S Satoh

Shonan Fujisawa Tokushukai Hospital, Fujisawa, Kanagawa, Japan

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Publications (80)267.25 Total impact

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    ABSTRACT: Aims/IntroductionTo define a set of criteria using indices of β-cell function, including results from the glucagon stimulation test, for liraglutide introduction in patients with type 2 diabetes. Materials and Methods In the present retrospective cohort study, patients were included in our analysis if their β-cell function had been evaluated with a glucagon stimulation test and a 24-h urinary C-peptide (U-CPR) excretion test before switching from insulin therapy to liraglutide monotherapy. The efficacy of liraglutide was determined by the extent to which glycemic control was achieved or if glycated hemoglobin levels were maintained at <7.0% after liraglutide monotherapy for 24 weeks. ResultsLiraglutide was effective in 36 of 77 patients. In the liraglutide-effective cases, the following parameters were higher: fasting C-peptide (CPR0) levels, C-peptide levels 6 min after glucagon stimulation (CPR6), the C-peptide index (CPI; CPR0 × 100/fasting plasma glucose) and stimulated C-peptide index (S-CPI; CPR6 × 100/plasma glucose 6 min after glucagon stimulation). U-CPR did not differ between liraglutide-effective and liraglutide-ineffective cases. Using receiver operating characteristic analysis adjusted for baseline characteristics, the independent cut-off value for effective liraglutide introduction was 0.72 for CPI and 1.92 for S-CPI. Conclusions Evaluation of β-cell function using the glucagon stimulation test is useful for determining the efficacy of liraglutide introduction in patients with type 2 diabetes.
    Journal of Diabetes Investigation. 04/2013;
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    ABSTRACT: Objective To examine risk factors for coronary artery disease (CAD) and retinopathy in patients with type 2 diabetes mellitus (DM) and assess the relationship between CAD and retinopathy. Methods A total of 1,003 outpatients with type 2 DM (578 men and 425 women) were classified into two groups according to the presence (based on ischemic findings on a resting electrocardiogram or a history of angina or myocardial infarction) or absence of CAD and four retinopathy stages based on the International Clinical Classification of Diabetic Retinopathy. Results Stepwise multiple regression analyses showed that independent risk factors for CAD were age, the triglyceride (TG) level and smoking, while those for retinopathy included age, age of DM diagnosis, the HbA1c level and a female gender. The prevalence of CAD increased in association with the progression of retinopathy (p<0.01). Conclusion Since it is difficult to distinguish macrovascular and microvascular diseases, diabetic vascular disorders require comprehensive approaches to assessment and treatment.
    Internal Medicine 01/2013; 52(22):2483-7. · 0.97 Impact Factor
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    ABSTRACT: Usefulness of abdominal ultrasonography for quantitative estimation of fatty liver by measurement of para- and perirenal sonographic fat thickness (UFT) was investigated. Study subjects were 286 patients hospitalized for the treatment of diabetes. These subjects underwent blood chemistry studies, abdominal ultrasonography, and CT. On sonography, the thickness of combined para- and perirenal fat was measured between the kidney and the inner aspect of the abdominal musculature. Measurements on both sides were averaged as the UFT. Fatty liver infiltration was graded on a scale of grade 0 to 3: 0, none; 1, mild; 2, moderate; and 3, severe. With abdominal CT, the ratio of CT attenuation value of the liver to that of the spleen (L/S ratio) was measured. A positive correlation was found between UFT and FL grade or between UFT and L/S ratio (p < 0.0001). Positive correlations were also found between UFT and glutamic pyruvic transaminase (p < 0.05), or cholinesterase (p < 0.0001). Measurement of UFT is a useful method for the quantification of fatty liver as well as for the quantification of visceral fat.
