PMID- 11913712 OWN - NLM STAT- MEDLINE DCOM- 20020911 LR - 20151119 IS - 1078-0297 (Print) IS - 1078-0297 (Linking) VI - 108 IP - 3-4 DP - 2000 TI - Metabolic changes in DOCA-salt hypertensive rats. PG - 201-11 AB - In a previous report, we observed an altered proportion of fiber types and a reduction of capillary per fiber ratio in extensor digitorus longus (EDL) and soleus (SOL) muscles of deoxicorticosterone acetate (DOCA)-salt hypertensive rats when compared with controls. The aim of the present study was to ascertain various carbohydrate and lipid enzyme activities and substrates that may be involved in the morphological changes reported. In the SOL muscle of hypertensive rats, glucose, glycogen and triglycerides (TG) levels were increased, citrate synthase (CS) and beta-hydroxy-acyl-CoA dehydrogenase (HAD) activities were reduced, while hexokinase (HK) and lipoprotein lipase (LPL), LPL mass, lactate and free fatty acids (FFA) levels were unchanged. In EDL muscles of hypertensive rats, glycogen levels and LPL mass were higher than in controls, while CS, HAD, HK, and LPL activities and glucose, lactate, FFA and TG levels were unmodified. Serum levels of insulin, TG, cholesterol and FFA were increased while glucose levels were decreased and high-density lipoprotein-cholesterol levels were similar in hypertensive rats when compared with controls. In conclusion, hypertensive rats showed increased glycogen in both EDL and SOL muscles, with hyperinsulinemia and reduced glycemia. Hyperinsulinemia might have been a compensatory response to insulin resistance. The oxidative capacity of SOL muscle was reduced indicating that glucose uptake was conduced via non-oxidative metabolism. TG, FFA and cholesterol were increased in serum and TG in SOL muscle. FAU - Hernandez, N AU - Hernandez N AD - Institute of Experimental Medicine, Faculty of Medicine, Central University of Venezuela, Caracas. hernandn@camelot.rect.ucv.ve FAU - Torres, S H AU - Torres SH FAU - De Sanctis, J B AU - De Sanctis JB FAU - Sosa, A AU - Sosa A LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Res Commun Mol Pathol Pharmacol JT - Research communications in molecular pathology and pharmacology JID - 9437512 RN - 0 (Blood Glucose) RN - 0 (Fatty Acids, Nonesterified) RN - 0 (Insulin) RN - 0 (Triglycerides) RN - 33X04XA5AT (Lactic Acid) RN - 40GP35YQ49 (Desoxycorticosterone) RN - 451W47IQ8X (Sodium Chloride) RN - 9005-79-2 (Glycogen) RN - 97C5T2UQ7J (Cholesterol) RN - EC 1.1.1.- (3-Hydroxyacyl CoA Dehydrogenases) RN - EC 2.3.3.1 (Citrate (si)-Synthase) RN - EC 2.7.1.1 (Hexokinase) RN - EC 3.1.1.34 (Lipoprotein Lipase) RN - IY9XDZ35W2 (Glucose) SB - IM MH - 3-Hydroxyacyl CoA Dehydrogenases/metabolism MH - Animals MH - Blood Glucose/metabolism MH - Cholesterol/blood MH - Citrate (si)-Synthase/metabolism MH - Desoxycorticosterone/toxicity MH - Fatty Acids, Nonesterified/blood/metabolism MH - Glucose/metabolism MH - Glycogen/metabolism MH - Hexokinase/metabolism MH - Hypertension/blood/*chemically induced/*metabolism MH - Insulin/blood MH - Lactic Acid/metabolism MH - Lipoprotein Lipase/metabolism MH - Muscle, Skeletal/metabolism MH - Rats MH - Rats, Sprague-Dawley MH - Sodium Chloride MH - Triglycerides/blood/metabolism EDAT- 2002/03/27 10:00 MHDA- 2002/09/12 10:01 CRDT- 2002/03/27 10:00 PHST- 2002/03/27 10:00 [pubmed] PHST- 2002/09/12 10:01 [medline] PHST- 2002/03/27 10:00 [entrez] PST - ppublish SO - Res Commun Mol Pathol Pharmacol. 2000;108(3-4):201-11.