Glucose Transport and Protein Trafficking
Karin Stenkula, PI
The group is focused on exploring the molecular events regulating adipose cell function and how that is associated with whole-body glucose homeostasis. Specifically, we are intere3sted in the plasma membrane environment, including the cytoskeleton network, and how changes during cell expansion influence the insulin signaling transducation and glucose uptake.
We have previously characterized the dynamic of the main-insulin responsive golucose transporter, GLUT4, by live-cell imaging in primalry adipocytes [1, 2]. Recently, we found that the GLUT4 translocation process itself is impaired in human adipose cells isolated from obese and insulin resistant subjects, and that cells displayed a bimodal switch (either responding or non-responding to insulin( [3, 4]. We are now in the process further exploring this bimodal behavior, to see if that could expalin why some humans can handle excess fat mass without developing insulin resistance3 whereas other, equally obese, become insulin resistant.
Another focus is to identify early events in mature adipocytes associated with the development of insulin resistance and pre-diabetes. We are studying both processes during adipose cell expansion to identify factors regulating adipocyte recruitment , and the initial alteration of glucose uptake and lipid metabolism in mature adipocytes induced by increased calorie intake.
In a recent project, we have focused on transcriptional regulation of the plasma membrane components caveolin and cavins in adipocytes, where we found one of the commonly used insulin sensitizer drug, Rosiglitazone, to induce expression of cavin-2 in both pre-and mature adipocytes.
In most of our research studies, we are applying live-cell imaging and confocal microscopy. This in combination with different molecular- and cell biology techniques of gene expression, glucose uptake, lipogenesis and signal transduction analaysis makes the frame-work of the methods used in our lab.
Send an e-mail: karin [dot] stenkula [at] med [dot] lu [dot] se