PMID- 24685128
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20140410
LR  - 20220408
IS  - 2049-3002 (Print)
IS  - 2049-3002 (Electronic)
IS  - 2049-3002 (Linking)
VI  - 2
IP  - 1
DP  - 2014 Mar 31
TI  - Leucine supplementation differentially enhances pancreatic cancer growth in lean 
      and overweight mice.
PG  - 6
LID - 10.1186/2049-3002-2-6 [doi]
AB  - BACKGROUND: The risk of pancreatic cancer, the 4th deadliest cancer for both men 
      and women in the United States, is increased by obesity. Calorie restriction (CR) 
      is a well-known dietary regimen that prevents or reverses obesity and suppresses 
      tumorigenesis in a variety of animal models, at least in part via inhibition of 
      mammalian target of rapamycin (mTOR) signaling. Branched-chain amino acids 
      (BCAA), especially leucine, activate mTOR and enhance growth and proliferation of 
      myocytes and epithelial cells, which is why leucine is a popular supplement among 
      athletes. Leucine is also increasingly being used as a treatment for pancreatic 
      cancer cachexia, but the effects of leucine supplementation on pancreatic tumor 
      growth have not been elucidated. RESULTS: Supplementation with leucine increased 
      pancreatic tumor growth in both lean (104 +/- 17 mm3 versus 46 +/- 13 mm3; P <0.05) 
      and overweight (367 +/- 45 mm3 versus 230 +/- 39 mm3; P <0.01) mice, but tumor 
      enhancement was associated with different biological outcomes depending on the 
      diet. In the lean mice, leucine increased phosphorylation of mTOR and downstream 
      effector S6 ribosomal protein, but in the overweight mice, leucine reduced 
      glucose clearance and thus increased the amount of circulating glucose available 
      to the tumor. CONCLUSIONS: These findings show that leucine supplementation 
      enhances tumor growth in both lean and overweight mice through diet-dependent 
      effects in a murine model of pancreatic cancer, suggesting caution against the 
      clinical use of leucine supplementation for the purposes of skeletal muscle 
      enhancement in cachectic patients.
FAU - Liu, Kristyn A
AU  - Liu KA
AD  - Department of Nutritional Sciences, University of Texas at Austin, Austin, TX 
      78723, USA.
FAU - Lashinger, Laura M
AU  - Lashinger LM
AD  - Department of Nutritional Sciences, University of Texas at Austin, Austin, TX 
      78723, USA.
FAU - Rasmussen, Audrey J
AU  - Rasmussen AJ
AD  - Department of Nutritional Sciences, University of Texas at Austin, Austin, TX 
      78723, USA.
FAU - Hursting, Stephen D
AU  - Hursting SD
AD  - Department of Nutritional Sciences, University of Texas at Austin, Austin, TX 
      78723, USA.
AD  - Department of Molecular Carcinogenesis, University of Texas M.D. Anderson Cancer 
      Center, 1808 Park Road 1c, Smithville, TX 78957, USA.
LA  - eng
PT  - Journal Article
DEP - 20140331
PL  - England
TA  - Cancer Metab
JT  - Cancer & metabolism
JID - 101607582
PMC - PMC4392529
EDAT- 2014/04/02 06:00
MHDA- 2014/04/02 06:01
PMCR- 2014/03/31
CRDT- 2014/04/02 06:00
PHST- 2013/10/03 00:00 [received]
PHST- 2014/03/18 00:00 [accepted]
PHST- 2014/04/02 06:00 [entrez]
PHST- 2014/04/02 06:00 [pubmed]
PHST- 2014/04/02 06:01 [medline]
PHST- 2014/03/31 00:00 [pmc-release]
AID - 2049-3002-2-6 [pii]
AID - 10.1186/2049-3002-2-6 [doi]
PST - epublish
SO  - Cancer Metab. 2014 Mar 31;2(1):6. doi: 10.1186/2049-3002-2-6.