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It's All about Balance: Cellular Responses to Nutrients and Development of Disease

Hatzoglou, Maria, Snider, Martin D., Maruvada, Padma
Advances in nutrition 2014 v.5 no.5 pp. 558-560
amino acids, cell growth, diabetes, fatty acid-binding proteins, glucose, hydrogen sulfide, inflammation, islets of Langerhans, lipolysis, lithium, mammals, neoplasm cells, nutrient availability, nutrients, protein synthesis, receptors, retinoic acid, signal transduction, sodium, tissues, transcription (genetics)
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 δ (PPARδ). 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 β-cells can contribute to the progression of diabetes.