Literature DB >> 9202100

Dietary linoleic acid intake controls the arterial blood plasma concentration and the rates of growth and linoleic acid uptake and metabolism in hepatoma 7288CTC in Buffalo rats.

L A Sauer1, R T Dauchy, D E Blask.   

Abstract

In this study, we tested the hypothesis that dietary linoleic acid intake controls the arterial blood plasma linoleic acid concentration and the rates of tumor growth and linoleic acid metabolism in vivo. Seven groups of young male Buffalo rats (11-21 rats/group) were given free access to semipurified diets containing different amounts of corn and/or olive oils. Four other groups (7-11 rats/group) were 30% energy-restricted. Each experiment included periods for rat growth and plasma lipid stabilization (6 wk), measurement of mean daily arterial blood plasma fatty acid concentrations (3 wk), surgical implantation of a subcutaneous tissue-isolated hepatoma 7288CTC, tumor growth and harvest (2-4 wk). Linoleic + arachidonic acid (P = 0.007) and oleic acid (P = 0.002) concentrations in arterial blood plasma were increased as dietary intake of linoleic and oleic acids was increased, respectively. In rats given free access to food, tumor growth was directly dependent on the plasma concentrations of linoleic (P < 0.001) and arachidonic acids (P = 0.04). Tumor growth in energy-restricted rats was dependent only on the linoleic acid concentration (P = 0.008). Energy restriction itself caused a growth inhibition independent of plasma linoleic acid. The linoleic acid and total fatty acid concentrations of tumor triacylglycerols were directly dependent on the plasma linoleic acid concentration in rats given free access to food (P = 0.009). Hepatoma 7288CTC (both in vivo and during perfusion in situ) supported a dose-dependent conversion (P < 0.001) of plasma linoleic acid to the mitogen, 13-hydroxy-9, 11-octadecadienoic acid. We conclude that increased arterial blood plasma linoleic acid concentrations, caused by increased dietary intakes, specifically stimulate growth, lipid storage and linoleic acid metabolism in hepatoma 7288CTC in vivo.

Entities:  

Mesh:

Substances:

Year:  1997        PMID: 9202100     DOI: 10.1093/jn/127.7.1412

Source DB:  PubMed          Journal:  J Nutr        ISSN: 0022-3166            Impact factor:   4.798


  5 in total

Review 1.  Melatonin: an inhibitor of breast cancer.

Authors:  Steven M Hill; Victoria P Belancio; Robert T Dauchy; Shulin Xiang; Samantha Brimer; Lulu Mao; Adam Hauch; Peter W Lundberg; Whitney Summers; Lin Yuan; Tripp Frasch; David E Blask
Journal:  Endocr Relat Cancer       Date:  2015-04-15       Impact factor: 5.678

Review 2.  Putting cancer to sleep at night: the neuroendocrine/circadian melatonin signal.

Authors:  David E Blask; Robert T Dauchy; Leonard A Sauer
Journal:  Endocrine       Date:  2005-07       Impact factor: 3.633

3.  Effects of spectral transmittance through standard laboratory cages on circadian metabolism and physiology in nude rats.

Authors:  Robert T Dauchy; Erin M Dauchy; John P Hanifin; Sheena L Gauthreaux; Lulu Mao; Victoria P Belancio; Tara G Ooms; Lynell M Dupepe; Michael R Jablonski; Benjamin Warfield; Melissa A Wren; George C Brainard; Steven M Hill; David E Blask
Journal:  J Am Assoc Lab Anim Sci       Date:  2013-03       Impact factor: 1.232

4.  Dietary Melatonin and Omega-3 Fatty Acids Induce Human Cancer Xenograft Regression In Vivo in Rats by Suppressing Linoleic Acid Uptake and Metabolism.

Authors:  Erin M Dauchy; Robert T Dauchy; Robert P Tirrell; Leslie K Davidson; Steven M Hill; Leonard A Sauer; David E Blask
Journal:  Comp Med       Date:  2021-06-29       Impact factor: 0.982

5.  Light exposure at night disrupts host/cancer circadian regulatory dynamics: impact on the Warburg effect, lipid signaling and tumor growth prevention.

Authors:  David E Blask; Robert T Dauchy; Erin M Dauchy; Lulu Mao; Steven M Hill; Michael W Greene; Victoria P Belancio; Leonard A Sauer; Leslie Davidson
Journal:  PLoS One       Date:  2014-08-06       Impact factor: 3.240

  5 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.