Search results for "Phosphofructokinase"
showing 5 items of 25 documents
Fructose 2,6-bisphosphate as a signal for changing from sugar to lipid oxidation during flight in locusts
1986
AbstractFlight in locusts is initially powered mainly by carbohydrate but if flight is to be sustained, as in migration, the animals have to utilize fat as the predominant fuel. The molecular basis of this metabolic switch has not been identified. Fructose 2,6-bisphosphate is a potent activator of 6-phosphofructokinase (EC 2.7.1.11) purified from locust flight muscle. After the first few minutes of flight in the locust the concentration of fructose 2,6-bisphosphate in the flight muscle falls dramatically, which should lead to a decrease in the activity of 6-phosphofructokinase as part of the mechanism to conserve carbohydrate during prolonged flight.
Properties of locust muscle 6-phosphofructokinase and their importance in the regulation of glycolytic flux during prolonged flight
1987
6-Phosphofructokinase (PFK, EC 2.7.1.11) from the flight muscle of the locust (Locusta migratoria) was purified to a specific activity of 80 μmol min−1 (mg protein)−1 (at 25°C). 1. The enzyme is made up from subunits ofMr-81600, and the smallest catalytically active form is likely to be a tetramer. 2. PFK activity is markedly affected by the pH of the assay; the optimum pH was at about 8. 3. Physiological concentrations of ATP strongly inhibit locust PFK by shifting the S0.5 for fructose 6-phosphate (concentration required for 50% of maximum activity) out of the physiological concentration range. At pH 7.4 and about physiological concentrations of ATP, the curve of PFK activity against the …
Different modes of activating phosphofructokinase, a key regulatory enzyme of glycolysis, in working vertebrate muscle
2002
Glycolytic flux in white muscle can be increased several-hundredfold by exercise. Phosphofructokinase (PFK; EC 2.7.1.11) is a key, regulatory enzyme of glycolysis, but how its activity in muscle is controlled is not fully, understood. In order not to neglect integrative aspects of metabolic regulation, we have studied in frogs (Rana temporaria) a physiological form of muscle work (swimming) that can be triggered like a reflex. We analysed swimming to fatigue in well rested frogs, recovery from exercise, and repeated exercise after 2 h of recovery. At various times, gastrocnemius muscles were tested for glycolytic intermediates and effectors of PFK. All metabolites responded similarly to the…
Fructose 2,6-bisphosphate and glycolytic flux in skeletal muscle of swimming frog
1990
AbstractGlycolytic flux in skeletal muscle is controlled by 6-phosphofructokinase but how this is achieved is controversial. Brief exercise (swimming) in frogs caused a dramatic increase in the phosphofructokinase activator, fructose 2,6-bisphosphate, in working muscle. The kinetics of phosphofructokinase suggest that in resting muscle, the enzyme is inhibited by ATP plus citrate and that the increase in fructose 2,6-bisphosphate is part of the mechanism to activate phosphofructokinase when exercise begins. When exercise was sustained, fructose 2,6-bisphosphate in muscle was decreased as was the rate of lactate accumulation. Glycolytic flux and the content of fructose 2,6-bisphosphate appea…
The HIF1α-PFKFB3 Pathway: A Key Player in Diabetic Retinopathy
2021
Abstract Diabetic retinopathy (DR) is the leading cause of blindness for adults in developed countries. Both microvasculopathy and neurodegeneration are implicated in mechanisms of DR development, with neuronal impairment preceding microvascular abnormalities, which is often underappreciated in the clinic. Most current therapeutic strategies, including anti-vascular endothelial growth factor (anti-VEGF)-antibodies, aim at treating the advanced stages (diabetic macular edema and proliferative diabetic retinopathy) and fail to target the neuronal deterioration. Hence, new therapeutic approach(es) intended to address both vascular and neuronal impairment are urgently needed. The hypoxia-induci…