6-phosphofructokinase glucose oxidation

Glycolysis and the citric acid cycle (to be discussed in Chapter 20) are coupled via phosphofructokinase, because citrate, an intermediate in the citric acid cycle, is an allosteric inhibitor of phosphofructokinase. When the citric acid cycle reaches saturation, glycolysis (which feeds the citric acid cycle under aerobic conditions) slows down. The citric acid cycle directs electrons into the electron transport chain (for the purpose of ATP synthesis in oxidative phosphorylation) and also provides precursor molecules for biosynthetic pathways. Inhibition of glycolysis by citrate ensures that glucose will not be committed to these activities if the citric acid cycle is already saturated. 

Figure 16.1 The glucose/fatty add cycle. The dotted Lines represent regulation. Glucose in adipose tissue produces glycerol 3-phosphate which enhances esterification of fatty acids, so that less are available for release. The effect is, therefore, tantamount to inhibition of lipolysis. Fatty acid oxidation inhibits pyruvate dehydrogenase, phosphofructokinase and glucose transport in muscle (Chapters 6 and 7) (Randle et al. 1963).

The number of ATPs produced by complete oxidation of a molecule of glucose can be calculated at this point. This calculation is not directly relevant to detenrunation of the energy requirement. NADH from the Krebs cycle is responsible for the production of many more ATPs than is glycolysis. In glycolysis, an ATP is expended at the points of hexokinase and phosphofructokinase. For each molecule... 

Endogenous nitric oxide inhibits glucose-induced insulin secretion by suppression of phosphofructokinase activity in pancreatic islets. Biochem Biophys Res Commun 252 34-38. 

In addition to stimulating the synthesis and release of LPL, insulin stimulates glucose metabolism in adipose cells. Insulin leads to the activation of the glycolytic enzyme phosphofructokinase-1 by an activation of PFK-2, which increases fructose 2,6-bisphosphate levels. Insulin also stimulates the dephosphorylation of pyruvate dehydrogenase, so that the pyruvate produced by glycolysis can be oxidized in the TCA cycle. Furthermore, insulin stimulates the conversion of glucose to fatty acids in adipose cells, although the liver is the major site of fatty acid synthesis in humans. 

Figure 8.1 Biochemical pathways involved in glucose catabolism in Pseudomonas putida KT2440. The metabolic network depicted is sketched around four main metabolic blocks, identified with different colors (i) the peripheral oxidative pathways, that encompass the oxidative transformation of glucose into gluconate and 2-ketogluconate (and the corresponding phosphorylated derivatives of these metabolites) (ii) the Embden-Meyerhof-Pamas (EMP) pathway (nonfunctional, due to the absence of a 6-phosphofructokinase activity) (iii) the...

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