Glucose transporters in chromaffin cells: Subcellular distribution and characterization

Abstract

The glucose transporter was identified and characterized by cytochalasin B binding in subcellular membrane fractions of chromaffin tissue. The binding was saturable with a Kd of about 0.3/zM for each subceilular fraction. The Bm~ capacity was 12-16 pmol/mg protein for enriched plasma membrane fractions, 6.3 pmol/mg protein for mierosomal membrane preparations and 5.4 pmol/mg protein for chromaitin granule membranes. Irreversible photoaffinity labelling of the glucose-protectable binding sites with [aH]cytochaiasin B followed by solubilization and polyacrylamide gel electrophoresis from enriched plasma membrane preparations demonstrated the presence of three molecular species: 97+ 10, 51.5 + 6 and 30 + 4 kDa. The chromaffin granule membranes showed only a molecular species of 80__+ 10 kDa.

Effect of 5′‐(N‐Ethylcarboxamido)adenosine on Adenosine Transport in Cultured Chromaffin Cells

“…It is well known that insulin increases glucose transport by translocation of transporters from the microsomal fraction to plasma membranes (Simpson et al, 1983;Simpson and Cushman, 1986). In chromaffin cells, insulin and other secretagogues also increase glucose transport by a parallel increase in number of glucose transporters at the plasma membrane level (Delicado and Miras-Portugal, 1987;Delicado et al, 1988). Thus, it will be necessary to study the nucleoside transporter number at the plasma membrane of chromaffin cells in the presence or absence of the A2 agonist NECA.…”

Induced Pluripotent Stem (iPS) Cells Inhibit Apoptosis and Fibrosis in Streptozotocin-Induced Diabetic Rats

“…The World Health Organization (WHO) predicts that this number will more than double to an astounding 366 million people by the year 2030 . Type 1 diabetes is an autoimmune disease characterized by destruction of insulin-producing beta cells of the islets of Langerhans in the pancreas. , Normally, insulin functions to regulate blood glucose levels and to increase cellular absorption of glucose by enhancing membrane expression of glucose receptors . Loss of insulin production leads to high circulating blood glucose, or hyperglycemia, which causes many complications, including retinopathy, nephropathy, neuropathy, impaired wound healing, osteoporosis, and cardiomyopathy. ,,, Moreover, diabetic cardiomyopathy (DCM) alters many pathways mediated by oxidative stress and hyperglycemia, which leads to an increase in cellular death via apoptosis and necrosis. , In the diabetic heart, apoptosis is well documented by various investigators. , Following apoptotic cell death, adverse ventricular remodeling occurs, which involves interstitial and vascular fibrosis. , Fibrosis alters cardiac structure and geometry as well as initiates stiffening of the heart that further significantly reduces cardiac function, which leads to congestive heart failure and death. ,, The exact mechanisms of increased fibrosis in diabetic cardiomyopathy are still being elucidated .…”

“…4,41 Normally, insulin functions to regulate blood glucose levels and to increase cellular absorption of glucose by enhancing membrane expression of glucose receptors. 13 Loss of insulin production leads to high circulating blood glucose, or hyperglycemia, which causes many complications, including retinopathy, nephropathy, neuropathy, impaired wound healing, osteoporosis, and cardiomyopathy. 4,11,18,21 Moreover, diabetic cardiomyopathy (DCM) alters many pathways mediated by oxidative stress and hyperglycemia, 6 which leads to an increase in cellular death via apoptosis and necrosis.…”