Solmonson, Ashley; Faubert, Brandon; Gu, Wen; Rao, Aparna; Cowdin, Mitzy A.; Menendez-Montes, Ivan; Kelekar, Sherwin; Rogers, Thomas J.; Pan, Chunxiao; Guevara, Gerardo; Tarangelo, Amy; Zacharias, Lauren G.; Martin-Sandoval, Misty S.; Do, Duyen; Pachnis, Panayotis; Dumesnil, Dennis; Mathews, Thomas P.; Tasdogan, Alpaslan; Pham, An; Cai, Ling; Zhao, Zhiyu; Ni, Min; Cleaver, Ondine; Sadek, Hesham A.; Morrison, Sean J.; DeBerardinis, Ralph J. published the artcile< Compartmentalized metabolism supports midgestation mammalian development>, Category: esters-buliding-blocks, the main research area is midgestation mammalian embryogenesis metabolome LIPT1.
Mammalian embryogenesis requires rapid growth and proper metabolic regulation. Midgestation features increasing oxygen and nutrient availability concomitant with fetal organ development. Understanding how metabolism supports development requires approaches to observe metabolism directly in model organisms in utero. Here we used isotope tracing and metabolomics to identify evolving metabolic programs in the placenta and embryo during midgestation in mice. These tissues differ metabolically throughout midgestation, but we pinpointed gestational days (GD) 10.5-11.5 as a transition period for both placenta and embryo. Isotope tracing revealed differences in carbohydrate metabolism between the tissues and rapid glucose-dependent purine synthesis, especially in the embryo. Glucoses contribution to the tricarboxylic acid (TCA) cycle rises throughout midgestation in the embryo but not in the placenta. By GD12.5, compartmentalized metabolic programs are apparent within the embryo, including different nutrient contributions to the TCA cycle in different organs. To contextualize developmental anomalies associated with Mendelian metabolic defects, we analyzed mice deficient in LIPT1, the enzyme that activates 2-ketoacid dehydrogenases related to the TCA cycle. LIPT1 deficiency suppresses TCA cycle metabolism during the GD10.5-GD11.5 transition, perturbs brain, heart and erythrocyte development and leads to embryonic demise by GD11.5. These data document individualized metabolic programs in developing organs in utero.
Nature (London, United Kingdom) published new progress about Anemia. 112-63-0 belongs to class esters-buliding-blocks, and the molecular formula is C19H34O2, Category: esters-buliding-blocks.
Referemce:
Ester – Wikipedia,
Ester – an overview | ScienceDirect Topics