Disease relevance of McN 3802

• To test whether induction of additional myocyte hypertrophy might prevent pathological LV remodeling after large MI, we administered 2-tetradecylglycidic acid (TDGA) 20 mg/kg/day to sham-operated (n = 12) and MI (n = 10) rats for 10 days, beginning the third day after infarction [1].

High impact information on McN 3802

• The effects of glucose and lactate infusion on palmitate oxidation were compared with the effect of 2-tetradecylglycidic acid (TDGA), an irreversible inhibitor of the carnitine acyltransferase I, in normoxic canine myocardium [2].
• In primary hepatocyte cultures, oleic acid had no inducing effect, but in the presence of 2-tetradecylglycidic acid (TDGA), an inhibitor of carnitine palmitoyltransferase I, it induced P-450 4A1, peroxisomal beta-oxidation, and L-FABP pretranslationally [3].
• When an erythrocyte suspension was incubated with [1-14C]palmitoyl-L-carnitine, radiolabeled palmitate was recovered in the phospholipid fraction, and the carnitine palmitoyltransferase inhibitor, 2-tetradecylglycidic acid, completely abolished the incorporation [4].
• Action of the oral hypoglycemic agent 2-tetradecylglycidic acid on hepatic fatty acid oxidation and gluconeogenesis [5].
• 1. The induction of peroxisomal beta-oxidation activities by bezafibrate in cultured rat hepatocytes and in the rat in vivo was prevented by inhibitors of carnitine acyltransferase, e.g. 2-bromopalmitate, 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate or 2-tetradecylglycidic acid [6].

Biological context of McN 3802

• Inhibition of hepatic lipogenesis by 2-tetradecylglycidic acid [7].
• Effects of 2-tetradecylglycidic acid on rat platelet energy metabolism and aggregation [8].

Anatomical context of McN 3802

• The effects of 2-tetradecylglycidic acid (TDGA), TDGA-CoA and TDGA-carnitine were examined in purified hepatic CPT (carnitine palmitoyltransferase) and in hepatic mitochondria and inverted submitochondrial vesicles derived from Sprague-Dawley rats [9].
• Effect of the fatty acid oxidation inhibitor 2-tetradecylglycidic acid (TDGA) on glucose and fatty acid oxidation in isolated rat soleus muscle [10].

Associations of McN 3802 with other chemical compounds

• Indeed, in isolated hepatocytes from 24-h-old rabbits, the 75% inhibition of the oxidation by 2-tetradecylglycidic acid, resulted in a total redirection of oleate metabolized towards triacylglycerol synthesis [11].
• This protective effect of octanoate against inhibition of gluconeogenesis by 2-tetradecylglycidic acid was seen even though in some experiments the mitochondrial redox state remained two to three times the magnitude observed prior to octanoate addition [12].
• 3. Gluconeogenesis from 4 mM glycerol was not inhibited and gluconeogenesis from 4 mM propionate was only slightly inhibited by 2-tetradecylglycidic acid [12].

Gene context of McN 3802

• To accomplish this objective, fed or overnight fasted rats were treated with 2-tetradecylglycidic acid (TDGA), a specific, irreversible CPT1 inhibitor, and acute changes in rat epididymal leptin expression and serum leptin content were measured using Northern, RT-PCR, and radioimmunoassay analyses [13].
• Inhibition of the mitochondrial uptake of long-chain fatty acids was achieved by treating rats with 2-tetradecylglycidic acid (TDGA), a potent inhibitor of the overt form of carnitine palmitoyltransferase (CPT-I) [8].

References