Effect of glucose on the utilization of palmitate 1 14C by rat kidney cortex slices.

The authors studied the effect of glucose on the uptake and utilization of palmitate 1 14C by rat kidney cortex slices. They found that its inhibitory effect on free fatty acid (FFA) uptake was caused by inhibition of the incorporation of 1 14C-labelled palmitate into the total lipids and FFA and by reduced oxidation to 14CO2. Glucose has a regulative function in the utilization of FFA by the kidneys.     

Effect of hippurate on tissue fatty acid metabolism

The authors studied 1-14C-palmitate metabolism in rat muscle, renal cortex and liver incubated with synthetic hippurate in vitro (1 mmol/l). a) Hippurate did not affect 1-14C-palmitate uptake and utilization in the muscle (hemidiaphragm). b) In the renal cortex it stimulated only the incorporation into total lipids and from the individual lipid fractions into mono- and diglycerides and free fatty acids (FFA). c) In the liver it stimulated the uptake, oxidation to 14CO2 and incorporation into total lipids and, out of the individual lipid fractions, into phospholipids, triacylglycerols and free fatty acids. d) Hippurate already had a significant effect in the concentration of 0.5 mmol/l, i.e. during the development of the disturbance and not just as a supplementary factor in advanced renal insufficiency. It is concluded that, by interfering with fatty acid metabolism, the hippurate present in the serum of patients with renal insufficiency plays an active role in the development of dyslipoproteinaemia in such patients.     

Synthesis of 8-diamino-substituted adenosine, inosine, and guanosine

Adenosine, inosine and guanosine derivatives were prepared, modified at the C-8 atom with the aid of diamines (1,3-diaminopropane, 1,4-diaminobutane and 1,5-diaminopentane).     

Specific binding of human alpha interferon to a high affinity cell surface binding site on bovine kidney cells

Virus-induced human alpha interferon (HuIFN-alpha) derived from Namalwa cells and purified to a specific activity of 2 X 10(8) units/mg of protein was radiolabeled with 125I-labeled Bolton and Hunter reagent to a specific activity of 4-12 microCi/micrograms of protein. The binding of this 125I-IFN to bovine kidney cells was examined at 4 degrees C. Scatchard analysis of the binding data indicate the presence of 650 binding sites/cell and binding of the ligand with an apparent Kd of 6 X 10(-11) M. Trypsin or acid treatment of cells to which 125I-IFN was bound resulted in the release of greater than or equal to 77% of the radioactivity, indicating a majority of radiolabeled material was bound to the cell surface. Antibodies against human leukocyte IFN but not antibodies against human fibroblast IFN inhibited the binding of radiolabeled IFN to the cells. The binding of 125I-IFN was not inhibited by a 75-fold molar excess of mouse IFN but was inhibited 30% by a 200-fold molar excess of human beta (fibroblast) IFN. These data are compatible with the Lower biological activities of these IFNs on bovine kidney cells. Several Escherichia coli derived HuIFN-alpha s inhibited the binding of the radiolabeled IFN to the same extent as native HuIFN-alpha s, but four fragments of HuIFN-alpha 1, an E. coli-derived 86 amino acid NH2-terminal fragment as well as 3 different synthetic carboxy-terminal fragments of 140, 56, or 46 amino acids did not inhibit binding.     

Release of free fatty acids by the rat kidney.

The authors studied the release of free fatty acids (FFA) by the rat kidney cortex. They found that the kidney cortex released FFA into the incubation medium like adipose tissue. The presence of Ca2+ ions did not affect FFA release. Glucose significantly inhibited it. It was further shown that the kidney cortex is sensitive to the akipokinetic action of adrenaline and the antilipolytic action of insulin, in the same way as adipose tissue. It is concluded from the results that the kidney cortex has a lipolytic system which seems to be subject to higher hormonal regulatory mechanisms.     

Effect of hippurate on glucose utilization in rat kidney cortex slices.

Hippurate action on glucose utilization was evaluated in rat kidney cortex slices. Studies have shown the following. (1) Hippurate inhibits markedly basal as well as insulin-stimulated glucose utilization and basal gluconeogenesis. (2) Ca deficiency and specific Ca channel blockers diltiazem and isradipine abolish the hippurate inhibition of glucose utilization. (3) K+ channel blockers, i.e. the increased K+ concentration in incubation medium, procaine and sulfonylurea drugs also abolish the hippurate inhibition of glucose utilization. It is concluded that hippurate and benzoate operate through the ATP-dependent K+ channel.