    Journal of Clinical Ultrasound 08/2010; 38(9):470-4. · 0.70 Impact Factor
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    ABSTRACT: To analyze the functional differences of the insulin receptor substrate (IRS) family, the N-terminal fragments containing the pleckstrin homology (PH) domains and the phosphotyrosine-binding (PTB) domains of IRS (IRS-N) proteins, as well as intact IRS molecules, were expressed in Cos-1 cells, and insulin-induced tyrosine phosphorylation and subcellular distribution of IRS proteins were analyzed. In contrast to the distinct affinities toward phosphoinositides, these IRS-N fragments non-selectively inhibited insulin-induced tyrosine phosphorylation of IRS-1, IRS-2 and IRS-3, among which IRS3-N was most effective. The mutations of IRS-1 disrupting all the phosphoinositide-binding sites in both the PH and PTB domains significantly but not completely suppressed tyrosine phosphorylation of IRS-1, which was further inhibited by coexpression of all the IRS-N proteins examined. In contrast, the N-terminal PH domain-interacting region (PHIP-N) of PH-interacting protein (PHIP) did not impair tyrosine phosphorylation of either IRS molecule. The analysis using confocal microscopy also demonstrated that all the IRS-N proteins, but not PHIP-N, suppressed targeting of IRS-1 to the plasma membrane in response to insulin. Moreover, the phosphoinositide affinity-disrupting mutations of IRS-1 significantly impaired but did not completely abrogate the insulin-induced translocation of IRS-1 to the plasma membrane, which was further suppressed by IRS1-N overexpression. These findings suggest that both insulin-induced tyrosine phosphorylation and the cell surface targeting of IRS proteins may be regulated in a similar manner through a target molecule common to the members of the IRS family, and distinct from phosphoinositides or PHIP.
    Cell Structure and Function 02/2007; 32(1):69-78. · 1.65 Impact Factor
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    ABSTRACT: To examine factors that affect the development of retinopathy after short-term inpatient management of diabetes. The subjects were 143 patients with type 2 diabetes who were admitted for inpatient management of diabetes, and did not have retinopathy of the right eye at admission, and had an HbA1c level of > or =8.0%. We studied the characteristics of patients who developed retinopathy within one year after discharge. Between the admission date and one year after discharge, twenty-six patients developed retinopathy and the retinopathy subsequently regressed in 5 patients. The 26 patients who developed retinopathy had a significantly longer duration of diabetes (p<0.005), had a higher fasting blood glucose level at admission (p=0.06), and received insulin therapy during the admission at a higher rate (p=0.06) than the 117 patients without retinopathy. The magnitude of the reduction in HbA1c level at 3 months after discharge was smaller in the 13 patients who developed retinopathy within 3 months after discharge than in the 130 patients who did not. Among the 26 patients who developed retinopathy, the HbA1c level at one year after discharge of the 5 patients whose retinopathy regressed was lower than that of the 21 patients whose retinopathy did not regress (p=0.06). A long duration of diabetes, high fasting blood glucose level at admission, and treatment with insulin were associated with the development of retinopathy. Patients with these characteristics should undergo frequent fundus examinations after correction of hyperglycemia. The retinopathy was likely to improve if patients maintained strict glycemic control after discharge.
    Internal Medicine 02/2006; 45(22):1267-71. · 0.97 Impact Factor
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    ABSTRACT: Dehydroepiandrosterone (DHEA), the most abundant human adrenal steroid, improves insulin sensitivity and obesity in human and model animals. In a previous study, we reported that orally administered DHEA suppresses the elevated activities of hepatic gluconeogenic enzymes like glucose-6-phosphatase (G6Pase) in C57BL/KsJ-db/db mice. However, the molecular mechanisms by which DHEA ameliorates insulin resistance are not clearly understood. In the present study, we cultured the human hepatoma cell line HepG2 with DHEA and measured the enzyme activity and protein expression of G6Pase to investigate the direct effect of DHEA on glucose metabolism in hepatocytes. DHEA significantly suppressed both the activity and protein expression of G6Pase. Moreover, DHEA decreased the gene expression of G6Pase and phosphoenolpyruvate carboxykinase, both of which were maximal at 1 microM DHEA, whereas the mRNA level of glucose-6-phosphate translocase was unchanged. Furthermore, DHEA enhanced 2-deoxyglucose uptake, although its effect was much smaller than that of insulin. These results suggest that DHEA may act at multiple steps in the regulation of glucose metabolism in the liver.
