Dietary arachidonic acid and hepatic desaturation of fatty acids in obese zucker rats

1998 ◽  
Vol 75 (2) ◽  
pp. 269-274 ◽  
Author(s):  
Jean Paul Blond ◽  
Georges Durand ◽  
Jean Bézard
2009 ◽  
Vol 139 (8) ◽  
pp. 1495-1501 ◽  
Author(s):  
Barbara Batetta ◽  
Mikko Griinari ◽  
Gianfranca Carta ◽  
Elisabetta Murru ◽  
Alessia Ligresti ◽  
...  

2008 ◽  
Vol 295 (4) ◽  
pp. H1522-H1528 ◽  
Author(s):  
Adam G. Goodwill ◽  
Milinda E. James ◽  
Jefferson C. Frisbee

This study determined if altered vascular prostacyclin (PGI2) and/or thromboxane A2 (TxA2) production with reduced Po2 contributes to impaired hypoxic dilation of skeletal muscle resistance arterioles of obese Zucker rats (OZRs) versus lean Zucker rats (LZRs). Mechanical responses were assessed in isolated gracilis muscle arterioles following reductions in Po2 under control conditions and following pharmacological interventions inhibiting arachidonic acid metabolism and nitric oxide synthase and alleviating elevated vascular oxidant stress. The production of arachidonic acid metabolites was assessed using pooled arteries from OZRs and LZRs in response to reduced Po2. Hypoxic dilation, endothelium-dependent in both strains, was attenuated in OZRs versus LZRs. Nitric oxide synthase inhibition had no significant impact on hypoxic dilation in either strain. Cyclooxygenase inhibition dramatically reduced hypoxic dilation in LZRs and abolished responses in OZRs. Treatment of arterioles from OZRs with polyethylene glycol-superoxide dismutase improved hypoxic dilation, and this improvement was entirely cyclooxygenase dependent. Vascular PGI2 production with reduced Po2 was similar between strains, although TxA2 production was increased in OZRs, a difference that was attenuated by treatment of vessels from OZRs with polyethylene glycol-superoxide dismutase. Both blockade of PGH2/TxA2 receptors and inhibition of thromboxane synthase increased hypoxic dilation in OZR arterioles. These results suggest that a contributing mechanism underlying impaired hypoxic dilation of skeletal muscle arterioles of OZRs may be an increased vascular production of TxA2, which competes against the vasodilator influences of PGI2. These results also suggest that the elevated vascular oxidant stress inherent in metabolic syndrome may contribute to the increased vascular TxA2 production and may blunt vascular sensitivity to PGI2.


2009 ◽  
Vol 103 (6) ◽  
pp. 869-878 ◽  
Author(s):  
Susana V. Martins ◽  
Paula A. Lopes ◽  
Cristina M. Alfaia ◽  
Pedro O. Rodrigues ◽  
Susana P. Alves ◽  
...  

Conjugated linoleic acid (CLA) has been reported as having body fat lowering properties and the ability to modulate the inflammatory system in several models. In the present study, the effects of CLA added to saturated fat diets, from vegetable and animal origins, on the serum adipokine profile of obese Zucker rats were assessed. In addition, the fatty acid composition of epididymal and retroperitoneal adipose tissues was determined and a principal component analysis (PCA) was used to assess possible relationships between fatty acids and serum metabolites. Atherogenic diets (2 % cholesterol) were formulated with palm oil and ovine fat and supplemented or not with 1 % of a mixture (1:1) ofcis-9,trans-11 andtrans-10,cis-12-CLA isomers. CLA-fed animals exhibited lower daily feed intake, final body and liver weights, and hepatic lipids content. Total and LDL-cholesterol levels were increased in CLA-supplemented groups. CLA also promoted higher adiponectin and lower plasminogen activator inhibitor-1 (PAI-1) serum concentrations. In contrast to palm oil diets, ovine fat increased insulin resistance and serum levels of leptin, TNF-α and IL-1β. Epididymal and retroperitoneal adipose tissues had similar deposition of individual fatty acids. The PCA analysis showed that thetrans-10,cis-12-CLA isomer was highly associated with adiponectin and PAI-1 levels. Summing up, CLA added to vegetable saturated enriched diets, relative to those from animal origin, seems to improve the serum profile of adipokines and inflammatory markers in obese Zucker rats due to a more favourable fatty acid composition.


1996 ◽  
Vol 271 (1) ◽  
pp. E44-E49 ◽  
Author(s):  
B. H. Jones ◽  
M. A. Maher ◽  
W. J. Banz ◽  
M. B. Zemel ◽  
J. Whelan ◽  
...  

Stearoyl-CoA desaturase (SCD) is a key regulatory enzyme in the synthesis of unsaturated fatty acids. Although regulation of hepatic SCD by obesity and polyunsaturated fatty acids (PUFA) has been well investigated, no studies have addressed whether similar regulation occurs in adipose tissue. We addressed these questions by feeding control (12% corn oil) and high-PUFA (48% corn oil) diets to lean and obese Zucker rats and analyzing SCD mRNA levels in adipose tissue and liver. We report that SCD mRNA content was dramatically elevated in adipose tissue of obese vs. lean rats on both diets and was significantly decreased by PUFA in both genotypes. Interestingly, we demonstrate that SCD expression was directly downregulated in a dose dependent manner by PUFA in 3T3-L1 adipocytes. We conclude that 1) obese Zucker rats overexpress the SCD gene in both liver and adipose tissue and 2) PUFA directly suppress SCD expression in adipocytes. Further studies will elucidate the mechanisms responsible for obesity- and PUFA-mediated regulation of SCD in adipose cells.


2014 ◽  
Vol 30 (4) ◽  
pp. 643-651 ◽  
Author(s):  
A. Boglino ◽  
M. J. Darias ◽  
K. B. Andree ◽  
A. Estévez ◽  
E. Gisbert

2009 ◽  
Vol 296 (3) ◽  
pp. R715-R721 ◽  
Author(s):  
Benjamin L. Hodnett ◽  
Jennifer A. Dearman ◽  
Cory B. Carter ◽  
Robert L. Hester

In obesity, skeletal muscle blood flow during exercise (functional hyperemia) is impaired. We have indirectly demonstrated that an altered arachidonic acid metabolism is responsible for the impaired functional vasodilation in the obese Zucker rat (OZR), a model of obesity. In this study, we tested the hypothesis that there is an impaired release of PGI2 due to a nitration of PGI2 synthase (PGIS), which is associated with a decreased prostanoid receptor expression. PGI2, PGE2, and thromboxane A2 (TXA2) release were determined in vitro using ELISA under basal conditions and in response to arachidonic acid (AA) administration (50 μM). Immunofluorescence of PGI2 and TXA2 receptors (IP and TP, respectively) was determined in dispersed vascular smooth muscle cells (VSMCs). Nitration of tyrosine residues of the PGIS enzyme was determined using immunoprecipitation and Western blot analysis. Following AA administration, PGI2 and PGE2 release were attenuated in OZR compared with lean Zucker rats (LZR; controls). Basal and AA-induced TXA2 release were not significantly different between groups. IP and TP immunofluorescence were not significantly different between OZR and LZR groups. OZR exhibited elevated nitration of tyrosine residues of PGIS compared with LZR. These results suggest that alterations in the PGI2 pathway (attenuated PGI2 synthesis), and not the TXA2 pathway (normal TXA2 synthesis/no change in TP receptor expression), underlie the attenuated functional hyperemia in the OZR.


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