Polysaccharide-rich hydrolysate fromSaccharomyces cerevisiae(LipiGo®) increases fatty acid and neutral sterol excretion in guinea pigs fed with hypercholesterolemic diets

2017 ◽  
Vol 119 (11) ◽  
pp. 1700104
Author(s):  
Jonathan Santas ◽  
Magda Rafecas ◽  
Jordi Cuñé
1961 ◽  
Vol 39 (4) ◽  
pp. 739-746 ◽  
Author(s):  
Frank Sauer

Non-diabetic ketosis was produced experimentally in fasted pregnant guinea pigs. Total CO2output of ketotic animals was less than that of appropriate controls but there was no impairment in the conversion of acetate-1-C14to C14O2. Sterol synthesis increased in ketotic animals while fatty acid synthesis, particularly in carcass, showed the expected decrease. Ketosis was accompanied by an increase in plasma total fatty acids and in the fatty acid concentration of liver. The experimental findings support the hypothesis that ketosis is a manifestation of increased ketogenesis rather than impaired utilization of ketone bodies.


2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Allison L McDaniel ◽  
Ryan E Temel ◽  
J M Brown ◽  
Richard G Lee ◽  
Mark J Graham ◽  
...  

Transintestinal cholesterol excretion (TICE) is a recently discovered pathway by which cholesterol travels from plasma to the small intestine for direct excretion into the feces. Hallmarks of animal models with TICE include severely diminished biliary cholesterol secretion but near normal levels of hepatic cholesterol and fecal neutral sterol excretion. Using an ATP binding cassette transporter G8 (ABCG8) antisense oligonucleotide (ASO) to knock down ABCG8 specifically in liver (G8 HKD ), we created a novel mouse model with significantly decreased biliary cholesterol excretion but a 658% increase in hepatic cholesterol accumulation and a 78% reduction in fecal neutral sterol excretion, indicating a dysfunction in the TICE pathway. LXR agonists have previously been shown to stimulate the TICE pathway. In order to more definitively prove the TICE pathway was disfunctional in G8 HKD mice, we treated wild type (WT) and G8 HKD mice with the LXR agonist T0901317 and measured markers of TICE stimulation. As expected, in WT mice, T0901317 doubled biliary cholesterol concentrations. A similar effect was seen in G8 HKD mice treated with T0901317, but biliary cholesterol concentrations remained significantly less than their WT counterparts. These levels of biliary cholesterol closely mirrored hepatic ABCG8 mRNA expression. T0901317 stimulated fecal neutral sterol excretion by >1000% in wild type mice but only by 190% in G8 HKD mice. These data indicate that TICE is disfunctional in G8 HDK mice since the pathway was not stimulated to the same extent in WT and G8 HKD mice by an LXR agonist. Some controversy remains over whether the TICE pathway transports macrophage derived cholesterol. In order to address this issue, we performed a macrophage RCT assay on WT and TICE disfunctional G8 HKD mice. T0901317 stimulated macrophage RCT (fecal neutral sterol 3H dpm) by >2300% in wild type mice but only by 370% in G8 HKD mice. T0901317 increased fecal acidic sterol 3H count by 65-75% in both wild type and G8 HKD mice. These results indicate that macrophage RCT is impaired when the TICE pathway is decreased. In sum, our data shows that hepatic ABCG8 plays a key role in the TICE pathway and that impairing the TICE pathway through hepatic ABCG8 knockdown causes decreased macrophage RCT.


1960 ◽  
Vol 38 (1) ◽  
pp. 635-641
Author(s):  
Frank Sauer

Fatty acid, cholesterol, and acetoacetate biosynthesis was studied with liver homogenates from normal and starved guinea pigs. Starvation suppressed the incorporation of acetate into fatty acids and cholesterol but not into acetoacetate. The in vitro biosynthesis of cholesterol and fatty acids was not restored by the addition of either G-6-P or isocitrate in combination with TPN, nor was it restored by orally dosing the starved animals with dextrose. The addition of isocitrate to normal homogenates depressed cholesterogenesis and stimulated lipogenesis.


2003 ◽  
Vol 89 (3) ◽  
pp. 375-382 ◽  
Author(s):  
Caroline M. Pond ◽  
Christine A. Mattacks

To explore the hypothesis that proliferating lymphoid cells in immune-stimulated lymph nodes obtain nutrients locally from adjacent adipose tissue, adult guinea pigs were fed for 6 weeks on standard chow or on chow supplemented with 100 g suet, sunflower oil or fish oi/g. All the guinea pigs ate standard chow for the last 5 d, during which swelling of one popliteal lymph node was stimulated by repeated local injection of lipopolysaccharide. The fatty acid compositions of phospholipids in both popliteal and in several mesenteric lymph nodes, and of triacylglycerols in eleven samples of adipose tissue defined by their anatomical relations to lymph nodes, were determined by GC. The proportions of fatty acids in the phospholipids extracted from the stimulated popliteal node correlated best with those of triacylglycerols in the surrounding adipocytes, less strongly with those of adipocytes elsewhere in depots associated with lymphoid tissue, but not with those of nodeless depots. The composition of triacylglycerols in the perinodal adipose tissue changed under local immune stimulation. We conclude that proliferating lymphoid cells in activated lymph nodes obtain fatty acids mainly from the triacylglycerols in adjacent perinodal adipose tissue. Immune stimulation prompts changes in the fatty acid composition of the triacylglycerols of adipocytes in node-containing depots that equip the adipose tissue for provisioning immune responses. Such local interactions show that specialised adipocytes can act as an interface between whole-body and cellular nutrition, and may explain why mammalian adipose tissue is partitioned into a few large and many small depots.


1997 ◽  
Vol 77 (4) ◽  
pp. 621-643 ◽  
Author(s):  
Christine A. Mattacks ◽  
Caroline M. Pond

The effects of diet on the composition and properties of adipose tissue in relation to lymph nodes were studied in adult guinea-pigs. The proportions of monoenoic triacylglycerol fatty acids were constant in all sites in adipose tissue of similarly fed guinea-pigs, but were substantially greater in samples from guinea-pigs fed on suet-enriched chow. Triacylglycerols in adipose tissue from near nodes contained significantly fewer saturated fatty acids, and significantly more 18:2n−6 and 18:3n−3 than those in samples from sites remote from nodes within the same depot. Depots that interact most strongly with lymphoid cellsin vitrohad the largest and most consistent within-depot differences. The gradients of triacylgiycerol fatty acid composition with distance from lymph nodes in two small intermuscular depots were similar in guinea-pigs fed on plain or suet-enriched chow. These findings are consistent with the hypothesis that adipose tissue around lymph nodes is specialized for local interactions with the lymphoid cells therein, and help to explain the variability of serial or duplicate measurements of adipose tissue composition. When cultured alone, lipopolysaccharide-stimulated lymph node lymphoid cells from suet-fed guinea-pigs incorporated as much labelled thymidine as the controls. Adipose tissue explants from suet-fed guinea-pigs inhibited lymphocyte proliferation much less than those of the controls, although the site-specific differences were similar. The pattern of site-specific differences in glycerol released from explants incubated alone was generally similar for both dietary groups, but except in the popliteal depot, the increases following co-culturing with lymphoid cells were smaller for samples from suet-fed guinea-pigs. These experiments show that minor changes in the fatty acid composition of the diet can substantially alter the interactions between adipose tissue and lymphoid cells.


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