eicosapentaenoic fatty acid
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Animals ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 150
Author(s):  
Ariane Martins Guimarães ◽  
Cristhiane Guertler ◽  
Gabriella do Vale Pereira ◽  
Jaqueline da Rosa Coelho ◽  
Priscila Costa Costa Rezende ◽  
...  

This work aimed to evaluate Nannochloropsis spp. as feed additive in the diet of Pacific white shrimp for their effect on midgut microbiology, thermal shock resistance and immunological parameters. Initially, the digestibility of the microalgae meal was assessed, and the apparent digestibility coefficient (ADC) was determined. The ADC was, in general, high in lipids (78.88%) and eicosapentaenoic fatty acid (73.86%). Then, Nannochloropsis spp. were included in diets at four levels (0, 0.5, 1 and 2% inclusion). The shrimp were reared in 500 L clear water tanks containing 20 shrimp per tank with an initial weight of 6.05 ± 0.06 g and fed four times a day. Shrimp fed with supplemented diets containing Nannochloropsis spp. (0.5 and 2%) presented higher resistance to thermal shock when compared to the non-supplemented group (control). Shrimp fed with 1 and 2% of algae inclusion had a higher production of reactive oxygen species (ROS) when compared to other treatments. No statistical difference was observed in the immunological parameters and microbiology of the intestinal tract. Thus, the inclusion of Nannochloropsis spp. in shrimp diets at 0.5 and 2% levels increases resistance to thermal shock and ROS production in shrimp.


2005 ◽  
Vol 288 (6) ◽  
pp. R1682-R1688 ◽  
Author(s):  
Patricia Pérez-Matute ◽  
Amelia Marti ◽  
J. Alfredo Martínez ◽  
M. P. Fernández-Otero ◽  
Kimber L. Stanhope ◽  
...  

Eicosapentaenoic acid (EPA), one of the n-3 polyunsaturated fatty acids, has been shown to stimulate leptin mRNA expression and secretion in 3T3-L1 cells. However, other studies have reported inhibitory effects of EPA on leptin expression and secretion in vivo and in vitro. To determine the direct effects of EPA on basal and insulin-stimulated leptin secretion, isolated rat adipocytes were incubated with EPA in the absence and presence of insulin. EPA (10, 100, and 200 μM) increased basal leptin gene expression and secretion (+43.8%, P < 0.05; +71.1%, P < 0.01; and +73.7%, P < 0.01, respectively). EPA also increased leptin secretion in the presence of 1.6 nM insulin; however, the effect was less pronounced than in the absence of it. Because adipocyte glucose and lipid metabolism are involved in the regulation of leptin production, the metabolic effects of this fatty acid were also examined. EPA (200 μM) increased basal glucose uptake in isolated adipocytes (+50%, P < 0.05). Anaerobic metabolism of glucose, as assessed by lactate production and proportion of glucose metabolized to lactate, has been shown to be inversely correlated to leptin secretion and was decreased by EPA in both the absence and presence of insulin. EPA increased basal glucose oxidation as determined by the proportion of 14C-labeled glucose metabolized to CO2. Lipogenesis (14C-labeled glucose incorporation into triglyceride) was decreased by EPA in the absence of insulin, whereas lipolysis (glycerol release) was unaffected. The EPA-induced increase of basal leptin secretion was highly correlated with increased glucose utilization ( r = +0.89, P < 0.01) and inversely related to the anaerobic glucose metabolism to lactate. EPA’s effect on insulin-stimulated leptin secretion was not related to increased glucose utilization but was inversely correlated with anaerobic glucose metabolism to lactate ( r = −0.84, P < 0.01). Together, the results suggest that EPA, like insulin, stimulates leptin production by increasing the nonanaerobic/oxidative metabolism of glucose.


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