    Endocrine Journal 01/2006; 52(6):727-33. · 2.23 Impact Factor
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    ABSTRACT: Dehydroepiandrosterone (DHEA) is known to improve hyperglycemia in diabetic db/db mice that are obese and insulin resistant. In a previous study, we reported that DHEA suppresses the elevated hepatic gluconeogenic glucose-6-phosphatase (G6Pase) activity and gene expression in C57BL/KsJ-db/db mice. In the present study, we evaluated the total amount of gluconeogenesis using NaH[(14)C]CO(3) and hepatic glucose production using fructose as a substrate in primary cultured hepatocytes. Despite hyperinsulinemia, the glucose production of db/db mice in the total body and hepatocytes was elevated as compared to their heterozygote littermate C57BL/KsJ-db/+m mice. Administration of DHEA significantly decreased the blood glucose level and increased the plasma insulin level in db/db mice. Administration of DHEA decreased the elevated total body and hepatic glucose production in db/db mice. In addition, the glucose production in the primary cultured hepatocytes of db/db mice was decreased significantly by the direct addition of DHEA or DHEA-S to the medium. These results suggest that administration of DHEA suppresses the elevated total body and hepatic glucose production in db/db mice, and this effect on the liver is considered to result from increased plasma insulin and DHEA or DHEA-S itself.
    Life Sciences 06/2004; 74(25):3075-84. · 2.56 Impact Factor
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    ABSTRACT: In primary adipocytes, insulin receptor substrate (IRS)-1 and -3 are expressed in a comparable amount and play distinct roles in insulin signaling. To examine the roles of these IRS in apoptosis inhibition, we evaluated staurosporine-induced apoptosis in Chinese hamster ovary (CHO) cells overexpressing human insulin receptor and IRS-1 or IRS-3. Overexpression of both IRS protected CHO cells from staurosporine-induced apoptosis. Overexpressed IRS-3 as well as IRS-1 enhanced phosphoinositide (PI) 3-kinase activity in response to insulin and increased phosphorylation of protein kinase B (PKB) at S473 and phosphorylation of one of the members of the forkhead transcription factor FKHRL1 on T32 in both insulin-untreated and -treated states. Treatment of these cells with a PI 3-kinase inhibitor LY294002 suppressed apoptosis-inhibitory effects of IRS-1 and IRS-3 as well as the phosphorylation of PKB and FKHRL1. These results indicate that both IRS-1 and IRS-3 take part in apoptosis inhibition through the PI 3-kinase/PKB/forkhead cascade.
    Biochemical and Biophysical Research Communications 02/2003; 300(2):371-7. · 2.41 Impact Factor
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    ABSTRACT: Telemedicine was used for taking ocular fundus images of diabetic patients, which were subsequently sent by electronic mail to experienced ophthalmologists at a university hospital. The ophthalmologists provided reports on the patients to the internists. The objective of the study was to evaluate the effectiveness of this telemedicine system. A total of 279 diabetic patients were admitted to the Third Department of Internal Medicine of Yokohama City University Hospital, School of Medicine, for blood sugar control or for education on lifestyle between April, 1999, and October, 2000. The subjects did not have eye disease nor diabetic retinopathy when evaluated by an ophthalmologist (at either Yokohama City University Hospital or other facility) within 3 months before enrollment in the study. After dilation of the pupil, fundus images were taken of each eye from four angles using a nonmydriatic fundus camera. The images were transmitted by electronic mail to the Division of Ophthalmology of Tokyo University Branch Hospital along with other patient information. The ophthalmologists there evaluated the images on the screen according to Fukuda's classification of diabetic retinopathy. They sent ophthalmologic reports to the internists at the Third Department of Internal Medicine of Yokohama City University Hospital, School of Medicine, and recommended whether the patient should be seen by his/her regular ophthalmologist earlier than the next scheduled visit. Fundus images were obtained at the time of admission, at 1, 3, and 6 months after discharge, and at every 6 months thereafter. Out of the images of 1170 eyes obtained at various time points from the 279 patients, 1076 (92.0%) were successfully evaluated by the ophthalmologists at the University of Tokyo, while 60 (5.1%) could not be evaluated and there was a communication problem for the images of 34 eyes. The ophthalmologists determined that 5 eyes of 3 patients required further evaluation by the patient's regular ophthalmologist based on the images transferred by telemedicine. No patient dropped out during the study period.
