PMID- 21462085
OWN - NLM
STAT- MEDLINE
DCOM- 20110815
LR  - 20211203
IS  - 1532-7914 (Electronic)
IS  - 0163-5581 (Linking)
VI  - 63
IP  - 3
DP  - 2011
TI  - Effects of intermittent and chronic calorie restriction on mammalian target of 
      rapamycin (mTOR) and IGF-I signaling pathways in mammary fat pad tissues and 
      mammary tumors.
PG  - 389-401
LID - 10.1080/01635581.2011.535968 [doi]
AB  - Chronic calorie restriction (CCR) prevents mammary tumor (MT) development in 
      rodents. We reported that intermittent calorie restriction (ICR) provides greater 
      protection than CCR in MMTV-TGF-alpha mice. The mammalian target of rapamycin (mTOR) 
      pathway is involved in MT development. Here the impact of ICR versus CCR on 
      proteins associated with mTOR signaling in mammary tissues and MTs from 
      MMTV-TGF-alpha mice was determined. Mice were enrolled at 10 wk of age into ad 
      libitum-fed (AL), CCR, and ICR groups and followed until 37/38 or 73/74 wk of 
      age. Time points 37 and 73 followed 3 wk of 50% restriction for ICR mice, while 
      38 and 74 followed 1 wk of refeeding of ICR mice. Calorie restriction reduced 
      serum IGF-I levels except for older CCR mice. At 37/38 wk, calorie restriction 
      decreased mTOR, p70S6K, HIF-1, EGFR, and Erk protein activation and increased 
      p4EBP1 and VEGF in mammary fat pads. At 73/74 wk, both modes of calorie 
      restriction lowered IGF-I protein expression levels and Akt activation in MTs and 
      mammary fat pads, and CCR increased mTOR, p70S6K, p4EBP1, and HIF-1 expression. 
      ICR had inconsistent effects on these proteins in older mice. These results 
      indicate that mTOR signaling proteins are modulated by age and type of calorie 
      restriction.
FAU - Dogan, Soner
AU  - Dogan S
AD  - Hormel Institute, University of Minnesota, Austin, Minnesota 55912, USA.
FAU - Johannsen, Anna C
AU  - Johannsen AC
FAU - Grande, Joseph P
AU  - Grande JP
FAU - Cleary, Margot P
AU  - Cleary MP
LA  - eng
GR  - CA101858/CA/NCI NIH HHS/United States
GR  - DK16105/DK/NIDDK NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Nutr Cancer
JT  - Nutrition and cancer
JID - 7905040
RN  - 0 (Transforming Growth Factor alpha)
RN  - 0 (insulin-like growth factor-1, mouse)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 2.7.1.1 (mTOR protein, mouse)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Adipose Tissue/*pathology
MH  - Analysis of Variance
MH  - Animals
MH  - Body Weight
MH  - Breast/pathology
MH  - *Caloric Restriction
MH  - Cell Line, Tumor
MH  - Disease Models, Animal
MH  - Eating
MH  - Energy Intake
MH  - Female
MH  - Humans
MH  - Insulin-Like Growth Factor I/analysis/*metabolism
MH  - Mammals/metabolism
MH  - Mammary Neoplasms, Experimental/*diet therapy
MH  - Mammary Tumor Virus, Mouse/genetics
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - *Signal Transduction
MH  - TOR Serine-Threonine Kinases/*genetics/metabolism
MH  - Transforming Growth Factor alpha/genetics
EDAT- 2011/04/05 06:00
MHDA- 2011/08/16 06:00
CRDT- 2011/04/05 06:00
PHST- 2011/04/05 06:00 [entrez]
PHST- 2011/04/05 06:00 [pubmed]
PHST- 2011/08/16 06:00 [medline]
AID - 935891616 [pii]
AID - 10.1080/01635581.2011.535968 [doi]
PST - ppublish
SO  - Nutr Cancer. 2011;63(3):389-401. doi: 10.1080/01635581.2011.535968.