I have more than a decade of research experience in studying the regulation of intestinal epithelial nutrient/electrolyte transport in both in-vitro and in-vivo systems during physiological and pathophysiological states like inflammatory bowel disease (IBD) and obesity. My work on B0AT1 during my postdoctoral training identifies that Na-glutamine co-transporter, B0AT1, present only in the absorptive villus cells, is inhibited secondary to a transcriptional reduction in the synthesis of the protein, most likely by the immune inflammatory mediator, prostaglandin E2, in IBD. In contrast, Na-glutamine co-transporter, SN2, the only nutrient absorptive system in the secretory crypt cells, was stimulated secondary to increased affinity of the co-transporter from its altered phosphorylation, most likely by the immune inflammatory mediator leukotriene D4 in IBD.
My research area of interest is obesity, diabetes, and especially in Exosomal communications between adipose tissue and nutrient transporters in intestinal epithelial cells (IECs). Deregulation of glucose homeostasis not only results in diabetes but also obesity, as hyperglycemia promotes excessive insulin release and causes subsequent fat deposition. During obesity, adipose tissue secreted exosomes are transported to IECs via circulation. In IECs, obese exosomes mediate the stimulation of SGLT1, which results in increased glucose absorption. This altered glucose homeostasis is the underlying cause of diabetes; thus, it is critical to understand the cellular mechanism of intestinal absorptive pathways associated with glucose.