Glycolysis and gluconeogenesis

Glycolysis and gluconeogenesis are not individual molecular targets but rather two fundamental metabolic pathways. Glycolysis is the process by which glucose is broken down in the cytoplasm to generate pyruvate, ATP, and NADH; it provides energy for cells—especially those lacking mitochondria—and intermediates for other biosynthetic processes. Gluconeogenesis is essentially the reverse process; it synthesizes glucose from non-carbohydrate precursors such as lactate, glycerol, amino acids, and odd-chain fatty acids. This occurs mainly in the liver and helps maintain blood glucose levels during fasting or starvation. Both pathways are tightly regulated by hormones—insulin stimulates glycolysis while glucagon stimulates gluconeogenesis—and key rate-limiting enzymes such as phosphofructokinase 1 for glycolysis and fructose 1,6-bisphosphatase for gluconeogenesis. Dysregulation contributes to diseases like type 2 diabetes mellitus (where excess hepatic gluconeogenesis leads to hyperglycemia), cancer (where increased glycolytic flux supports tumor growth), neurodegeneration, and some infections. Therapeutically relevant drugs include metformin—which inhibits hepatic gluconeogenesis to lower blood sugar in type 2 diabetes patients—and potential inhibitors or modulators targeting specific enzymes within these pathways. Biomarkers often involve expression levels or activity states of key enzymes like hexokinase or ALDOA/FBP1 ratios in cancer prognosis. Safety concerns center on hypoglycemia risk if these pathways are excessively inhibited. Note: "Glycolysis/gluconeogenesis" refers collectively to two entire metabolic processes rather than a single protein target; thus this entry should be flagged as incorrect if a specific molecular target is required. Individual proteins/enzymes within these pathways—such as hexokinase or fructose 1,6-bisphosphatase—are valid therapeutic targets themselves.

Other names

Glycolytic pathwayGluconeogenic pathwayEmbden-Meyerhof pathway (for glycolysis)

Inhibition of gluconeogenesis (e.g., by metformin)