Evidence for expression of the facilitated glucose transporter in rat hepatocytes.

Abstract

The eukaryotic facilitated glucose transporter (GT) is expressed by many cell types, with the notable exception of hepatocytes; however, GT is expressed by several hepatoma cell lines, including the well-differentiated lines Fao, Hep3B, and HepG2. We report on studies carried out to determine the aspect(s) of the transformed phenotype that might be responsible for activating GT expression. Using RNA blot analysis with probes derived from rat GT cDNA, we found that GT was expressed by rat hepatocytes under two conditions (i) in vitro, when isolated hepatocytes were placed in cell culture, and (a) in vivo, when rats were subjected to starvation for .2 days. However, GT expression was not an obligatory feature of hepatomas, since two primary hepatocellular carcinomas did not express any GT mRNA. GT expression in hepatocytes was reduced by addition of dimethyl sulfoxide or sodium butyrate to the culture medium. Since these reagents are known to promote differentiation in some cell culture systems, their effect on hepatocytes may be to maintain the GT repression normally observed in vivo. Inclusion or exclusion in the culture medium of several other agents that enhance hepatocyte viability (serum, insulin, corticosteroids, epidermal growth factor, or triiodothyronine) did not affect GT expression. It is unclear whether the two conditions that led to GT expression in hepatocytes are related by a common signaling mechanism. Possibly, both cases involve a "stress" response: in vivo, a normal physiological response to starvation; in vitro, a response to a major alteration in the cellular environment.

Fructose transporter Glut5 expression in clear renal cell carcinoma

“…Overexpression of the facilitative glucose-transporter has been observed for a wide range of human cancers (41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53)(54)(55)(56)(57)(58) with the degree of overexpression generally being inversely correlated with prognosis. The mechanisms by which GLUTs promote malignant cellular behaviour have focused on factors inducing its expression, such as local hypoxia (37), oncogenes such as Ras, Scr (15) or Myc (38).…”

Gene therapy of diabetes: glucose-stimulated insulin secretion in a human hepatoma cell line (HEP G2ins/g)

“…The parental HEP G2 cells express the erythrocyte/brain may be overcome by engineering, from the patient's own glucose transporter GLUT 1, 4 but do not express the cells, an 'artificial beta cell', ie a non-islet cell capable of liver/islet glucose transporter GLUT 2. 5 This facilitative synthesising, storing and secreting mature insulin in transporter has a low affinity for glucose but a high response to metabolic signals, thus correcting diabetes capacity for transport.…”

Restricted expression of the erythroid/brain glucose transporter isoform to perivenous hepatocytes in rats. Modulation by glucose.

“…Since expression of the erythroid/brain GT is high in all cultured hepatomas tested, some of these hepatomas could arise from the perivenous hepatocytes that naturally express it. Other human primary hepatocellular carErythroid/Brain Glucose Transport in Perivenous Hepatocytes 991 cinomas, as the two described by Rhoads and his colleagues (10), that do not express the erythroid/brain GT, may arise from the periportal zone and might express only the liver GT.…”

“…This might derive from low expression of this mRNA in hepatocytes, from non-hepatocyte mRNA, or might be due to crosshybridization to other GT mRNAs in the liver (5). Rhoads et al (10) showed that hepatocytes do express the erythroid/brain GT only under stress conditions, such as 3 d of starvation in vivo or in cell culture in response to major alterations in the cellular environment.…”