    Telemedicine and e-Health 02/2003; 9(3):235-9. · 1.40 Impact Factor
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    ABSTRACT: The role of phosphatidylinositol (PI) 3-kinase in the regulation of pancreatic beta-cell function was investigated. PI 3-kinase activity in p85 alpha regulatory subunit-deficient (p85 alpha(-/-)) islets was decreased to approximately 20% of that in wild-type controls. Insulin content and mass of rough endoplasmic reticula were decreased in beta-cells from p85 alpha(-/-) mice with increased insulin sensitivity. However, p85 alpha(-/-) beta-cells exhibited a marked increase in the insulin secretory response to higher concentrations of glucose. When PI 3-kinase in wild-type islets was suppressed by wortmannin or LY294002, the secretion was also substantially potentiated. Wortmannin's potentiating effect was not due to augmentation in glucose metabolism or cytosolic [Ca(2+)] elevation. Results of p85 alpha(-/-) islets and wortmannin-treated wild-type islets stimulated with diazoxide and KCl showed that inhibition of PI 3-kinase activity exerted its effect on secretion, at least in part, distal to a cytosolic [Ca(2+)] elevation. These results suggest that PI 3-kinase activity normally plays a crucial role in the suppression of glucose-stimulated insulin secretion.
    Diabetes 02/2002; 51(1):87-97. · 7.90 Impact Factor
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    ABSTRACT: To evaluate the importance of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) in insulin resistant diabetic C57BL/KsJ-db/db mice, we measured the activity and mRNA level of 11beta-HSD1 in the liver of db/db mice and their heterozygote litter mates, db/+m mice. The blood glucose, plasma insulin, and corticosterone levels of db/db mice were significantly higher than those of db/+m mice. Despite hyperinsulinemia, the activity level of this enzyme was significantly higher in db/db mice, and the mRNA level of hepatic 11beta-HSD1 was also significantly higher in db/db mice. Since hepatic 11beta-HSD1 in vivo mainly functions as 11-keto-reductase and does not work as 11beta-oxidase, these results suggest that the rate of hepatic conversion of 11-dehydrocorticosterone to corticosterone is increased in db/db mice, resulting in higher glucocorticoid activity in the liver. The increased hepatic corticosterone concentration due to the elevation of 11beta-HSD1 and high plasma corticosterone concentration may antagonize the action of insulin and cause insulin resistance. These findings have a potentially important implication for relationships between increased hepatic 11beta-HSD1 and insulin resistance in db/db mice. The present paper is the first to demonstrate the increased activities and mRNA level of hepatic 11beta-HSD1 in db/db mice.
    Life Sciences 11/2001; 69(21):2543-9. · 2.56 Impact Factor
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    ABSTRACT: In primary adipocytes, although IRS-1 and IRS-3 are expressed in comparable amounts, these proteins manifest distinct distribution and significance in insulin signalling. We investigated the molecular basis of the difference between these two proteins. In Cos-1 cells transiently expressing rat IRS-1, IRS-3, or chimeric proteins of these two proteins we examined the tyrosine phosphorylation via the wild-type or mutant insulin receptors and evaluated their targeting to the plasma membrane by immunostaining the membrane ghost. In contrast to IRS-1, IRS-3 was tyrosine-phosphorylated by the insulin receptor altering Tyr960 to Phe (Y960F), which disrupts the binding site of the PTB domain of IRSs, to an extent comparable to the wild-type receptor. The tyrosine phosphorylation of IRS-3 with the PH domain replacement via the Y960F insulin receptor markedly decreased, whereas that of IRS-3 with the PTB domain alteration was mildly impaired. Insulin-stimulated translocation of IRS-1 to the plasma membrane, as well as that of IRS-3 with the PH domain replacement, was wortmannin-sensitive, although that of IRS-3 was insulin-independent and wortmannin-resistant. The affinity of the PH domain for the phospholipids in the plasma membrane seems to influence the receptor-substrate interaction required for IRS tyrosine phosphorylation, indicating that the PH domain and the PTB domain of IRSs cooperatively function in insulin-stimulated tyrosine phosphorylation of these proteins.
