Carrageenan-induced granuloma and iron status in rats with dietary polyunsaturated fatty acid deficiency

Sprague–Dawley rats were fed for 4 months on a control diet or a polyunsaturated-fatty-acid (PUFA)-deficient diet. The combined effects of iron overload (Fe dextran) or Fe deficiency (desferrioxamine) on carrageenan-induced granuloma were studied. PUFA deficiency induced changes in Fe metabolism, but no alterations in lipid peroxidation variables were observed. Inflammation implied an increase in lipid peroxidation, Fe storage and caeruloplasmin concentration, together with symptoms of anaemia. PUFA deficiency in inflamed rats gave rise to a lower inflammatory response (granuloma weight and prostaglandin E2concentration) and ethane exhalation. Fe overload potentiated inflammatory and lipid peroxidation processes, whereas Fe deficiency decreased them.

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Independent mechanisms underlie the protective effect of dietary polyunsaturated fatty acid supplementation and Gαz deficiency on the early type 1 diabetes phenotype of Non-obese diabetic (NOD) mice

10.1101/2021.03.13.435254 ◽

2021 ◽

Author(s):

Rachel J. Fenske ◽

Haley N. Wienkes ◽

Darby C. Peter ◽

Michael D. Schaid ◽

Andrea Pennati ◽

...

Keyword(s):

Fatty Acid ◽

Glucose Tolerance ◽

Polyunsaturated Fatty Acid ◽

Ex Vivo ◽

Control Diet ◽

Nod Mice ◽

Future Research ◽

Prostaglandin E ◽

Wild Type ◽

Cellular Mechanisms

AbstractNon-obese diabetic (NOD) mice deficient in Gz alpha subunit (Gαz) are protected from developing hyperglycemia, even with early islet insulitis similar to wild-type mice. Similarly, wild-type (WT) NOD mice are protected from glucose intolerance when fed a diet enriched in eicosapentaneoic acid (EPA). In the beta-cell, Prostaglandin EP3 receptor (EP3), whose primary endogenous ligand is the arachidonic acid (AA) metabolite, prostaglandin E2, is specifically coupled to Gαz. In this work, we tested whether dietary EPA supplementation, thereby reducing systemic PGE2 levels, would complement Gαz loss in the NOD mouse model. WT and Gαz-null NOD mice were fed an AA-enriched diet, EPA-enriched diet, or control diet upon weaning. After 12 weeks of diet feeding, glucose tolerance tests were performed and pancreatic islets and whole pancreas collected for ex vivo analyses, with the longer-term effect of an EPA-enriched diet on splenic T-cell populations quantified via flow cytometry. Our results reveal a polyunsaturated fatty acid-enriched diet, whether AA or EPA, improves wild-type NOD glucose tolerance by the same magnitude as Gαz loss, but through almost completely different physiological and cellular mechanisms. Our results shed critical light on future research into novel pharmacological and dietary adjuvant therapies for T1D.

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Dietary conjugated linoleic acid (CLA) induces apoptosis of colonic mucosa in 1,2-dimethylhydrazine-treated rats: a possible mechanism of the anticarcinogenic effect by CLA

British Journal Of Nutrition ◽

10.1079/bjn2001445 ◽

2001 ◽

Vol 86 (5) ◽

pp. 549-555 ◽

Cited By ~ 77

Author(s):

Hyun S. Park ◽

Ji H. Ryu ◽

Yeong L. Ha ◽

Jung H. Y. Park

Keyword(s):

Linoleic Acid ◽

Conjugated Linoleic Acid ◽

Control Diet ◽

Terminal Deoxynucleotidyl Transferase ◽

Prostaglandin E ◽

Dependent Manner ◽

Sprague Dawley ◽

Tumour Incidence ◽

Sprague Dawley Rats ◽

Dietary Conjugated Linoleic Acid

One of the objectives of the present study was to investigate whether 1 % conjugated linoleic acid (CLA) in the diet reduced tumour incidence in the colon of 1,2-dimethylhydrazine (DMH)-treated rats. Colon cancer was induced by injecting 6-week-old, male, Sprague–Dawley rats with 15 mg/kg DMH twice per week for 6 weeks. They were fed either 1 % CLA or a control diet ad libitum for 30 weeks. Dietary CLA significantly decreased colon tumour incidence (P<0·05). Our second objective was to investigate whether apoptosis in the colon mucosa of DMH-treated rats was affected by the amount of dietary CLA and whether the changes in apoptosis were related to those in fatty acid-responsive biomarkers. For this purpose, rats were killed after being fed a diet containing 0 %, 0·5 %, 1 % or 1·5 % CLA for 14 weeks. CLA was undetected in the mucosa of rats fed the 0 % CLA diet and increased to 5·9 mg/g phospholipid in rats fed the 0·5 % diet. The apoptotic index estimated by the terminal deoxynucleotidyl transferase-mediated dUTP nick and labelling technique was increased by 251 % and the 1,2-diacylglycerol content was decreased by 57 % in rats fed 0·5 % CLA. No further changes in these variables were observed when CLA in the diet was raised to 1·0 % or 1·5 %. However, dietary CLA decreased mucosal levels of prostaglandin E2, thromboxane B2 and arachidonic acid in a dose-dependent manner. The present data indicate that dietary CLA can inhibit DMH-induced colon carcinogenesis by mechanisms probably involving increased apoptosis.

