Abstract
The sulfonylureas (SULF) have long been utilized as oral agents in the treatment of type 2 diabetes mellitus (1). The primary effect of SULF is the stimulation of insulin secretion following binding to specific SULF receptors (SUR) on pancreatic β-cells. However, SUR have extensive representation in a multitude of extrapancreatic tissues. Therefore, it is not unanticipated that SULF may induce metabolic changes aside from that of insulin secretion. These drugs have been shown to increase glucose uptake and glucose transporter (GLUT) expression in myocytes, adipocytes, and skeletal muscle cells (2–5). Moreover, we have documented significant SULF-induced metabolic effects in cultured rat mesangial cells (MCs), including alterations in mesangial matrix metabolism and MC contractility, independent of their effect on the ambient level of glycemia. The latter effect mimicked that provided by other known MC effectors of contractility, for example, atrial natriuretic peptide and angiotensin II.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Lebovitz HE, Feinglos MN. Sulfonylurea drugs: mechanism of antidiabetic action and therapeutic usefulness. Diabetes Care 1978;1:189–198.
Jacobs DB, Hayes GR, Lockwood DH. In vitro effects of sulfonylurea on glucose transport and translocation of glucose transporters in adipocytes from streptozotocin-induced diabetic rats. Diabetes 1989;38:205–211.
Wang PH, Moller D, Flier JR, Nayak RC, Smith RJ. Coordinate regulation of glucose transporter function, number, and gene expression by insulin and sulfonylureas in L6 rat skeletal muscle cells. J Clin Invest 1989;84:62–67.
Müller G, Wied S. The sulfonylurea drug glimepiride stimulates glucose transport, glucose transporter translocation, and dephosphorylation in insulin-resistant rat adipocytes in vitro. Diabetes 1993;42:1852–1867.
Rogers BJ, Standaert ML, Pollet RJ. Direct effects of sulfonylurea agents on glucose transport in the BC3H-1 myocyte. Diabetes 1987;36:1292–1296.
Cortes P, Riser BL, Asano K, Rodrígez-Barbero A, Narins RG, Yee J. Effects of oral antihyperglycemic agents on extracellular matrix synthesis by mesangial cells. Kidney Int 1998;54:1985–1998.
Giannico G, Biederman J, Hasset C, Yee J, Cortes P. Amelioration of glucose-induced extracellular matrix formation (ECM) by the sulfonylurea glibenclamide (GLIB) in cultured mesangial cells (MC). J Am Soc Nephrol 2002;13:318A.
Asano K, Cortes P, Garvin JL, et al. Characterization of the rat mesangial cell type 2 sulfonylurea receptor. Kid Int 1999;55:2289–2298.
Inagaki N, Gonoi T, Clement IV JP, et al. A family of sulfonylurea receptors determines the pharmacological properties of ATP-sensitive K+ channels. Neuron 1996;16:1011–1017.
Chutkow WA, Simon MC, Le Beau MM, Burant CF. Cloning, tissue expression, and chromosomal localization of SUR2, the putative drug-binding subunit of cardiac, skeletal muscle, and vascular KATP channels. Diabetes 1996;45:1439–1445.
Higgins CF. The ABC of Channel Regulation. Cell 1995;82:693–696.
Philipson LH, Steiner DF. Pas de deux or more: The sulfonylurea receptor and K+ channels. Science 1995;268:372, 373.
Garlid KD, Paucek P, Yarov-Yarovoy P, Sun X, Schindler PA. The mitochondrial KATP channel as a receptor for potassium channel openers. J Biol Chem 1996;271:8796–8799.
Suzuki M, Kotake K, Fujikura K, et al. Kir6.1: A possible subunit of ATP-sensitive K+ channels in mitochondria. Biochem Biophys Res Comm 1997;241:693–697.
Geng X, Li L, Watkins S, Robbins PD, Drain P. The insulin secretory granule is the major site of KATP channels of the endocrine pancreas. Diabetes 2003;52:767–776.
Suzuki M, Sasaki N, Miki T, et al. Role of sarcolemmal KATP channels in cardioprotection against ischemia/reperfusion injury in mice. J Clin Invest 2002;109:509–516.
Carpentier J-L, Sawano F, Ravazzola M, Malisse WJ. Internalization of 3H-glibenclamide in pancreatic islet cells. Diabetologia 1996;29:259–261.
Kawaki J, Nagashima K, Tanaka J, et al. Unresponsiveness to glibenclamide during chronic treatment induced by reduction of ATP-sensitive K+ channel activity. Diabetes 1999;48:2001–2006.
