Fish oil prevents effect of high cholesterol diet on active intestinal transport of galactose

1989 ◽  
Vol 67 (8) ◽  
pp. 829-836 ◽  
Author(s):  
A. B. R. Thomson ◽  
M. Keelan ◽  
M. L. Garg ◽  
M. T. Clandinin

We tested the hypothesis that diets containing fish oils prevent the effects of a high cholesterol diet on the morphology and nutrient uptake of the intestine. Isocaloric semisynthetic diets were supplemented with beef tallow or fish oil containing low or high amounts of cholesterol and were fed to growing female Wistar rats for 14 days, after which the in vitro jejunal and ileal uptake of glucose, galactose, long-chain fatty acids, and cholesterol was determined. Feeding cholesterol with beef tallow was associated with a 12% decrease in the jejunal mucosal surface area. Feeding fish oil decreased jejunal mucosal surface area by 24%, as compared with the beef tallow diet, but the reduction was increased to 42% when fish oil and cholesterol were fed together. Ileal surface area was unaffected by varying the major source of dietary lipid, or by adding cholesterol. Despite the effect of fish oil on the mucosal surface area, the jejunal and ileal uptake of saturated as well as unsaturated long-chain fatty acids and cholesterol was similar in the four diet groups. Cholesterol supplementation enhanced the jejunal uptake of high concentrations of galactose only when fed with beef tallow, i.e., feeding fish oil prevented the enhancing effect of cholesterol on galactose uptake observed when beef tallow was fed. Thus, (i) a fish oil diet prevents the enhancing effect of cholesterol on jejunal active transport of galactose, an effect not explained by the reduction in jejunal mucosal surface area observed with the fish oil diet; (ii) these dietary manipulations result in a clear dissociation of the morphological from the transport adaptation of the intestine; and (iii) substitution of fish oil for beef tallow as the major source of lipid in the diet prevents the influence of cholesterol on the active intestinal transport of galactose.Key words: adaptation, dietary cholesterol, galactose, glucose, long-chain fatty acids, permeation, fish oil.

1988 ◽  
Vol 66 (7) ◽  
pp. 985-992 ◽  
Author(s):  
A. B. R. Thomson ◽  
M. Keelan ◽  
M. Garg ◽  
M. T. Clandinin

Animals were fed for 2 weeks on one of four isocaloric and isocholesterolic semisynthetic diets: high 18:3ω3, low 18:3ω3, high 20:5ω3, or low 20:5ω3. The weight of the intestine and the percentage of the wall consisting of mucosa was greater in high 20:5ω3 than in high 18:3ω3, and greater in low 20:5ω3 than in low 18:3ω3, although the mucosal surface area was 26% lower in high 20:5ω3 than high 18:3ω3. The jejunal uptake of 40 mM glucose and ileal uptake of 40 mM galactose was greater in high 18:3ω3 than in high 20:5ω3; jejunal uptake of fatty acid 12:0 was higher, but 18:0 was lower in high 18:3ω3 than in high 20:5ω3. The jejunal or ileal uptake of cholesterol was not affected by 20:5ω3. However, 20:5ω3 had a variable effect on the uptake of medium- and long-chain fatty acids. Alterations in the uptake of fatty acids and glucose were not explained by any difference in the animals' food consumption, body weight gain, or intestinal weight, but the reduced jejunal uptake of 40 mM glucose in rats fed the high 20:5ω3 diet was associated with reduced mucosal surface area. Thus, (i) varying the source of ω3-fatty acids (vegetable, 18:3ω3 versus fish oil, 20:5ω3) altered the mucosal mass of the intestine, and (ii) the source of the dietary ω3-fatty acid (18:3ω3 versus 20:5ω3) influenced intestinal hexose uptake, with fish oil having an anti-absorptive effect on the jejunal uptake of D-glucose.


2001 ◽  
Vol 80 (6) ◽  
pp. 741-752 ◽  
Author(s):  
S. López-Ferrer ◽  
M.D. Baucells ◽  
A.C. Barroeta ◽  
M.A. Grashorn

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 682-682 ◽  
Author(s):  
Kayla Dillard ◽  
Morgan Coffin ◽  
Gabriella Hernandez ◽  
Victoria Smith ◽  
Catherine Johnson ◽  
...  

Abstract Objectives Non-alcoholic fatty liver disease (NAFLD) represents the major cause of pediatric chronic liver pathology in the United States. The objective of this study was to compare the relative effect of inclusion of isocaloric amounts of saturated medium-chain fatty acids (hydrogenated coconut oil), saturated long-chain fatty acids (lard) and unsaturated long-chain fatty acids (olive oil) on endpoints of NAFLD and insulin resistance. Methods Thirty-eight 15-d-old Iberian pigs were fed 1 of 4 diets containing (g/kg body weight × d) 1) control (CON; n = 8): 0 g fructose, 10.5 g fat, and 187 kcal metabolizable energy (ME), 2) lard (LAR; n = 10): 21.6 g fructose, 17.1 g fat (100% lard) and 299 kcal ME, 3) hydrogenated coconut oil (COCO; n = 10): 21.6 g fructose, 16.9 g fat (42.5% lard and 57.5% coconut oil) and 299 kcal ME, and 4) olive oil (OLV, n = 10): 21.6 g fructose, 17.1 g fat (43.5% lard and 56.5% olive oil) and 299 kcal ME, for 9 consecutive weeks. Body weight was recorded every 3 d. Serum markers of liver injury and dyslipidemia were measured on d 60 at 2 h post feeding, with all other serum measures assessed on d 70. Liver tissue was collected on d 70 for histology, triacylglyceride (TG) quantification, and metabolomics analysis. Results Tissue histology indicated the presence of steatosis in LAR, COCO and OLV compared with CON (P ≤ 0.001), with a further increase in in non-alcoholic steatohepatitis (NASH) in OLV and COCO compared with LAR (P ≤ 0.01). Alanine and aspartate aminotransferases were higher in COCO and OLV (P ≤ 0.01) than CON. All treatment groups had lower liver concentrations of methyl donor's choline and betaine versus CON, while bile acids were differentially changed (P ≤ 0.05). COCO had higher levels of TGs with less carbons (Total carbons < 52) than all other groups (P ≤ 0.05). Several long-chain acylcarnitines involved in fat oxidation were higher in OLV versus all other groups (P ≤ 0.05). Conclusions Inclusion of fats enriched in medium-chain saturated and long-chain unsaturated fatty acids in a high-fructose high-fat diet increased liver injury, compared with fats with a long-chain saturated fatty acid profile. Further research is required to investigate the mechanisms causing this difference in physiological response to these dietary fat sources. Funding Sources ARI, AcornSeekers.


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