scholarly journals Time-dependent behavioral, neurochemical, and metabolic dysregulation in female C57BL/6 mice caused by chronic high-fat diet intake

2016 ◽  
Vol 157 ◽  
pp. 196-208 ◽  
Author(s):  
Saritha Krishna ◽  
Zhoumeng Lin ◽  
Claire B. de La Serre ◽  
John J. Wagner ◽  
Donald H. Harn ◽  
...  
2016 ◽  
Vol 60 (1) ◽  
pp. 28536 ◽  
Author(s):  
Noemi A. V. Roza ◽  
Luiz F. Possignolo ◽  
Adrianne C. Palanch ◽  
José A. R. Gontijo

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Amy C Burke ◽  
Brian G Sutherland ◽  
Julia M Assini ◽  
Murray W Huff

Previous studies demonstrate that the addition of naringenin, a grapefruit flavonoid, to a high-fat diet prevents the development of many disorders of the metabolic syndrome and atherosclerosis in Ldlr-/- mice. Furthermore, in intervention studies, the addition of naringenin to a high-fat, high cholesterol (HFHC) diet reversed pre-established obesity, hyperlipidemia, hepatic steatosis, insulin resistance and improved atherosclerotic lesion pathology, but not lesion size. In the present intervention study, we tested the hypothesis that addition of naringenin to a chow diet would further improve pre-established metabolic dysregulation and attenuate lesion development, compared to chow alone. Ldlr-/- mice were fed a HFHC diet for 12 weeks to induce metabolic dysregulation. Subsequently, mice received one of 3 diets for another 12 weeks: 1) continuation of the HFHC diet, 2) an isoflavone-free chow diet or 3) isoflavone-free chow with 3% naringenin. At 12 weeks, the HFHC diet induced significant weight gain and increased adiposity. Intervention with chow alone reduced the weight gained during induction by 22%, whereas the addition of naringenin to chow induced a weight loss of 71%. Specifically, the reduction in adiposity was 2.75-times greater in naringenin-treated mice, compared to chow alone. The HFHC diet increased VLDL cholesterol 20-fold and LDL cholesterol 5-fold, which were reduced by intervention with both chow (>60%) and chow supplemented with naringenin (>80%). The HFHC diet induced insulin resistance and glucose intolerance. Naringenin improved insulin tolerance (plasma glucose AUC -38%) and glucose tolerance (plasma glucose AUC -58%), which was accompanied by normalization of plasma insulin and glucose. HFHC-induction promoted the development of intermediate atherosclerotic lesions. Continuation of the HFHC diet doubled lesion size. Intervention with chow alone attenuated lesion size progression by 65%. The addition of naringenin to chow slowed lesion progression by 90%, resulting in smaller lesions compared to chow intervention alone (P=0.042). We conclude that intervention with naringenin-supplemented chow enhances weight loss, improves metabolic dysregulation and halts the progression of atherosclerosis.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Valter T. Boldarine ◽  
Amanda P. Pedroso ◽  
Nelson I. P. Neto ◽  
Ana P. S. Dornellas ◽  
Cláudia M. O. Nascimento ◽  
...  

2020 ◽  
Vol 22 ◽  
pp. 100736 ◽  
Author(s):  
Eri Nanizawa ◽  
Yuki Tamaki ◽  
Reika Sono ◽  
Rintaro Miyashita ◽  
Yumi Hayashi ◽  
...  

2020 ◽  
Vol 11 (2) ◽  
pp. 1547-1559 ◽  
Author(s):  
C. A. Lamas ◽  
L. A. Kido ◽  
F. Montico ◽  
C. B. Collares-Buzato ◽  
M. R. Maróstica ◽  
...  

Jaboticaba extract prevented the prostatic lesion development in aging and/or overweight mice, mainly interfering in cell proliferation, hormonal and angiogenesis pathways.


2013 ◽  
Vol 28 (10) ◽  
pp. 2464-2476 ◽  
Author(s):  
C. S. Pinhal ◽  
A. Lopes ◽  
D. B. Torres ◽  
S. L. Felisbino ◽  
J. A. Rocha Gontijo ◽  
...  

Molecules ◽  
2018 ◽  
Vol 23 (3) ◽  
pp. 705 ◽  
Author(s):  
Soo-min Lim ◽  
Eunju Kim ◽  
Jae-Ho Shin ◽  
Pu Seok ◽  
Sangwon Jung ◽  
...  

2009 ◽  
Vol 15 (S3) ◽  
pp. 21-22 ◽  
Author(s):  
I. Tomada ◽  
N. Tomada ◽  
H. Almeida ◽  
P. Vendeira ◽  
D. Neves

AbstractErectile dysfunction (ED) is considered equivalent to endothelial dysfunction and thus an early manifestation of atherosclerosis and cardiovascular disease (CVD). Atherosclerosis that is frequently provoked by regular consumption of high-fat diet (HFD) has been recently recognized as a chronic inflammation condition associated to vessel lipid deposition and vascular smooth cells proliferation that together impair endothelium-dependent relaxation of corpus cavernosum (CC) smooth muscle. It is also well established that HFD regular intake by its own induces endothelial dysfunction. The main objective of this study was to evaluate effects of HFD continuous intake on atherosclerosis progression of CC vessels of the rat. Due to their intervention on atherosclerosisrelated vascular remodelling pathways, angiopoietins (Ang1, Ang2) expression in erectile tissue of this rat experimental model was characterized.


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