Localization of the GLUT8 glucose transporter in murine kidney and regulation in vivo in nondiabetic and diabetic conditions

Schiffer, Mario; Suszták, Katalin; Ranalletta, Mollie; Raff, Amanda; Böttinger, Erwin P.; Charron, Maureen J.

doi:10.1152/ajprenal.00234.2004

Cited by 45 publications

(23 citation statements)

References 36 publications

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“…The increase in glucose uptake was not abolished completely, which may be explained by incomplete knockdown or by the contribution of other glucose transporters. We have demonstrated the presence of GLUT2 in podocytes (M. A. Saleem, unpublished data) and GLUT8 has also been reported to have high levels of production in the kidney [36].…”

Section: Discussionmentioning

confidence: 69%

Rosiglitazone enhances glucose uptake in glomerular podocytes using the glucose transporter GLUT1

et al. 2009

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Aims/hypothesis Peroxisome proliferator-activated receptor (PPAR) γ agonists are used increasingly in the treatment of type 2 diabetes. In the context of renal disease, PPARγ agonists reduce microalbuminuria in diabetic nephropathy; however, the mechanisms underlying this effect are unknown. Glomerular podocytes are newly characterised insulin-sensitive cells and there is good evidence that they are targeted in diabetic nephropathy. In this study we investigated the functional and molecular effects of the PPARγ agonist rosiglitazone on human podocytes. Methods Conditionally immortalised human podocytes were cultured with rosiglitazone and functional effects were measured with glucose-uptake assays. The effect of rosiglitazone on glucose uptake was also measured in 3T3-L1 adipocytes, nephrin-deficient podocytes, human glomerular endothelial cells, proximal tubular cells and podocytes treated with the NEFA palmitate. The role of the glucose transporter GLUT1 was investigated with immunofluorescence and small interfering RNA knockdown and the plasma membrane expression of GLUT1 was determined with bis-mannose photolabelling. Results Rosiglitazone significantly increased glucose uptake in wild-type podocytes and this was associated with translocation of GLUT1 to the plasma membrane. This effect was blocked with GLUT1 small interfering RNA. Nephrin-deficient podocytes, glomerular endothelial cells and proximal tubular cells did not increase glucose uptake in response to either insulin or rosiglitazone. Furthermore, rosiglitazone significantly increased basal and insulinstimulated glucose uptake when podocytes were treated with the NEFA palmitate. Conclusions/interpretation In conclusion, rosiglitazone has a direct and protective effect on glucose uptake in wild-type human podocytes. This represents a novel mechanism by which PPARγ agonists may improve podocyte function in diabetic nephropathy.

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Section: Discussionmentioning

confidence: 69%

Rosiglitazone enhances glucose uptake in glomerular podocytes using the glucose transporter GLUT1

et al. 2009

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“…Its entry is mediated by two distinct families of the hexose transporter proteins: facilitative glucose carriers (GLUTs) and sodium-glucose co-transporters (SGLTs; Mueckler, 1994;Wright, 2001). GLUT1, 2, 4, 5, 8, 12 and SGLT 1 and 2 are expressed in the kidney (Hoffman and Ziyadeh, 1995;Schiffer et al, 2005;Linden et al, 2006). GLUT2 and SGLT2, the high capacity and low-affinity transporters expressed in the S1 segment of the proximal tubule, are major transporters of glucose in the kidney.…”

Section: Journal Of Cellular Physiology G F a T 1 A N D O G T I N P Omentioning

confidence: 99%

Expression of GFAT1 and OGT in podocytes: Transport of glucosamine and the implications for glucose uptake into these cells

Rogacka

Piwkowska

Jankowski

et al. 2010

Journal Cellular Physiology

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Glutamine:fructose-6-phosphate amidotransferase (GFAT) and N-acetylglucosaminyltransferase (OGT) participate in glucosamine (GlcN) production and its utilization in O-glycosylation, one of key post-translational modifications of nuclear and cytoplasmic proteins. For this purpose, cells require a high rate of intracellular production of GlcN and/or significant GlcN delivery. We studied the expression of GFAT1 and OGT and measured uptake of glucose and GlcN in cultured rat podocytes, the main cellular component of glomerular filtration barrier. RT-PCR revealed the presence of both GFAT1 and OGT mRNA. Immunofluorescence of GFAT1 has shown staining signal diffused within the cytoplasm of the cell body and processes. However, OGT was distinctly visible around the nucleus and, in diffuse form, within the cytoplasm of cell bodies and processes. Glucose was transported (1.3 +/- 0.2 nmol/min/mg protein) mainly by facilitative transporter systems whilst GlcN uptake (1.1 +/- 0.2 nmol/min/mg protein) in a significant part, involved a sodium-dependent transporter. There was interplay between glucose and GlcN uptake. In the presence of GlcN (50 microM), the rate of glucose uptake decreased by about 50%. The rate of GlcN uptake decreased by 28% in the presence of 5.6 mM glucose. Our results suggest that cultured podocytes possess limited ability to synthesize GlcN internally and therefore may need to receive GlcN from the extracellular environment.

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“…26 Podocytes also express GLUT8; however, the subcellular localization of this transporter is not known. 24 GLUT3 is expressed in mesangial cells but not in podocytes. 22 All these data, however, are not enough to explain how podocytes utilize glucose under physiological and pathological conditions.…”

Section: Introductionmentioning

confidence: 97%

“…The passage of glucose across cell membranes is facilitated by glucose transporters (GLUTs), of which 14 members are currently known. 20 Several studies have determined GLUT1, 21,22 GLUT3, 22 GLUT4 22,23 and GLUT8 24 to be expressed in the glomerulus. Among these proteins, both GLUT1 and GLUT4 are localized in the cytoplasm and at the plasma membrane of podocytes in addition to their more abundant expression in the mesangial cells of the human glomerulus.…”

Section: Introductionmentioning

confidence: 99%

The struggle for energy in podocytes leads to nephrotic syndrome

et al. 2012

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Localization of the GLUT8 glucose transporter in murine kidney and regulation in vivo in nondiabetic and diabetic conditions

Abstract: tion of the GLUT8 glucose transporter in murine kidney and regulation in vivo in nondiabetic and diabetic conditions. Am J Physiol

Cited by 45 publications

References 36 publications

Rosiglitazone enhances glucose uptake in glomerular podocytes using the glucose transporter GLUT1

Rosiglitazone enhances glucose uptake in glomerular podocytes using the glucose transporter GLUT1

Expression of GFAT1 and OGT in podocytes: Transport of glucosamine and the implications for glucose uptake into these cells

The struggle for energy in podocytes leads to nephrotic syndrome

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