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transporters (GLUT) and the hormonal regulation of their expression and function ( Charron et al . 2005 ). The Glut4 (Slc2a4) is the main insulin-responsive transporter abundantly expressed in skeletal muscle, adipose tissue and heart ( Kahn 1992 , Mueckler
Instituto Reina Sofía de Investigación Renal and REDinREN from Instituto de Salud Carlos III, Madrid, Spain
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Instituto Reina Sofía de Investigación Renal and REDinREN from Instituto de Salud Carlos III, Madrid, Spain
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Biomedical Research Foundation and Nephrology Department, Hospital Príncipe de Asturias, Madrid, Spain
Department of Systems Biology, Physiology Unit, Universidad de Alcalá, Madrid, Spain
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Instituto Reina Sofía de Investigación Renal and REDinREN from Instituto de Salud Carlos III, Madrid, Spain
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Instituto Reina Sofía de Investigación Renal and REDinREN from Instituto de Salud Carlos III, Madrid, Spain
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Introduction Type 2 diabetes and metabolic syndrome (MS) are characterized by high blood glucose levels as a consequence of inappropriate peripheral glucose uptake. The insulin-responsive facilitative glucose transporter GLUT4 is strongly
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Introduction Insulin is a major effector of cardiac substrate utilization, regulating both glucose and long-chain fatty acid (LCFA) uptake into cardiomyocytes. Under basal conditions, more than 90% of the major glucose transporter isoform GLUT4 is
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. 2004 ). Accumulating evidence has indicated the involvement of Akt1 in many types of cancer ( Cheung & Testa 2013 ). Akt2, on the other hand, plays a pivotal role in glucose homeostasis. Akt2 stimulates translocation of the glucose transporter GLUT4
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Department of Endocrinology, Medical College, Department of Physiology, Department of Physical Education, Clinical Medical College, Yangzhou University, Nantong West Street No. 98, Yangzhou, Jiangsu 225001, China
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most important and abundant member is glucose transporter 4 (GLUT4; Absalan et al . 2012 ). After GLUT4 vesicles are trafficked from an intracellular pool to dock and fuse with the plasma membrane of cells, GLUT4 can benefit glucose uptake from
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Physiology 289 R947 – R954 . Garvey WT Maianu L Zhu JH Brechtel-Hook G Wallace P Baron AD 1998 Evidence for defects in the trafficking and translocation of GLUT4 glucose transporters in skeletal muscle as a cause of human insulin
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Abstract
The effect of GH, in vivo, on the glucose transport systems of rat adipocytes has been investigated. Lowering of serum GH levels, by treatment of rats with an antiserum specific for rat GH (anti-rGH), significantly decreased serum levels of both IGF-I and insulin. Treatment with anti-rGH also increased glucose oxidation and the conversion of glucose to lipid by isolated adipocytes. Adipocyte glucose oxidation and lipid synthesis were measured in the presence of a limiting concentration of glucose and therefore reflect changes in glucose transport. Immunoblot analysis of adipocyte subcellular fractions revealed that anti-rGH induced an increase in the amount of the glucose transporters GLUT1 (1·6-fold) and GLUT4 (2·5-fold) present in plasma membranes and a decrease (39%) in the amount of GLUT4 present in low-density microsomal fractions. Lowering of serum GH also increased, by 36%, the amount of GLUT1 present in a total membrane fraction but had no such effect on GLUT4 levels. Replenishment of serum GH, by concurrent administration of ovine GH to rats, prevented all of these effects of anti-rGH. It was concluded that GH in vivo down-regulates the amount of both GLUT1 and GLUT4 present in rat adipocyte plasma membranes. This reflects a decrease in the total cellular levels of GLUT1 and modification of the subcellular distribution of GLUT4 and results in restriction of adipocyte glucose uptake.
Journal of Endocrinology (1995) 145, 27–33
Provincial Hospital Affiliated to Shandong University, Qianfoshan Hospital of Shandong Province, Shandong University School of Medicine, 324, Jing 5 Road, Jinan 250021, Shandong Province, People's Republic of China
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? Wilkes found that long-term ethanol feeding (35% calories from ethanol) in a HF diet decreased SLC2A4 (GLUT4) translocation to the plasma membrane ( Wilkes et al . 1996 ), thus resulting in insulin resistance in rat adipocytes. However, similar studies
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Abstract
Skeletal muscle GLUT-4 content is decreased in streptozotocin (STZ)-diabetic rats. This decrease is associated with impairment in glucose transport across the plasma membrane. In this study we investigated whether islet transplantation might normalize GLUT-4 content. Transplantation of syngeneic islets restored long-term near-normoglycemia in STZ-diabetic Lewis rats. Transplanted rats, followed up to 6 months, maintained slightly but significantly higher fasting and fed glucose levels when compared with age-matched normal controls. Although fasting insulin levels of transplanted rats were significantly higher than those of controls, insulin levels did not increase significantly with feeding. Plasma glucose levels following an oral glucose load (2 g/kg) were only slightly higher than in normal controls 2 months after transplantation, whereas after 6 months more severe glucose intolerance was detected. Transplanted rats completely lost the first-phase insulin release in response to i.v. glucose although they showed an increased second phase and preserved response to arginine. Six months after transplantation, endocrine beta cell mass of the grafts was similar to pretransplantation values. GLUT-4 protein content in skeletal muscle homogenates was reduced in untreated diabetic animals whereas it was completely restored by islet transplantation. In conclusion, achievement of long-term near-normoglycemia after islet transplantation was associated with complete normalization of skeletal muscle GLUT-4 content in the diabetic animals, even in the presence of abnormal glucose tolerance and an altered pattern of insulin secretion.
Journal of Endocrinology (1996) 150, 255–263
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disposal by a mechanism that is not totally dependent on hypertrophy. The enhanced glucose disposal was associated with increases in total cell levels of both the GLUT1 (by a mean 34%, P =0.026; Fig. 4 B/D) and GLUT4 (by a mean 48%, P =0.0009; Fig. 4 C
