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The effects of 3‐hydroxy‐3‐methylglutaryl‐CoA reductase inhibition on tissue levels of carnitine and carnitine acyltransferase activity in the rabbit
Author(s) -
Bhuiyan Jalaluddin,
Seccombe David W.
Publication year - 1996
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/bf02522982
Subject(s) - carnitine , medicine , endocrinology , lovastatin , reductase , coenzyme a , acyltransferase , carnitine o palmitoyltransferase , biology , levocarnitine , chemistry , cholesterol , biochemistry , enzyme , metabolism , beta oxidation
Recently, a new class of lipid lowering agents [3‐hydroxy‐3‐methylglutaryl (HMG)‐CoA reductase inhibitors] was introduced into clinical practice. The use of these agents could lead to a secondary deficiency in carnitine, which may manifest clinically as a myalgia/myositis—a side effect that is occasionally seen with this class of drugs. In the present study, we examined the effect of an HMG‐CoA reductase inhibitor (lovastatin) on serum and tissue levels of carnitine and carnitine acyltransferase activities in the rabbit. Rabbits ( n =6) were fed chow containing lovastatin (30 mg/d) for 16 wk. Blood was collected and tissues (liver, heart, and skeletal muscle) harvested at sacrifice. Free and total carnitine were measured in serum and tissues by a radioenzymatic method. Carnitine acetyltransferase and carnitine palmitoyltransferase (CPT) activities were determined and expressed relative to DNA. Serum free (24.0±2.6 vs. 29.4±3.1 μM) and total (35.1±4.7 vs. 52.8±8.8 μM) carnitine levels increased significantly with 16 wk of treatment. This increase in total carnitine was mainly due to an increase in the levels of serum acylcarnitine (12.7±3.1 vs 26.5±5.7 μM). Tissue levels of total carnitine were significantly decreased by the treatment. Carnitine acetyltransferase was unaffected by the treatment, whereas there was a significant increase in the activity of CPT in the liver and heart.