Schwanstecher M, Schwanstecher C, Dickel C, Chudziak F, Moshiri A, Panten U. Location of the sulfonylurea receptor at the cytoplasmic face of the beta-cell membrane. Brit J Pharmacol 1994;113:903–911.
Zunkler BJ, Trube G, Panten U. How do sulfonylureas approach their receptor in the P-cell plasma membrane? Naunyn-Schmiedeberg’s Arch Pharmacol 1989;340:328–332.
Ashcroft SJH, Ashcroft FM. The sulfonylurea receptor. Biochem Biophys Acta 1992;1175:45–59.
Dukes ID, Philipson LH. K+ channels: generating excitement in pancreatic P-cells. Diabetes 1996;45:845–853.
Suzuki M, Fujikura K, Inagaki N, Seino S, Takata K. Localization of the ATP-sensitive K+ channel subunit Kir6.2 in mouse pancreas. Diabetes 1997;46:1440–1444.
Brian J, Aguilar-Brian L. The ABCs of ATP-sensitive potassium channels-more pieces of the puzzle. Curr Opin Cell Biol 1997;9:553–559.
Babenko AP, Aguilar-Bryan L, Bryan J. A View of SUR/KIR6.X, K channels. Annu Rev Physiol 1998;60:667–687.
Ashcroft FM. Adenosine 5′-triphosphate-sensitive potassium channels. Ann Rev Neurosci 1988;11:97–118.
Seino S, Iwanaga T, Nagashima K, Miki T. Diverse roles in KATP channels learned from Kir6.2 genetically engineered mice. Diabetes 2000;49:311–318.
Lorenz E, Terzic A. Physical association between recombinant cardiac ATP-sensitive K+channel subunits Kir6.2 and SUR2A. J Mol Cell Cardiol 1999;31:425–434.
Ashcroft SJ, Ashcroft FM. Properties and function of ATP-sensitive K+ channels. Cell Signal 1990;2:197–214.
Gopalakrishnan M, Whitaker KL, Molinari EJ, et al. Characterization of the ATP-Sensitive Potassium Channels (KATP) Expressed in Guinea Pig Bladder Smooth Muscle Cells. J Pharmacol Exper Therap 1998;289:551–558.
Tune JD, Yeh C, Setty S, Downey F ATP-dependent K+ channels contribute to local metabolic coronary vasodilatation in experimental diabetes. Diabetes 2002;51:1201–1207.
Duncker DJ, van Zon NS, Ishibashi Y, Bache RJ. Role of K channels and adenosine in the regulation of coronary blood flow during exercise with normal and restricted coronary blood flow. J Clin Invest 1996;97:996–1009.
Edwards G, Weston AH. The pharmacology of ATP-sensitive potassium channels. Ann Rev Pharmacol Toxicol 1993;33:597–637.
Yokoshiki H, Katsube Y, Sunagawa M, Seki T, Sperelakis N. Disruption of actin cytoskeleton attenuates sulfonylurea inhibition of cardiac ATP-sensitive K+ channels. Eur J Physiol 1997;434:203–205.
Song DK, Ashcroft FM. ATP modulation of ATP-sensitive potassium channel ATP sensitivity varies with the type of SUR subunit. J Biol Chem 2001;276:7143–7149.
Loffler-Waltz C, Quast U. Disruption of the actin cytoskeleton abolishes high affinity 3H gliben-clamide binding in rat aortic rings. Naunyn-Schmiedebergs Arch Pharmacol 1998;357:183–185.
Brady PA, Alekseev AE, Alesandrova LA, Gomez LA, Terzic A. A disrupter of actin filaments impairs sulfonylurea-inhibitory gating of cardiac K channels. Am J Physiol 1996;271:H2710–H2716.
Dlugosz JA, Munk S, Ispanovic E, Goldberg HJ, Whiteside C. Mesangial cell filamentous actin disassembly and hypocontractility in high glucose are mediated by PKC-ζ. Am J Physiol Renal Physiol 2002;282:F151–F163.
Alto N, Michel JJC, Dodge KL, Langeberg LK, Scott JD. Intracellular targeting of protein kinases and phosphatases. Diabetes 2002;51(3):S385–S388.
Beesley AH, Qureshi IZ, Giesberts AN, Parker AJ, J White SJ. Expression of sulfonylurea receptor protein in mouse kidney. Pflugers Arch-Eur J Physiol 1999;438:1–7.
