a biotin-dependent enzyme (Figure 2).Methylmalonyl-CoA racemasecatalyzes the conversion of d-methylmalonyl-CoA to l-methylmalonyl-CoA, which then undergoes isomerization to succinyl-CoA catalyzed by methylmalonyl-CoA mutase. In nonruminants, including human beings, propionate arises from the β-oxidation of odd-chain fatty acids that occur in ruminant lipids , as well as the oxidation of isoleucine and the side chain of cholesterol, and is a (relatively minor) substrate for gluconeogenesis. Methylmalonyl-CoA mutase is a vitamin B12-dependent enzyme, and in B12 deficiency, methylmalonic acid is excreted in the urine (methylmalonic aciduria).

Fig2. Metabolism of propionate.

Glycerol is released from adipose tissue as a result of lipolysis of lipoprotein triacylglycerol in the fed state; it may be used for reesterification of free fatty acids to triacylglycerol, or may be a substrate for gluconeogenesis in the liver. In the fasting state, glycerol released from lipolysis of adipose tissue triacylglycerol is used as a substrate for gluconeogenesis in the liver and kidneys.

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مواضيع ذات صلة

Blood Glucose is Derived From the Diet, Gluconeogenesis, & Glycogenolysis

Glycolysis & gluconeogenesis share the same pathway but in opposite directions, & are reciprocally regulated

Thermodynamic Barriers Prevent a Simple Reversal of Glycolysis

Gluconeogenesis & the Control of Blood Glucose: Biomedical Importance

Glycogen Metabolism is Regulated by A Balance in Activities Between Glycogen Synthase & Phosphorylase

cAMP Activates Glycogen Phosphorylase

Cyclic AMP Integrates The Regulation of Glycogenolysis & Glycogenesis

Glycogenolysis is not the Reverse of Glycogenesis, it is A Separate Pathway

Glycogenesis Occurs Mainly in Muscle & Liver

The Oxidation of Pyruvate to Acetyl-COA is The Irreversible Route from Glycolysis to The Citric Acid Cycle

Glycolysis is Regulated at Three Nonequilibrium Reactions

Tissues That Function Under Hypoxic Conditions or have Intrinsically High Rates of Glucose Oxidation Produce Lactate