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Biomedical subjects

G Dietze

Publications and source records attributed to G Dietze.

At least 91 records · Page 5Linked to original sources
PubMed1978

Effect of phenformin on hepatic balances of gluconeogenic substrates in man.

The effect of a five day pretreatment with phenformin (3 X 50 mg daily) on hepatic metabolism was studied in six healthy volunteers. Arterial and hepatic venous concentrations of substrates and hepatic blood flow were estimated during a basal period and during a low-dose lactate infusion (0,03 mmol . kg-1 . min-1). The results have been compared with those obtained from untreated normal subjects in a previous study (16). During the baseline period arterial concentration of alanine and the hepatic venous concentration ratios of alanine: pyruvate and beta-hydroxybutyrate: acetoacetate were significantly increased with phenformin treatment, while the balances of carbon dioxide and glucose and the fractional extraction of alanine were decreased compared to the values obtained in untreated subjects. During lactate infusion mean arterial lactate concentration was significantly increased and hepatic lactate extraction was decreased compared to untreated persons under the same conditions. In the phenformin-treated group lactate infusion resulted in hepatic output of pyruvate and the hepatic glucose balance remained unchanged compared to baseline. Since the rate of hepatic blood flow was not increased during lactate infusion a significantly smaller glucose output and lactate uptake was obtained with phenformin. These findings support the present view that the hypoglycaemic effect of biguanides is due, at least in part, to inhibition of hepatic gluconeogenesis.

Adult↗
PubMed1978

On the mechanism of glucose release from the muscle of juvenile diabetics in acute insulin deficiency.

In fifty-three healthy subjects and twenty-three juvenile diabetics the measurement of arterial and deep venous glucose concentrations showed that the substrate was taken up by the tissues of the forearm of all the healthy subjects and released from it in all the diabetic ones. In six of the diabetics glucose output was accelerated almost five-fold during the intrabrachial arterial administration of metaproterenol (1.62 nmol/min), indicating that basal glucose release from muscle may result from enhanced glycogenolysis during acute insulin deficiency. In line with this view a reduction of glucose uptake by muscle was observed in six healthy subjects receiving metaproterenol infusion. However, since the production of lactate by the forearm appeared to be smaller in the diabetics, the basal glucose output could also partly be due to impaired glycolysis. These data suggest that the glucose released from muscle during acute insulin deficiency may be of clinical importance, especially when the rate of glycogenolysis is further stimulated by, for example, enhanced catecholamine drive.

Acute Disease↗
PubMed1978

Effect of continuously increasing concentrations of plasma ketone bodies on the uptake and oxidation of glucose by muscle in man.

Muscle metabolism in man was studied by measuring the arterial and deepvenous concentrations of glucose, lactate, pyruvate, free fatty acids, beta-hydroxybutyrate and aceacetoacetate, and forearm blood flow. After the subjects had fasted overnight, their arterial free fatty acid and ketone levels rose continuously during a period of 90 min, leading to increased ketone body uptake by muscle. Hence, for each subject, a relation was obtained between arterial concentrations and arterial-deepvenous differences of beta-hydroxybutyrate and acetoacetate. As the ketone body utilization increased, the release of lactate rose as well. In spite of these alterations the uptake of glucose remained unchanged. These findings underline the current notion that accelerated ketone uptake reduces pyruvate oxidation but not glucose uptake by muscle.

Acetoacetates↗
PubMed1978

Antiketogenic action of fructose in man.

The effect of fructose infusion (10 gm. every five minutes as a bolus followed by 0.5 gm. per kilogram X hours) on arterial concentrations and hepatic balances of ketones was studied in four juvenile diabetics 24 hours after the withdrawal of insulin. Arterial and hepatic venous concentrations of beta-hydroxybutyrate, acetoacetate, free fatty acids, fructose, and oxygen were measured. Hepatic blood flow was also determined. At constant rates of splanchnic fructose extraction, an 82 per cent diminution of the arterial hepatic venous concentration difference of the ketones was observed but the arteriovenous difference of free fatty acis rose moderately. Since hepatic blood flow was only slightly increased (17 per cent) there was no doubt that total hepatic ketone body formation was reduced. The magnitude of this antiketogenic action became apparent from the continuous fall of the arterial ketone concentrations. Since splanchnic oxygen uptake rose 40 per cent, it is suggested that the antiketogenic effect of fructose was due not only to enhanced re-esterification but also to accelerated oxidation of free fatty acids.

Acetoacetates↗
PubMed1978

[Substrate metabolism of muscles during the early postoperative period: the effect of glucose infusions].

Muscle substrate metabolism was studied by measuring arterial deep-venous substrate concentration differences across the forearm in metabolically healthy volunteers 3 h after abdominal surgery. Despite elevation of insulin levels following glucose infusion, no effect on muscular fractional extraction of glucose and no decrease of lactate and alanine production was found, whereas muscular lipolysis was inhibited to a normal extent and ketone utilization was reduced.