Brochiero E, Wallendorf B, Gagnon D, Laprade R, LaPointe JY Cloning of rabbit Kir6.1, SUR2A, and SUR2B: possible candidates for a renal K channel. Am J Physiol Renal Physiol 2002;282:F289–F300.
Tanemoto M, Vanoye CG, Dong K, et al. Rat homolog of sulfonylurea receptor 2B determines glibenclamide sensitivity of ROMK2 in Xenopus laevis oocyte. Am J Physiol Renal Physiol 2000;278:F659–F666.
Szamosfalvi B, Cortes P, Alviani R, et al. Putative subunits of the rat mesangial K: A type 2B sulfonylurea receptor and an inwardly rectifying K+ channel. Kid Int 2002;61:1739–1749.
Pendergast BD. Glyburide and glipizide, second generation oral sulfonylurea hypoglycemic agents. Clin Pharm 1984;3:473–485.
Russ U, Hambrock A, Artunc F, et al. Coexpression with the inward rectifier K+ channel Kir6.1 increases the affinity of the vascular sulfonylurea receptor SUR2B for glibenclamide. Mol Pharmacol 1999;56:955–961.
Peyrollier K, Heron Virsolvy-Vergine A, LeCam A, Bataille D. Alpha endosulfine is a novel molecule, structurally related to a family of phosphoproteins. Biochem Biophys Res Commun 1996;223:583–586.
Dulubova I, Horiuchi A, Snyder GL, et al. ARPP-16/ARPP-19: a highly conserved family of cAMP-regulated phosphoproteins. J Neurochem 2001;77:229–238.
Irwin N, Chao S, Gorichenko L, et al. Nerve growth factor controls GAP-43 mRNA stability via the phosphoprotein ARPP-19. Proc Natl Acad Sci 2002;99:12,427–12,431.
Heron L, Virsolvy A, Apiou F, Le Cam A, Bataille D. Isolation, characterization, and chromosomal localization of the human ENSA gene that encodes alpha-endosulfine, a regulator of beta-cell KATP channels. Diabetes 1999;48:1873–1876.
Bataille D, Heron L, Virsolvy A, et al. α-Endosulfine, a new entity in the control of insulin secretion. Cell Mol Life Sci 1999;56:78–84.
Gros L, Breant B, Duchene B, et al. Localization of α-endosulfine in pancreatic somatostatin 8-cells and expression during rat pancreas development. Diabetologia 2002;45:703–710.
Kim SH Lubec G. Brain a-endosulfine is manifold decreased in brains from patients with Alzheimer’s disease: a tentative marker and drug target? Neurosci Lett 2001;310:77–80.
Yee J, Cortes P, Barnes JL, Alviani R, Biederman JI, Szamosfalvi B. Rat mesangial a-endosulfine. Kid Int 2004;65:1731–1739.
Yee J, Szamosfalvi B. A New Mesangial Triumvirate: Sulfonylureas, Their Receptors and Endosulfines Exp Neph 2002;10:1–6.
UK Prospective Diabetes Study (UKPDS) Group. Intensive blood glucose control with sulfonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet 1998;352:837–853.
Klein R, Klein BEK, Moss SE, Cruickshanks K. Ten-year incidence of gross proteinuria in people with diabetes. Diabetes 1995;44:916–923.
Carpenter A-M, Goetz FC, LeCompte PM, Williamson JR. Glomerulosclerosis in type 2 (non-insulin-dependent) diabetes mellitus: relationship to glycemia in the University Group Diabetes Program (UGDP). Diabetologia 1993;36:1057–1063.
Biederman J, Vera E, Pankhaniya R, et al. Effects of sulfonylureas, a-endosulfine counterparts, on glomerulosclerosis in type 1 and type 2 models of diabetes. Kid Int 2005;67:554–565.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2006 Humana Press Inc., Totowa, NJ
About this chapter
Cite this chapter
Yee, J., Szamosfalvi, B. (2006). α-Endosulfine in Diabetic Nephropathy. In: Cortes, P., Mogensen, C.E. (eds) The Diabetic Kidney. Contemporary Diabetes. Humana Press. https://doi.org/10.1007/978-1-59745-153-6_17
Download citation
DOI: https://doi.org/10.1007/978-1-59745-153-6_17
Publisher Name: Humana Press
Print ISBN: 978-1-58829-624-5
Online ISBN: 978-1-59745-153-6
eBook Packages: MedicineMedicine (R0)