[77a] Phosphofructokinase

Ling, Kuo-Huang; Paetkau, Verner; Marcus, Frank I.; Lardy, Henry A.

doi:10.1016/0076-6879(66)09087-6

Cited by 110 publications

(56 citation statements)

References 8 publications

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“…L -1 ): sucrose (25), ethylene diamine tetraacetic acid (2), tris-hydroxymethyl-amino methane (10, pH 7.4). CS [17], HAD [18], HK [19], PFK [20] and LDH [21] activities were assessed using a Cobas-BIO autoanalyzer (Roche, Basle, Switzerland). Protein content in the homogenates was measured with the microbicinchoninic acid method of Pierce (Rockford, IL, USA) [22].…”

Section: Collection and Analysis Of Muscle Biopsiesmentioning

confidence: 99%

Muscle metabolic status in patients with severe COPD with and without long-term prednisolone

Pouw¹,

Lang²,

Gosker³

et al. 2000

Eur Respir J

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Both abnormalities in high energy phosphate metabolism and a decreased oxidative enzyme capacity have been reported in skeletal muscle of stable chronic obstructive pulmonary disease (COPD) patients. The first aim of this study was to investigate whether these findings are present in anterior tibialis muscle and whether or not they are associated. Abnormalities in mitochondrial structure and function as well as signs of myopathy have been found during corticosteroid treatment. The second aim of this study, therefore, was to investigate whether in COPD patients prolonged use of low dose prednisolone has effects on muscle energy metabolism and qualitative morphology.In a cross-sectional study 15 COPD patients (forced expiratory volume in one second (FEV1) 33 9 (mean SD) % predicted) who were steroid-naive (CORT-) were compared with 10 healthy control subjects (HC) and with 14 COPD patients (FEV1 30 11 % pred), who had been using oral prednisolone for at least 1 yr (CORT+).It was found that adenosine triphosphate (ATP)/adenosine diphosphate was lower in CORT-compared to HC (5.7 versus 6.2, p=0.03). Inosine monophosphate was detected in 13 of 15 CORT-compared to 3 of 10 HC (p=0.004). However, although indications were found for an imbalance in production and utilization of ATP, comparing CORT-and HC, no differences in oxidative (citrate synthase and 3-hydroxy-acylcoenzyme A dehydrogenase) and glycolytic (hexokinase, lactate dehydrogenase and phosphofructokinase) enzyme capacities were found.When, comparing steroid-treated and steroid-naive patient subgroups, no differences in the above mentioned parameters of muscle energy metabolism and of muscle qualitative morphology were found. Eur Respir J 2000; 16: 247±252. Supported by a scholarship from ASTRA BV, the Netherlands.Exercise intolerance and dyspnoea are the most frequently occurring complaints in patients with severe chronic obstructive pulmonary disease (COPD). Weakness of both skeletal and respiratory muscles contributes significantly to these complaints [1]. Recently it has been shown that muscle weakness in COPD patients can predominantly be explained by muscle atrophy [2]. However, several studies suggested that exercise tolerance might also be impaired by alterations in muscle energy metabolism [3±5].Experimental evidence is accumulating that in COPD patients muscle energy metabolism is already disturbed at rest. JAKOBSSON et al. [6] found a decreased oxidative capacity and an increased glycolytic capacity in quadriceps femoris muscle. MALTAIS et al.[3] reported a decreased oxidative capacity in quadriceps femoris muscle. In another recent study [4], in tibialis anterior muscle, indications for an imbalance in adenosine triphosphate (ATP) utilization and resynthesis were found, as suggested by increased inosine monophosphate (IMP) levels, which were negatively related with ATP/adenosine diphosphate (ADP) ratios. However, in that study oxidative and glycolytic enzyme capacities were not investigated.In view of the above mentioned findings in skel...

