Effects of a highly palatable diet on lipid and glucose parameters, nitric oxide, and ectonucleotidases activity.
Obesity has reached epidemic proportions worldwide and is stimulated by the ready availability of food rich in fat and sugar (highly palatable diet). This type of diet increases the risks of obesity-associated pathologies, such as insulin resistance and cardiovascular disease. Nitric oxide, a potent endogenous vasodilator, is decreased in these pathologies, mostly as a result of insulin resistance. Ectonucleotidases are ecto and soluble enzymes that regulate the availability of the nucleotides ATP, ADP, and AMP and the nucleoside adenosine in the vascular system, thereby affecting vasoconstriction, vasodilatation, and platelet aggregation homeostasis. The aim of this study was to evaluate the effects of a highly palatable diet on serum lipid and glucose parameters, nitric oxide, and ectonucleotidase activity. Forty male Wistar rats were fed 1 of 2 diets for either 45 days or 4 months: standard chow (SC, n = 10) or a highly palatable diet enriched with sucrose (HP, n = 10). Body mass, visceral fat mass, glucose tolerance, cholesterol (total, high-density lipoprotein (HDL) and non-HDL), serum triacylglycerol, liver triacylglycerol, and free glycerol were increased in the HP group after 45 days and after 4 months, whereas insulin levels were not different between the groups at either time. Furthermore, levels of nitric oxide metabolites and ATP, ADP, and AMP hydrolysis were significantly lower in the HP group (p < 0.05) after 4 months. In conclusion, the consumption of the HP diet for 4 months induced overall corporal and metabolic changes, and decreased nitric oxide metabolites and ectonucleotidase activity, thereby promoting an appropriate environment for the development of cardiovascular diseases, without apparent changes in insulin levels.
Souza
Carolina Guerini de
CG
Department of Biochemistry, Federal University of Rio Grande do Sul - UFRGS, Rua Ramiro Barcelos, 2600 anexo, CEP 90035003, Porto Alegre, RS, Brazil. carolguerini@hotmail.com
Böhmer
Ana Elisa
AE
Müller
Alexandre Pastoris
AP
Oses
Jean Pierre
JP
Viola
Giordano Gübert
GG
Lesczinski
Daniel Neumann
DN
Souza
Débora Guerini de
DG
Knorr
Luísa
L
Moreira
Júlia Dübois
JD
Lhullier
Francisco
F
Souza
Diogo Onofre
DO
Perry
Marcos Luiz Santos
ML
D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000255:Adenosine Triphosphate / Q000378:metabolism; D000821:Animal Feed; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D004041:Dietary Fats / Q000494:pharmacology; D019422:Dietary Sucrose / Q000494:pharmacology; D004789:Enzyme Activation / Q000502:physiology; D018149:Glucose Intolerance / Q000378:metabolism; D005990:Glycerol / Q000378:metabolism; D007328:Insulin / Q000097:blood; D008055:Lipids / Q000097:blood*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D009765:Obesity / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar
D001786:Blood Glucose; D004041:Dietary Fats; D019422:Dietary Sucrose; D007328:Insulin; D008055:Lipids; D009569:Nitric Oxide; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D000251:Adenosine Triphosphatases; C027201:ectoATPase; D005990:Glycerol