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Dietary Polyunsaturated Fatty Acid Promote Peroxidation and its Possible Role in the Promotion of Cancer

Advances in Experimental Medicine and Biology - Biological Reactive Intermediates IV ◽

10.1007/978-1-4684-5877-0_107 ◽

1991 ◽

pp. 789-791 ◽

Cited By ~ 8

Author(s):

Olalekan E. Odeleye ◽

Ronald R. Watson ◽

Cleamond D. Eskelson ◽

Siraj I. Mufti

Keyword(s):

Fatty Acid ◽

Polyunsaturated Fatty Acid ◽

Dietary Polyunsaturated Fatty Acid

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43 Dietary Polyunsaturated Fatty Acid (PUFA) Prevents Malformations in Offspring of Diabetic Rats

American Journal of Obstetrics and Gynecology ◽

10.1016/s0002-9378(12)90454-8 ◽

1993 ◽

Vol 168 (1) ◽

pp. 304

Keyword(s):

Fatty Acid ◽

Polyunsaturated Fatty Acid ◽

Diabetic Rats ◽

Dietary Polyunsaturated Fatty Acid

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The chemistry of lipid alkoxyl radicals and their role in metal-amplified lipid peroxidation

Biochemical Society Symposium ◽

10.1042/bss0610065 ◽

1995 ◽

Vol 61 ◽

pp. 65-72 ◽

Cited By ~ 19

Author(s):

Lawrence J. Marnett ◽

Allan L. Wilcox

Keyword(s):

Lipid Peroxidation ◽

Steady State ◽

Fatty Acid ◽

Hydroxyl Radical ◽

Metal Complexes ◽

Polyunsaturated Fatty Acid ◽

Ring Opening ◽

Steady State Concentration ◽

State Concentration ◽

Fatty Acid Hydroperoxides

Reaction of polyunsaturated fatty acid hydroperoxides with metal complexes generates lipid alkoxyl radicals and metal-oxo complexes. Lipid alkoxyl radicals are presumed to be the species responsible for metal-amplified lipid peroxidation because of the chemical analogy of simple organic alkoxyl radicals to the hydroxyl radical. However, polyunsaturated fatty acid alkoxyl radicals exhibit a rich and diverse chemistry that is dominated by intramolecular cyclization to epoxyallylic radicals. Studies described herein demonstrate that the equilibrium between cyclization and ring-opening of epoxyallylic radicals lies overwhelmingly toward cyclization. Thus lipid alkoxyl radicals have a steady-state concentration that is so low that their contribution to metal-amplified lipid peroxidation is insignificant. In fact, the species responsible for metal amplification of lipid peroxidation appears to be the epoxyperoxyl radical formed by coupling the epoxyallylic radical to molecular oxygen.

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Levels of polyunsaturated fatty acids in lymphocytes of rats fed on diets varying in polyunsaturated fatty acid content

British Journal Of Nutrition ◽

10.1079/bjn19800099 ◽

1980 ◽

Vol 43 (2) ◽

pp. 367-373 ◽

Cited By ~ 9

Author(s):

W. M. Tsagn ◽

J. Belin ◽

A. D. Smith

Keyword(s):

Fatty Acids ◽

Fatty Acid ◽

Polyunsaturated Fatty Acid ◽

Fatty Acid Content ◽

Inverse Correlation ◽

Normal Diet ◽

Deficient Diet ◽

Polyunsaturated Fatty Acid Content ◽

Weanling Rats ◽

Total Fatty Acids

1. When weanling rats were fed on a diet containing 0.1 g/kg of the diet as polyunsaturated fatty acid, it was found that after 2 weeks the level of linoleate in the lymphocyte total lipids was 56 mg/ g total fatty acids, as compared with a level of 138 mg/ g in rats on a normal diet (P < 0.005). Similar levels were obtained from rats which had been fed for up to 16 weeks on the deficient diet, but in a group killed after 28 weeks on the diet the level was found to be only 20 mg/ g total fatty acids. The arachidonate level was found to be approximately 220 mg/ g total fatty acids, regardless of whether the rats were fed on a diet deficient in linoleate for up to 16 weeks or on a normal diet. In the group of rats killed after 28 weeks on the linoleate deficient diet, however, the arachidonate level was only 60 mg/ g total fatty acids.2. Percentage values for total fatty acids are given for plasma, adipose tissue, and lymphocytes for rats on normal and experimental diets.3. Scatter diagrams of the levels of linoleate v. arachidonate in the lymphocyte total fatty acids showed no correlation between the levels of the two acids (r 0.05), but similar plots of linoleate and oleate levels showed an inverse correlation (r – 0.68).

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