Understand how metabolomics fits into your research program
Beginning with Antonie van Leeuwenhoek, scientists have been developing novel technologies to discover more about the world around them. However, in recent times, the development of technologies have become focused research areas unto themselves, in addition to remaining a means of support for countless areas of Basic Science Research.
Although it’s difficult to determine the exact starting point of the field of metabolomics, the observation of differential use of glycolysis by cancer cells by Otto Warburg jump-started the interest in metabolic differences relating to disease, and how these differences can be exploited for treatment. In recent years, Metabolism has been an increasingly active facet of many areas of research, including cancer, nutrition, immunology, microbiomes, and neuroscience. While Mass Spectrometry has long been utilized in molecular studies and proteomics, recent advances in combined separation techniques have allowed for the metabolite measurement of in a complex mixture, like cellular millieu.
Using techniques to measure the steady state levels of metabolites, a methodology called metabolomics, researchers can gain a better understanding of disease states, as well as normal physiological conditions. In 2002, Dr. Tomoyoshi Soga, of Keio University, established a new separation technique for MS based metabolomic studies: Capillary Electrophoresis. Capable of separating charged molecules based on mass, charge, and steric valence, this breakthrough became the groundwork for HMT. Having begun as a spinoff from an academic laboratory, HMT has never forgotten it’s roots: HMT is committed to working with basic science researchers to provide the highest quality metabolomics service, as well as collaborating with researchers to forge new paths to novel discoveries.
Metabolites released from apoptotic cells act as tissue messengers
Hypoxia tolerance in the Norrin-deficient retina and the chronically hypoxic brain studied at single-cell resolution
AMPK, a Regulator of Metabolism and Autophagy, Is Activated by Lysosomal Damage via a Novel Galectin-Directed Ubiquitin Signal Transduction System