    Diabetologia 09/2001; 44(8):992-1004. · 6.49 Impact Factor
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    ABSTRACT: To clarify the roles of insulin receptor substrate (IRS) family proteins in phosphatidylinositol (PI) 3-kinase activation and insulin actions in adipocytes, we investigated the intracellular localization of IRS family proteins and PI 3-kinase activation in response to insulin by fractionation of mouse adipocytes from wild-type and IRS-1 null mice. In adipocytes from wild-type mice, tyrosine-phosphorylated IRS-1 and IRS-2, which were found to associate with PI 3-kinase in response to insulin, were detected in the plasma membrane (PM) and low-density microsome (LDM) fractions. By contrast, tyrosine-phosphorylated IRS-3 (pp60), which was found to associate with PI 3-kinase, was predominantly localized in the PM fraction. In adipocytes from IRS-1-null mice, insulin-stimulated PI 3-kinase activity in anti-phosphotyrosine (alphaPY) immunoprecipitates in the LDM fraction was almost exclusively mediated via IRS-2 and was reduced to 25%; however, insulin-stimulated PI 3-kinase activity in the PM fraction was primarily mediated via IRS-3 and was reduced to 60%. To determine the potential functional impact of the distinct subcellular localization of IRSs and associating PI 3-kinase activity on adipocyte-specific metabolic actions, we examined lipolysis in IRS-1 null mice. The level of isoproterenol-induced lipolysis was increased 5.1-fold in adipocytes from IRS-1 null mice as compared with wild-type mice. Moreover, hormone-sensitive lipase (HSL) protein was increased 4.3-fold in adipocytes from IRS-1-null mice compared with wild-type mice, and HSL mRNA expression was also increased. The antilipolytic effect of insulin in IRS-1 null adipocytes, however, was comparable to that in wild-type mice. Thus, discordance between these two insulin actions as well as the transcriptional and translational effect (HSL mRNA and protein regulation) and the PM effect (antilipolysis) of insulin may be explained by distinct roles of both PI 3-kinase activity associated with IRS-1/IRS-2 and PI 3-kinase activity associated with IRS-3 in insulin actions related to their subcellular localization.
    Diabetes 07/2001; 50(6):1455-63. · 7.90 Impact Factor
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    ABSTRACT: Dehydroepiandrosterone (DHEA) is known to improve hyperglycemia of diabetic C57BL/KsJ-db/db mice that are obese and insulin resistant. In a previous study, we reported that DHEA as well as troglitazone suppresses the elevated hepatic gluconeogenic enzymes, glucose-6-phosphatase (G6Pase) and fructose-1,6-bisphosphatase (FBPase) activities in C57BL/KsJ-db/db mice. In the present study, we evaluated the changes in mRNA of G6Pase and FBPase in db/db mice. Despite hyperinsulinemia, the G6Pase mRNA level of db/db mice was elevated as compared to their heterozygote littermate db/+m mice. In contrast, the FBPase mRNA level was not elevated in db/db mice. Administration of DHEA for two weeks significantly decreased the blood glucose level and the elevated G6Pase mRNA level in db/db mice. No significant changes were seen in the FBPase mRNA level after the administration of DHEA. Administration of troglitazone also decreased the blood glucose and G6Pase mRNA level in db/db mice although no changes were seen in the FBPase mRNA level. These results suggest that the elevation of G6Pase mRNA is important in elucidating the cause of insulin resistance, and that the G6Pase gene is at least one target for the hypoglycemic effects of DHEA as an insulin sensitizing agent in db/db mice.
