Premium
Effects of streptozotocin‐induced diabetes on microsomal long‐chain fatty acyl‐CoA synthetase and hydrolase
Author(s) -
Dang A. Q.,
Faas F. H.,
Carter W. J.
Publication year - 1984
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02534714
Subject(s) - medicine , endocrinology , streptozotocin , hydrolase , clinical chemistry , diabetes mellitus , acyl coa , lipidology , microsome , chemistry , insulin , enzyme , biology , biochemistry
Streptozotocin‐induced diabetes significantly decreased rat liver microsomal long‐chain fatty acyl‐CoA (LCA‐CoA) hydrolase. The decrease was observed using either palmitoyl‐CoA (35 per cent, p<0.01) or oleoyl‐CoA (23 per cent, p<0.01) as the substrate for the enzyme. Under the same conditions, diabetes did not significantly alter activity of LCA‐CoA synthetase. Daily subcutaneous injections of protamine zinc insulin (10–12 units/day) into the diabetic rats returned their blood glucose to normal but only partially corrected the LCA‐CoA hydrolase activity and did not effect LCA‐CoA synthetase activity. The decreased LCA‐CoA hydrolase and the unchanged LCA‐CoA synthetase activities in the diabetic rat liver were interpreted as factors that may contribute to elevation of fatty acyl‐CoA levels in the diabetic liver.