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Section: Collection and Analysis Of Muscle Biopsiesmentioning

confidence: 99%

Muscle metabolic status in patients with severe COPD with and without long-term prednisolone

Pouw¹,

Lang²,

Gosker³

et al. 2000

Eur Respir J

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“…All the fructose 1, 6-diP was recoverable when incubated with the enzyme as determined by the method of Ling et al (15). In addition, the sedimentation characteristic of the enzyme determined on sucrose density gradients is not changed when the centrifugation is carried out in the presence of fructose 1, 6-diP, or a combination of fructose 1, 6-diP, ADP, and P-enolpyruvate.…”

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confidence: 74%

Some Properties of Partially Purified Pyruvate Kinase from Euglena gracilis Klebs var. bacillaris

Vaccaro¹,

Zeldin²

1974

Plant Physiol.

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A method of purification of pyruvate kinase (EC 2.7 The significance of the properties of pyruvate kinase in the regulation of photosynthetic carbohydrate metabolism, especially in connection with the inability of fructose 1, 6-diphosphate to reverse Ca2+ and ATP inhibitions, is emphasized.The formation of pyruvate and ATP from P-enolpyruvate and ADP is now recognized as a controlling step in the regulation of glycolysis in many organisms. During the last several years the enzyme pyruvate kinase, which catalyzes this conversion, has been isolated and purified from many sources and its properties described in some detail (4-7, 12, 14. 18-20, 24).Although information concerning the properties of pyruvate kinase in heterotrophic organisms is available, the situation in autotrophic organisms has not been examined extensively (8, 23,(26)(27)(28)

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“…In the present paper, we report on the quantification of rat liver and kidney phosphofructokinase, the eighth enzyme in the series, also by RIA. We minimized, if not prevented, aggregation by conducting the RIA under dilute conditions and by including 30mM-KF in the homogenization buffer (Ling et al, 1966). KF was included also to inhibit the activity of phosphofructokinase phosphatase, which might have altered the quaternary structure of the native enzyme (Soling et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

Quantification of liver and kidney phosphofructokinase by radioimmunoassay in fed, starved and alloxan-diabetic rats

Donofrio¹,

Thompson²,

Reinhart³

et al. 1984

Biochemical Journal

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A newly developed specific radioimmunoassay was used to quantify phosphofructokinase protein directly and independently of assayable activity in liver and kidney cytosol of normal fed, starved and alloxan-diabetic rats. In the fed state, liver phosphofructokinase concentration was 0.096 pm and the kidney enzyme was 0.086 pM (jumol/kg of tissue). In the starved state (24h), liver and kidney phosphofructokinase concentrations decreased by 30%. Prolonged starvation up to 72h did not further decrease enzyme concentration. In liver, total enzyme content during starvation declined by more than 50%, secondary also to a decrease in liver weight. In the alloxan-diabetic rats, there was a 22% decrease in enzyme protein concentration in liver and kidney. Total enzyme content per liver actually decreased much more (46%), because diabetes also resulted in a decrease in liver size. In conjunction with assayable activity measurements, the results of the radioimmunoassay allowed us to calculate the apparent specific activity of the enzyme. The specific activity of the kidney enzyme was 2-3 times that of the liver. Little or no change in specific activity of the liver or kidney enzyme occurred as a result of starvation or chemically induced diabetes. Tissue enzyme concentrations of phosphofructokinase unequivocally reconcile the ultimate results of changing rates of synthesis and degradation and are useful data in the design of spectrophotometric, kinetic, aggregation-disaggregation and other studies.

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[77a] Phosphofructokinase

Cited by 110 publications

References 8 publications

Muscle metabolic status in patients with severe COPD with and without long-term prednisolone

Muscle metabolic status in patients with severe COPD with and without long-term prednisolone

Some Properties of Partially Purified Pyruvate Kinase from Euglena gracilis Klebs var. bacillaris

Quantification of liver and kidney phosphofructokinase by radioimmunoassay in fed, starved and alloxan-diabetic rats

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