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Hypercaloric Diet Does Not Induce Metabolic Syndrome in Wistar Rats
Author(s) -
Medeiros Alessandra,
Moura Elizabeth O. C.,
Gomes Moisés F. P.,
Cardoso Naiara Magalhães,
Santos Ana Carolina C.,
Kubota Melina C.,
Estadella Débora
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.792.21
Subject(s) - ctl* , medicine , blood pressure , metabolic syndrome , endocrinology , obesity , immunology , immune system , cd8
BACKGROUND Studies have shown that metabolic syndrome (MS) is an important predictor of cardiovascular events. Although genetic susceptibility is essential, the MS components generally arise as a result of a sedentary lifestyle and diet rich in carbohydrates and lipids. To better understand the pathophysiological process of the disease becomes necessary to establish experimental models that have the same characteristics of the disease in humans. OBJECTIVE To evaluate the efficacy of a hypercaloric diet (HFFD 25% fructose and 25% saturated fat) in the induction of MS. METHODS Young (5 weeks old) or adult rats (12 weeks old) were randomly assigned into control or HFFD groups: control young (CTL‐Y, n=10) and HFFD young (HFFD‐Y, n=10); control adult (CTL‐A, n=10) and HFFD adult (HFFD‐A, n=10). All groups were subjected to analysis of blood glucose, triacylglycerol (TAG), body mass (BM) and blood pressure (BP) by tail plethysmography weekly, for 14 weeks. Furthermore, in the 13th week were performed ITT and GTT tests. RESULTS Even though the animals presented BM difference in the last week of the protocol (CTL‐Y=380.8 g vs. HFFD‐Y=451.7 g, p<0.001) and (CTL‐A=423.7 g vs. HFFD‐A=495.4 g, p<0.05), there were no significant changes in systolic BP (CTL‐Y=134 mmHg vs. HFFD‐Y=150 mmHg, p>0.05) and (CTL‐A=137 mmHg vs. HFFD‐A=127 mmHg, p>0.05) or diastolic BP (CTL‐Y=74 mmHg vs. HFFD‐Y=77 mmHg, p>0.05) and (CTL‐A=79 mmHg vs. HFFD‐A=64 mmHg, p>0.05). The TAG profile did not change, except in adult rats, when we performed t test only with the data from the last week (CTL‐Y=97 mg/dL vs. HFFD‐Y=95 mg/dL, p>0.05) and (CTL‐A=88 mg/dL vs. HFFD‐A=137 mg/dL, p<0.001; F=2.90). However, there was no difference in the two‐way analysis of variance in this variable in both groups. Finally, HFFD‐Y showed glucose tolerance, GTT (CTL‐Y=82 mg/dL vs. HFFD‐Y=92 mg/dL, p<0.001; F=6.94), but insulin tolerance ITT (CTL‐Y= 66 mg/dL vs. HFFD‐Y=63 mg/dL, p> 0.05, F=0.43). While HFFD‐A was not significantly different from CTL‐A in GTT (CTL‐A=78 mg/dL vs. HFFD‐A=79 mg/dL, p>0.05, F=0.06) and ITT (CTL‐A=78 mg/dL vs. HFFD‐A=79 mg/dL, p>0.05, F=0.07). CONCLUSION These data demonstrate that the hypercaloric diet used in our study was ineffective for the development of MS components in young and adult rats. Support or Funding Information FAPESP e CNPq