Abstract
We have previously shown that a high fat diet (20% w/w) containing 12% linoleic acid (18:2) can significantly increase the metastasis of mammary tumor cells when compared with high fat diets that contain 8% or less 18:2 with a constant level of oleic acid (18:1). This effect may have been due to an alteration of eicosanoid metabolism because the cyclooxygenase inhibitor, indomethacin, abolished the increase. Because 18:1 may interfere with the metabolism of 18:2 to 20:4, we have now tested whether the 18:1 that supplements the 18:2 diet can have an effect on spontaneous or experimental metastasis of the line 4526 murine mammary tumor. For this, six 20% fat diets were formulated with 1%, 6%, and 12% 18:2 and either high or low levels of 18:1. Our results indicate that the amount of select fatty acids other than 18:2 at 12% has no significant effect on mouse growth, tumor growth, or tumor latency. When spontaneous metastatic burden was calculated, no significant differences between mice fed diets containing 1% and 6% 18:2 were observed. However, 4 to 5 times more of a metastatic burden was observed in mice fed diets containing 12% 18:2. No significant differences were observed between high and low 18:1 diets when the 18:2 content was 1 or 12%. However, at 6% 18:2, 18:1 significantly decreased metastatic burden. When experimental metastasis was assessed, relatively low levels of surface lung nodules were observed at 1% and 6% 18:2, but significantly higher levels were observed at 12% 18:2. The results from these experiments along with our previous findings suggest that the type of fat supplementing the 12% 18:2 diet has no effect on altering 18:2-enhanced metastasis, but that it may have an effect of lowering metastasis when the level of 18:2 is decreased. Also, because there were no differences in growth in the primary tumor, and because increased experimental metastasis was observed in mice fed 12% 18:2, increased metastasis due to high levels of 18:2 may involve that part of the metastatic cascade after which the tumor cells are released from the primary site.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 165-171 |
| Number of pages | 7 |
| Journal | Cancer Letters |
| Volume | 56 |
| Issue number | 2 |
| DOIs | |
| State | Published - 1991 |
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Keywords
- cancer
- dietary fat
- mammary tumor
- metastasis
ASJC Scopus subject areas
- Cancer Research
- Molecular Biology
- Oncology
Cite this
Role of dietary oleic acid in linoleic acid-enhanced metastasis of a mouse mammary tumor. / Hubbard, Neil; Erickson, Kent L.
In: Cancer Letters, Vol. 56, No. 2, 1991, p. 165-171.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Role of dietary oleic acid in linoleic acid-enhanced metastasis of a mouse mammary tumor
AU - Hubbard, Neil
AU - Erickson, Kent L
PY - 1991
Y1 - 1991
N2 - We have previously shown that a high fat diet (20% w/w) containing 12% linoleic acid (18:2) can significantly increase the metastasis of mammary tumor cells when compared with high fat diets that contain 8% or less 18:2 with a constant level of oleic acid (18:1). This effect may have been due to an alteration of eicosanoid metabolism because the cyclooxygenase inhibitor, indomethacin, abolished the increase. Because 18:1 may interfere with the metabolism of 18:2 to 20:4, we have now tested whether the 18:1 that supplements the 18:2 diet can have an effect on spontaneous or experimental metastasis of the line 4526 murine mammary tumor. For this, six 20% fat diets were formulated with 1%, 6%, and 12% 18:2 and either high or low levels of 18:1. Our results indicate that the amount of select fatty acids other than 18:2 at 12% has no significant effect on mouse growth, tumor growth, or tumor latency. When spontaneous metastatic burden was calculated, no significant differences between mice fed diets containing 1% and 6% 18:2 were observed. However, 4 to 5 times more of a metastatic burden was observed in mice fed diets containing 12% 18:2. No significant differences were observed between high and low 18:1 diets when the 18:2 content was 1 or 12%. However, at 6% 18:2, 18:1 significantly decreased metastatic burden. When experimental metastasis was assessed, relatively low levels of surface lung nodules were observed at 1% and 6% 18:2, but significantly higher levels were observed at 12% 18:2. The results from these experiments along with our previous findings suggest that the type of fat supplementing the 12% 18:2 diet has no effect on altering 18:2-enhanced metastasis, but that it may have an effect of lowering metastasis when the level of 18:2 is decreased. Also, because there were no differences in growth in the primary tumor, and because increased experimental metastasis was observed in mice fed 12% 18:2, increased metastasis due to high levels of 18:2 may involve that part of the metastatic cascade after which the tumor cells are released from the primary site.
AB - We have previously shown that a high fat diet (20% w/w) containing 12% linoleic acid (18:2) can significantly increase the metastasis of mammary tumor cells when compared with high fat diets that contain 8% or less 18:2 with a constant level of oleic acid (18:1). This effect may have been due to an alteration of eicosanoid metabolism because the cyclooxygenase inhibitor, indomethacin, abolished the increase. Because 18:1 may interfere with the metabolism of 18:2 to 20:4, we have now tested whether the 18:1 that supplements the 18:2 diet can have an effect on spontaneous or experimental metastasis of the line 4526 murine mammary tumor. For this, six 20% fat diets were formulated with 1%, 6%, and 12% 18:2 and either high or low levels of 18:1. Our results indicate that the amount of select fatty acids other than 18:2 at 12% has no significant effect on mouse growth, tumor growth, or tumor latency. When spontaneous metastatic burden was calculated, no significant differences between mice fed diets containing 1% and 6% 18:2 were observed. However, 4 to 5 times more of a metastatic burden was observed in mice fed diets containing 12% 18:2. No significant differences were observed between high and low 18:1 diets when the 18:2 content was 1 or 12%. However, at 6% 18:2, 18:1 significantly decreased metastatic burden. When experimental metastasis was assessed, relatively low levels of surface lung nodules were observed at 1% and 6% 18:2, but significantly higher levels were observed at 12% 18:2. The results from these experiments along with our previous findings suggest that the type of fat supplementing the 12% 18:2 diet has no effect on altering 18:2-enhanced metastasis, but that it may have an effect of lowering metastasis when the level of 18:2 is decreased. Also, because there were no differences in growth in the primary tumor, and because increased experimental metastasis was observed in mice fed 12% 18:2, increased metastasis due to high levels of 18:2 may involve that part of the metastatic cascade after which the tumor cells are released from the primary site.
KW - cancer
KW - dietary fat
KW - mammary tumor
KW - metastasis
UR - http://www.scopus.com/inward/record.url?scp=0025981644&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025981644&partnerID=8YFLogxK
U2 - 10.1016/0304-3835(91)90092-V
DO - 10.1016/0304-3835(91)90092-V
M3 - Article
C2 - 1998946
AN - SCOPUS:0025981644
VL - 56
SP - 165
EP - 171
JO - Cancer Letters
JF - Cancer Letters
SN - 0304-3835
IS - 2
ER -