Abdomen↗
PubMed1977

[Effect of bradykinin on muscular glucose uptake in man (author's transl)].

Glucose metabolism of the human forearm was studied in 4 healthy volunteers by monitoring arterial deepvenous glucose concentration differences and by the determination of muscle blood flow, using 133xenon as a tracer, during 25 min intra-brachial-arterial infusion of bradykinin (13.3 ng per min). During the infusion of the kinine the forearms glucose uptake rose continuously from 0.64 +/- 0.11 micronmoles up to 1.68 +/- 0.22 micronmoles per 100 g x min after 25 min of the infusion (p less than 0.005). The enhancement of glucose uptake was partly due to the prompt small acceleration of muscle blood flow and partly to the continuously increasing glucose extraction of the forearm. From these data it is evident that besides insulin there is another physiological agent able to enhance glucose entry into the muscle cell.

Biological Transport↗
PubMed1977

Evidence for a participation of the kallikrein-kinin system in the regulation of muscle metabolism during hypoxia.

The effect of hypoxia on muscle metabolism was studied in the human forearm by the registration of arterial-deep venous concentration differences of oxygen, glucose, lactate, pyruvate, acetoacetate, and muscular blood flow after short, transient arrest of the forearm circulation. These studies were performed during the intravenous infusion of physiological saline (n=4), of a kallikrein-trypsin inhibitor (n=4), and of kallikrein-trypsin inhibitor plus the intrabrachial-arterial infusion of bradykinin (n=4). Infusion of the kallikrein-trypsin inhibitor significantly reduced the well known hypoxia-induced acceleration of nuscular glucose uptake due to a reduction of blood flow and of muscular glucose extraction. These changes of muscular glucose metabolism were accompanied by more or less striking effects on the balances of oxygen, lactate and acetoacetate. Physiological doses of bradykinin into the brachial artery during the infusion of a kallikrein-trypsin inhibitor restored almost completely the metabolic response during hypoxia. From these data there is further evidence for a participation of the kallikrein-kinin system in the physiological regulation of muscular substrate metabolism.

Acetoacetates↗
PubMed1976

On gluconeogenesis of human liver. Accelerated hepatic glucose formation induced by increased precursor supply.

In 8 subjects in whom portal vein catheters had been inserted 5-6 days previously during cholecystectomy, arterial and portal concentrations of glucose, lactate, pyruvate, glycerol, alanine, free fatty acids, beta-hydroxybutyrate and acetoacetate revealed no significant differences. This provided the basis for the calculation of hepatic balances from arterio-hepatic venous substrate-differences in 17 healthy volunteers. In eight of them metabolic balances were determined during elevated hepatic lactate supply. Kinetics of the substrates throughout the whole test period in 9 controls showed no gross interference from the catheterization or infusion procedure. The elevated hepatic lactate concentration caused a doubling of hepatic glucose output, which could almost entirely be accounted for by a fivefold increase of hepatic lactate uptake. This acceleration of hepatic gluconeogenesis was accompanied by a significant increment of hepatic free fatty acid uptake, whereas hepatic ketone body production did not change. These data seem to support the view that hepatic energy requirements caused by an accelerated gluconeogenesis might be covered from enhanced free fatty acid oxidation.

Adult↗
PubMed1976

[Utilization of glucose and fructose in human liver and muscle].

Hepatic metabolic balances derived from arterio-hepatic-venous substrate differences and hepatic blood flow exhibited similar results during fructose infusion (10 g/5 min., 0.5 g/kg x h) as compared to those from the isolated perfused organ: a portion of 55% of splanchnic fructose uptake was accountable for splanchnic glucose production, 25% for splanchnic lactate and pyruvate production and 20% for glycogen - of fat - synthesis and endoxidation. In account of this hepatic metabolism of fructose, glucose homeostasis and insulin secretion almost maintained. However, the small insulin response did not reduce hepatic free fatty acid utilization to such an extent as to increase pyruvate oxidation. Accordingly, splanchnic production of lactate and pyruvate, descending from fructose was enhanced. Since hepatic-venous lactate: pyruvate substrate ratios did not change, the rise of the arterial redox couple could not be due to hepatic fructose metabolism. According to the findings from the isolated perfused organ, fructose seemed to be phosphorylated at a rate which was found to be 2 to 3-fold that of glucose as calculated from splanchnic utilization rates. This high rate of fructose uptake was reduced with increasing insulin levels. The rapid ATP breakdown was followed by an increment of splanchnic oxygen consumption. The larger energy demand seemed to be satisfied by an enhanced endoxidation of free fatty acids. Since diabetics failed to increase their insulin production, their hepatic fructose phosphorylation rate and consequently their hepatic oxygen demand were not limited. Preliminary results concerning metabolic balances from the human forearm during a steady state of fructose supply, underline the notion that fructose has some effects on intermediary metabolism of skeletal muscle. Accordingly, in juvenile diabetics an enhancement of glucose-, lactate- and pyruvate-uptake could be demonstrated.

Abdomen↗