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Biomedical subjects

M Wicklmayr

Publications and source records attributed to M Wicklmayr.

At least 109 records · Page 6Linked to original sources
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↗
PubMed1975

[On the analysis of the hepatic-venous 133xenon-clearance after the application of the gas by inhalation].

After the inhalation of 133xenon continuous registrations of portal 133xenon concentrations showed that the monoexponential terminal component of the hepatic-venous 133xenon-clearance might be due to the recirculation of the gas from the gut. Accordingly, in all the cases, with the application of the wellknown "extrapolation and peeling off" of this monoexponential terminal component from this part of the hepatic-venous 133xenon-clearance, not affected any more by arterial recirculation a monoexponential 133xenon-clearance could be separated. The time-constant of the latter was similar to that of the well-knwon specific hepatic 133xenon-clearance after the application of the gas by injection into the portal vein.

Hepatic Veins↗
PubMed1975

[Oxygen, carbohydrate and fat metabolism of the splanchnic region under the influence of equimolecular parenteral doses of glucose and fructose].

Hepatic metabolic balances derived from arterio-hepatic venous substrate differences and hepatic blood flow exhibited similar results during fructose and glucose infusion (10 g/5 min, 0.5 g/kg X h) as compared to those from the isolated perfused organ. Accordingly, in account of hepatic utilization of fructose glucose homeostasis and secretion maintained during fructose infusion. However, the smaller insulin response during fructose infusion did not reduce hepatic free fatty acid utilization to such an extend as to increase pyruvate oxydation. Thus, splanchnic production of lactate and pyruvate descending from fructose was enhanced leading to a 7-fold increase of arterial lactate concentration. Since hepatic venous lactate to 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 2-3-fold that of glucose as calculated from splanchnic utilization rates. The rapid ATP-breakdown was followed by an increment in splanchnic oxygen consumption. The larger energy demand during fructose infusion seemed to be satisfied by an enhanced endoxydation of free fatty acids.

Adenosine Triphosphate↗
PubMed1975

[Influence of parenteral fructose or glucose administration on uric acid formation and phosphate uptake of the human liver].

15 min. after intravenous administration of fructose (10 g/5 min, 0,5 g/kg/h) the hepatic uric acid production in healthy volunteers increased from 0,07 mg/100 g X min to 0,52 mg/100 g X min. After one hour the enhanced uric acid production was 0,3 mg 100 g X min. The enhanced uric acid production was accompanied by an increased hepatic phosphate uptake. The highest value was 13 mumol/100 g X min. During the control period the liver released small amounts of phosphate into the hepatic vein. The increased hepatic uric acid output correlated with an enhanced renal clearance, therefore the peripheral venous uric acid concentrations remained unchanged.

Fructose↗