TRIACYLGLYCEROL BIOSYNTHETIC-ENZYMES IN LEAN AND OBESE ZUCKER RATS

Authors
Citation
Sc. Jamdar et Wf. Cao, TRIACYLGLYCEROL BIOSYNTHETIC-ENZYMES IN LEAN AND OBESE ZUCKER RATS, Biochimica et biophysica acta, L. Lipids and lipid metabolism, 1255(3), 1995, pp. 237-243
Citations number
53
Categorie Soggetti
Biology,Biophysics
ISSN journal
00052760
Volume
1255
Issue
3
Year of publication
1995
Pages
237 - 243
Database
ISI
SICI code
0005-2760(1995)1255:3<237:TBILAO>2.0.ZU;2-T
Abstract
In the present investigation, we have compared the potential of triacy lglycerol formation from sn-glycerol-3-phosphate (GP) and 2-monoacylgl ycerol (MG) in liver, adipose tissue and intestine from lean and obese Zucker rats. Microsomal fractions were used to measure the sn-glycero l-3-phosphate acyltransferase (GPAT), diacylglycerol acyltransferase ( DGAT) and monoacylglycerol acyltransferase (MGAT) activities and homog enates were used to measure NEM-sensitive and NEM-insensitive phosphat idate phosphohydrolase (PPH) activities. In adipose tissue and liver, the GP pathway served as the major route of glycerolipid formation, wi th adipose tissue being 5-20-fold more active. The activities of the G P pathway enzymes increased further in response to obesity, with some degree of organ specificity. In adipose tissue of obese rats, the acti vities of all the pathway enzymes increased; whereas, in liver and int estine, this response was limited to PPH and GPAT, respectively. In co ntrast with the GP pathway enzymes, obesity in Zucker rats was not ass ociated with alterations in the acylation of 2-monoacylglycerol. Compa rison of the activities of MGAT in different intestinal segments indic ated that the MG pathway was most active in the jejunum and least acti ve in the ileum and that this pattern did not change in response to ob esity. These measurements of the individual enzyme reactions provide e vidence that the entire process of esterification via sn-glycerol-3-ph osphate is accelerated in the various organs from obese rats and that this perturbation in lipid metabolism may contribute significantly to the increased deposition of body fat noted in this animal model.