PMID- 25469394
OWN - NLM
STAT- MEDLINE
DCOM- 20150623
LR  - 20230216
IS  - 2156-5376 (Electronic)
IS  - 2161-8313 (Print)
IS  - 2161-8313 (Linking)
VI  - 5
IP  - 5
DP  - 2014 Sep
TI  - It's all about balance: cellular responses to nutrients and development of 
      disease.
PG  - 558-60
AB  - Responding to nutrient availability is an important homeostatic mechanism in the 
      growth, development, and function of cells and tissues. However, these 
      adaptations can also play a role in the development of disease. Our symposium, 
      "Cellular Responses to Nutrients and Development of Disease," presented research 
      about how cells sense nutrients and how the resulting signal transduction 
      controls cellular processes from gene transcription to impacting various 
      pathophysiologic processes. Dr. Michael Kilberg discussed the transcription 
      program triggered by amino acid limitation that leads to growth arrest in normal 
      cells and sustained growth in tumor cells. Dr. Noa Noy elaborated on the role of 
      lipid-binding proteins in retinoic acid signaling, focusing on fatty acid-binding 
      protein 5 (FABP5), which promotes cell growth by delivering this molecule to the 
      nuclear receptor peroxisome proliferator-activated receptor delta (PPARdelta). Dr. Li-Na 
      Wei discussed the many functions of the protein receptor interacting protein 140 
      (RIP140) as a coregulator of nuclear receptors and as a cytoplasmic protein that 
      regulates insulin-stimulated glucose uptake, lipolysis, and inflammation. Dr. 
      Ruma Banerjee presented state-of-the-art approaches for studying the gaseous 
      signaling molecule hydrogen sulfide (H2S), discussing its concentrations, 
      metabolism, and functions in the regulation of redox signaling. Finally, Dr. 
      Maria Hatzoglou described how the stress-induced increases in amino acid 
      transport, mammalian target of rapamycin (mTOR) signaling, and protein synthesis 
      in pancreatic beta-cells can contribute to the progression of diabetes.
FAU - Hatzoglou, Maria
AU  - Hatzoglou M
FAU - Snider, Martin D
AU  - Snider MD
FAU - Maruvada, Padma
AU  - Maruvada P
LA  - eng
GR  - R37 DK060596/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Adv Nutr
JT  - Advances in nutrition (Bethesda, Md.)
JID - 101540874
RN  - 0 (Amino Acids)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Amino Acids/*pharmacology
MH  - Animals
MH  - Cell Line
MH  - Chronic Disease/*drug therapy/*prevention & control
MH  - Congresses as Topic
MH  - Disease Models, Animal
MH  - Homeostasis
MH  - Humans
MH  - JNK Mitogen-Activated Protein Kinases
MH  - Protein Serine-Threonine Kinases/metabolism
MH  - Receptors, Cytoplasmic and Nuclear/*drug effects/metabolism
MH  - *Signal Transduction
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Transcription, Genetic
PMC - PMC4188232
COIS- Author disclosures: M. Hatzoglou, M.D. Snider, and P. Maruvada, no conflicts of 
      interest
EDAT- 2014/12/04 06:00
MHDA- 2015/06/24 06:00
PMCR- 2015/09/01
CRDT- 2014/12/04 06:00
PHST- 2014/12/04 06:00 [entrez]
PHST- 2014/12/04 06:00 [pubmed]
PHST- 2015/06/24 06:00 [medline]
PHST- 2015/09/01 00:00 [pmc-release]
AID - S2161-8313(22)00880-8 [pii]
AID - 006544 [pii]
AID - 10.3945/an.114.006544 [doi]
PST - ppublish
SO  - Adv Nutr. 2014 Sep;5(5):558-60. doi: 10.3945/an.114.006544.