Peroxisomal enzyme activities in regenerating liver of rats

Abstract

The activities of five peroxisomal enzymes (fatty acyl-CoA oxidase, FAO; uricase, U; L-hydroxyacid oxidase, LHAO; D-aminoacid oxidase, DAO; and catalase, C and the triglyceride content were determined in the regenerating liver of rats after partial hepatectomy. The FAO activity was significantly increased on day 3. Thus, its rise followed the increase of the triglyceride content and preceded the disappearance of steatosis. For U and LHAO a similar progressive increase in activities was obtained on days 3, 5, and 7 of regeneration. DAO exhibited a highly significant increase on day 1. C increased on day 1 and then again after day 3. It is concluded that peroxisomal functions are not restored at parallel rates during liver regeneration.

Effects of antilipolytic agents on rat liver peroxisomes and peroxisomal oxidative activities

“…In accord with previous results [8,9], these data show that thè administration of antilipolytic drugs causes a remarkable decrease in thè peroxisomal /ì-oxidative activity of rat liver. Different antilipolytic drugs exhibited similar effects.…”

“…Recently, we explored thè effects of thè decrease in thè lipid supply to thè liver by giving antilipolytic agents to thè fasting rats. In these experiments, we were able to demonstrate that treatment with 3',5'-dimethylpyrazole or with Acipimox resulted in a significant decrease in thè peroxisomal fatty acid-oxidative actìvity within a very short time [8,9]. Here, we describe thè temporal pattern of thè decline and of thè subsequent restoration of peroxisomal enzyme activities after thè administration of antilipolytic agents and give an explanation of this phenomenon, together with a hypothesis concerning its physiological role.…”

“…Many of thè known effects of antilipolytic agents may be related to features of liver autophagy. For examples, with regard to prevention of peroxisome changes by glucose [8,9] or by glutamine, we may note that autophagy is under moment-to-moment control by thè cellular aminoacids [26] and thus may be sensitive to thè need of aminoacids for gluconeogenesis, rather than to thè decrease in supply of free fatty acids per se.…”

“…more than 10% to overall hepatic oxidation of thè physiologically important fatty acids palmitate and oleate, under normal conditions [3], and that this figure is greatly increased by hypolipidemic drugs (such as chlofibrate, tibric acid and Wy-14.683) [4,5] or by increasing thè lipid supply to thè liver. Indeed, thè /ì-oxidative enzyme activity in liver peroxisomes is increased by feeding rats a highlipid diet [6], after thè accumulation of endogenous lipid in thè liver (e.g., during liver regeneration [7]) or after stimulation of lipogenesis (by feeding glucose [8]).…”

Searching for the fountain of autophagy-dependent youth

“…3 Results of lowering the load (by the injection of an antilipolytic drug to fasted animals) proved to be too good: the expected decrease in fatty-acyl CoA oxidase was too big and too early (time-lag was shorter than three hours) to be accounted for by changes in enzyme synthesis. 4 Furthermore the decrease was associated with a parallel decrease in all peroxisomal enzyme activities.…”