title: Metabolic changes in DOCA-salt hypertensive rats.
abstract: 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.
authors.affiliation: Institute of Experimental Medicine, Faculty of Medicine, Central University of Venezuela, Caracas. hernandn@camelot.rect.ucv.ve
authors.forename: N
authors.initials: N
authors.lastname: Hernández
authors.forename: S H
authors.initials: SH
authors.lastname: Torres
authors.forename: J B
authors.initials: JB
authors.lastname: De Sanctis
authors.forename: A
authors.initials: A
authors.lastname: Sosa
mesh_terms: D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D002950:Citrate (si)-Synthase / Q000378:metabolism; D003900:Desoxycorticosterone / Q000633:toxicity; D005230:Fatty Acids, Nonesterified / Q000097:blood / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D006593:Hexokinase / Q000378:metabolism; D006973:Hypertension / Q000097:blood / Q000139:chemically induced* / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D019344:Lactic Acid / Q000378:metabolism; D008071:Lipoprotein Lipase / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012965:Sodium Chloride; D014280:Triglycerides / Q000097:blood / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D014280:Triglycerides; D019344:Lactic Acid; D003900:Desoxycorticosterone; D012965:Sodium Chloride; D006003:Glycogen; D002784:Cholesterol; D015094:3-Hydroxyacyl CoA Dehydrogenases; D002950:Citrate (si)-Synthase; D006593:Hexokinase; D008071:Lipoprotein Lipase; D005947:Glucose