Carbohydrate synthesis from lactate in pigeon-liver homogenate

Krebs, Harald; Dierks, Christa; Gascoyne, T.

doi:10.1042/bj0930112

Cited by 128 publications

(43 citation statements)

References 30 publications

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“…Glucose production by renal cortical slices was estimated according to Krebs et al [8] by incubating the washed cells in saline medium to which the substrate has been added in a 10 mM concentration, at 40°C for 1 h, with O2 t CO2 (95:s) as the gas phase. Glucose was determined by the glucose oxidase method [8,9]. Phosphoenolpyruvate carboxykinase activity was measured spectrophotometrically in the direction of oxaloacetate synthesis in the presence of an excess of malate dehydrogenase at 3O"C, as described previously …”

Section: Methodsmentioning

confidence: 99%

Stimulation of rat kidney gluconeogenic ability by inhibition of liver gluconeogenesis

et al. 1976

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Section: Methodsmentioning

confidence: 99%

Stimulation of rat kidney gluconeogenic ability by inhibition of liver gluconeogenesis

et al. 1976

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“…Blood glucose was assayed by the glucose oxidase method as described by Krebs et al (1963Krebs et al ( , 1964. Blood samples were collected in a heparinized tube after cutting the jugular vein.…”

Section: Methodsmentioning

confidence: 99%

Stimulation of phosphoenolpyruvate carboxykinase (guanosine triphosphate) activity by low concentrations of circulating glucose in perfused rat liver

Moreno¹,

Sanchez-Urrutia²,

Medina³

et al. 1975

Biochemical Journal

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(Received I1 Febrmary 1975) 1. After nicotinic acid treatment, rat liver glycogen is depleted and phosphoenolpyruvate carboxykinase activity increased, to about twice the initial value. 2. The increase in phosphoenolpyruvate carboxykinase activity promoted by nicotinic acid is prevented by cycloheximide or actinomycin D, suggest-ing that this effect is produced by synthesis of the enzyme de novo. 3. Despite the enhancement of phosphoenolpyruvate carboxykinase activity and glycogen depletion, which occurs 5h after the injection of nicotinic acid, the gluconeogenic capacity of liver is low and considerably less than the values found in rats starved for 48h. 4. When the livers of well-fed rats are perfused in the presence of low concentrations of glucose, the activity of phosphoenotpyruvate carboxykinase significantly incteases compared with the control. 5. This increase is not related to the glycogen content, but seemns to be also the result of synthesis of the enzyme de novo, since this effect is coumteracted by previous treatment with cycloheximide or actinomycin D. 6. Phosphoenolpyruvate carboxykinase activity is not increased in the presence of low concentrations of circulating glucose when 40mnM-imidaiole (an activator of phosphodiesterase) is added to the perfusion medium. 7. Addition of dibutyryl cyclic AMP to the perfusion medium reguftsg in an incrtease in phosphoenolpyruvate carboxykinase activity, in spite of the presenCe of normal concentrations of circulating glucose. On the other hand, the concentration of cyclic AMP in the liver increases when that of glucose in the medium is low. 8.These results suggest that, in the absence of hormonal factors, the regulation of phosphoenolpyruvate carboxykinase can be accomplished by glucose itself, inadequate concentrations of it resulting in the induction of the enzyme. The mediator in this regulation, as in hormonal regulation, seems to be cyclic AMP.

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“…Blood glucose was estimated by glucose oxidase method (Krebs et al, 1964). Urinary glucose was detected with Labstix(R) (Ames Company Co.).…”

Section: Methodsmentioning

confidence: 99%

General Survey of Diabetic Features of Yellow KK Mice

1970

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SynopsisYellow KK mice, carrying the yellow obese gene (Ay), developed marked adiposity and diabetic symptoms in comparison with their control littermates, black KK mice. The blood glucose and circulating insulin levels were increased progressively from 5 weeks of age in yellow KK mice. Age dependent alterlations were also observed in pancreas and kidney. Namely, degranulation and glycogen infiltration of B cells, first observed at 5 weeks of age, were followed by hypertrophy and central cavitation of islets. Renal glomerular changes, which were very similar to diffuse or exudative type of sclerosis in human diabetes, were also recognized in the mice at 16 weeks of age. These changes, though less remarkable, were also noted in their control littermates older than 16 weeks of age. Some metabolic defects were developed, as demonstrated by in vitro experiments. At younger age, lipogenesis by liver and adipose tissue was increased in yellow KK mice, but there was no noticeable difference in glucose oxidation by adipose tissue between both mice. Insulin sensitivity of adipose tissue was decreased with age in both mice, especially in yellow KK mice being reduced more remarkably to its complete loss at 16 weeks of age. These findings indicate that the yellow obese gene not only induces adiposity but also accelerates development of diabetic traits of KK mice. A possible mechanism for the observed diabetogenic action of the gene will be discussed.

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Carbohydrate synthesis from lactate in pigeon-liver homogenate

Cited by 128 publications

References 30 publications

Stimulation of rat kidney gluconeogenic ability by inhibition of liver gluconeogenesis

Stimulation of rat kidney gluconeogenic ability by inhibition of liver gluconeogenesis

Stimulation of phosphoenolpyruvate carboxykinase (guanosine triphosphate) activity by low concentrations of circulating glucose in perfused rat liver

General Survey of Diabetic Features of Yellow KK Mice

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