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At least 217 records · Page 12Linked to original sources
PubMed1990

Intestinal absorption of arachidonic acid in experimental azotemia.

The effect of renal failure (RF) on intestinal absorption of dietary fatty acids is not known. We studied the intestinal absorption of arachidonic acid (AA) in rats with experimental short-term (2 weeks post-subtotal nephrectomy) and long-term (5-6 weeks post-subtotal nephrectomy) RF. The results were compared with those obtained in sham-operated animals on liberal food intake (NL) and in those pair-fed (PF) with the respective RF groups. In vivo perfusion and in vitro incubation experiments were performed at a wide range of AA concentrations. The rates of AA transport determined both in vivo and in vitro were significantly lower in the short-term RF group than those found in the NL controls and the PF animals who showed comparable values. In contrast animals with long-term RF exhibited an increased rate of AA transport as compared with the respective controls. The observed changes in the transport rates appeared to parallel directional changes in mucosal mass which was reduced in animals with short-term RF and restored in those with long-term RF.

Animals↗
PubMed1979

Impact of hemodialysis on the abnormal glucose and alanine kinetics of chronic azotemia.

Rates of alanine and glucose turnover and precursor-product interrelationships were determined in patients on chronic hemodialysis and in matched controls using simultaneous primed injection-continuous infusions of [U-14C] alanine and [2-3h] glucose. In eight chronically dialyzed patients studied before their first dialysis of the week, glucose turnover was 866 +/- 120 micromole/min (mean +/- SE); after their last dialysis of the week, glucose turnover was 880 +/- 63 micromole/min. These rates were 35% (p less than 0.05) and 37% (p less than 0.01) greater than rates observed in ten normal volunteers (642 +/- 28.3 micromole/min). Fasting glucose and insulin levels in dialyzing patients were unchanged from normal. Alanine turnover was increased predialysis (318 +/- 55.2 micromoles/min; p less than 0.01) and postdialysis (248 +/- 32.4 micromole/min; p less than 0.01) as compared to normal (168 +/- 14.3 micromole/min). In patients pre- and postdialysis, gluconeogenesis from alanine was increased to 34.6 +/- 10.9 micromole/min (p less than 0.05) and 39.0 +/- 6.33 micromole/min (p less than 0.05) compared to 20.9 +/- 1.63 micromole/min in normal subjects. We conclude that neither acute nor chronic hemodialysis corrects the increased glucose and alanine production and utilization and gluconeogenesis observed in chronic renal failure.

Adult↗