PMID- 18001216
OWN - NLM
STAT- MEDLINE
DCOM- 20080219
LR  - 20220318
IS  - 0163-5581 (Print)
IS  - 0163-5581 (Linking)
VI  - 59
IP  - 2
DP  - 2007
TI  - High-fat, high-sucrose, and high-cholesterol diets accelerate tumor growth and 
      metastasis in tumor-bearing mice.
PG  - 207-16
AB  - Epidemiological studies indicate that the risk factors for the development of 
      various cancers are closely associated with metabolic symptoms such as obesity, 
      hyperlipidemia, and insulin resistance caused by the excess consumption of 
      high-calorie diets. However, the mechanisms of tumor growth and metastasis caused 
      by feeding a high-calorie diet have not been clarified yet in tumor-bearing mice. 
      In this study, we examined the effects of a high-fat (HF), a high-sucrose (HS), a 
      high-cholesterol (HC) or a low-fat/low-sucrose (LF/LS) diet on tumor growth and 
      metastasis in tumor-bearing mice. Angiogenic factors such as plasma leptin and 
      monocyte chemoattractant protein-1 (MCP-1) were increased after the implantation 
      of tumors, whereas conversely, an antiangiogenic factor, adiponectin, was reduced 
      after the implantation of tumors in mice fed the HF, the HS, or the HC diet 
      compared to LF/LS diet. Furthermore, we found that vascular endothelial growth 
      factor, hypoxia inducible factor-1alpha and MCP-1 expression levels in tumors of 
      mice fed the HF, the HS, or the HC diet were increased compared to those of mice 
      fed the LF/LS diet. These findings suggest that the acceleration of tumor growth 
      and metastasis by feeding the 3 diets may be due to the increase of angiogenic 
      factors and the reduction of antiangiogenic factors.
FAU - Kimura, Yoshiyuki
AU  - Kimura Y
AD  - Division of Biochemical Pharmacology, Department of Basic Medical Research, 
      School of Medicine, Ehime University, Shitsukawa, Toon-City, Ehime, Japan. 
      yokim@m.ehime-u.ac.jp
FAU - Sumiyoshi, Maho
AU  - Sumiyoshi M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Nutr Cancer
JT  - Nutrition and cancer
JID - 7905040
RN  - 0 (Adiponectin)
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cholesterol, Dietary)
RN  - 0 (Dietary Fats)
RN  - 0 (Dietary Sucrose)
RN  - 0 (Leptin)
SB  - IM
MH  - Adiponectin/blood
MH  - Animals
MH  - Body Weight
MH  - Carcinoma, Lewis Lung
MH  - Chemokine CCL2
MH  - Cholesterol, Dietary/*administration & dosage
MH  - *Diet
MH  - Dietary Fats/*administration & dosage
MH  - Dietary Sucrose/*administration & dosage
MH  - Disease Progression
MH  - Dose-Response Relationship, Drug
MH  - Glucose Intolerance
MH  - Glucose Tolerance Test
MH  - Hyperinsulinism/complications
MH  - Hyperlipidemias/complications
MH  - Immunohistochemistry
MH  - Insulin Resistance
MH  - Leptin/blood
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neoplasm Metastasis
MH  - Neoplasm Transplantation
MH  - Neoplasms, Experimental/etiology/*pathology
MH  - Obesity/complications
MH  - Random Allocation
EDAT- 2007/11/16 09:00
MHDA- 2008/02/20 09:00
CRDT- 2007/11/16 09:00
PHST- 2007/11/16 09:00 [pubmed]
PHST- 2008/02/20 09:00 [medline]
PHST- 2007/11/16 09:00 [entrez]
AID - 10.1080/01635580701499537 [doi]
PST - ppublish
SO  - Nutr Cancer. 2007;59(2):207-16. doi: 10.1080/01635580701499537.