    Endocrine Journal 01/2001; 47(6):799-804. · 2.23 Impact Factor
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    ABSTRACT: To investigate the role of insulin receptor substrate (IRS)-2 in vivo, we generated IRS-2-deficient mice by gene targeting. Although homozygous IRS-2-deficient mice (IRS-2-/- mice) had a body weight similar to wild-type mice, they progressively developed type 2 diabetes at 10 weeks. IRS-2-/- mice showed insulin resistance and a defect in the insulin-stimulated signaling pathway in liver but not in skeletal muscle. Despite insulin resistance, the amount of beta-cells was reduced to 83% of that in wild-type mice, which was in marked contrast to the 85% increase in the amount of beta-cells in IRS-1-deficient mice (IRS-1-/- mice) to compensate for insulin resistance. Thus, IRS-2 plays a crucial role in the regulation of beta-cell mass. On the other hand, insulin secretion by the same number of cells in response to glucose measured ex vivo was significantly increased in IRS-2-/- mice compared with wild-type mice but was decreased in IRS-1-/- mice. These results suggest that IRS-1 and IRS-2 may play different roles in the regulation of beta-cell mass and the function of individual beta-cells.
    Diabetes 12/2000; 49(11):1880-9. · 7.90 Impact Factor
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    ABSTRACT: We attempted to suppress glucose transporter 1 (GLUT1) expression by transfecting MKN45 cells with cDNA for antisense GLUT1. Glucose transport was significantly decreased in cells with antisense GLUT1 compared with wild-type cells or cells with vector alone. Suppression of GLUT1 mRNA resulted in a decreased number of cells in the S phase. This was accompanied by overexpression of p21 protein. Tumorigenicity in the nude mice injected with antisense GLUT1 expressing cells was significantly slower than in those with wild-type MKN45 cells. These results suggest that antisense GLUT1 mRNA inhibits tumor growth through a G(1) arrest and that expression of antisense GLUT1 mRNA via gene therapy can be used as a tool in the treatment of cancer.
    Cancer Letters 07/2000; 154(2):175-82. · 4.26 Impact Factor
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    ABSTRACT: Three patients with functional adrenal tumors, Cushing's syndrome, primary aldosteronism and pheochromocytoma, who underwent adrenalectomy and were subsequently cured, were studied. All these patients had been treated for diabetes for several years before the diagnosis of adrenal tumors. In each case the state of diabetes before and after surgery, including parameters of insulin secretion and insulin resistance, was compared to demonstrate how the adrenal disorder influenced the nature of diabetes. In the case of Cushing's syndrome the hypercortisolemia caused insulin resistance in the peripheral tissues. In the case of primary aldosteronism, excessive production of aldosterone diminished insulin secretion possibly through hypokalemia. Pheochromocytoma affected both insulin secretion and insulin sensitivity through hypersecretion of catecholamines. In all these patients the adrenal tumors were found in clinical contexts other than management of diabetes itself. By careful retrospective review of these three patients' history, several important points that might have drawn the physician's attention to the underlying adrenal disorders were pointed out. These included past history of acute myocardial infarction with onset at unexpectedly young age in the case of Cushing's syndrome and unexpectedly high insulin resistance for the patient's body mass index in the case of pheochromocytoma.
    Biomedecine [?] Pharmacotherapy 07/2000; 54 Suppl 1:198s-202s. · 2.07 Impact Factor
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    ABSTRACT: The expression of facilitative glucose transporter isoforms in colon adenocarcinoma and the possible role of k-ras in inducing GLUT (glucose transporter) mRNA were studied. RT-PCR demonstrated GLUT2 and GLUT3 expression in 100% of the ten normal colon mucosa samples but detected no GLUT1 mRNA. By contrast, GLUT1 mRNA was detected in all 20 (100%) colon cancer samples examined. GLUT4 mRNA was not detected in either normal mucosa or colon cancer tissues. Semiquantitative PCR demonstrated equal amounts of GLUT2 and GLUT3 mRNA in both normal mucosa and colon cancer samples. A point mutation in codon 12 of k-ras was detected in only six of the 20 (30%) colon cancer samples. Thus, a major difference between normal colon epithelia and colon cancer was the acquisition of GLUT1 expression, which was unlikely to have been induced by a point mutation in codon 12 of k-ras.
    Cancer Letters 07/2000; 154(2):137-42. · 4.26 Impact Factor
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    ABSTRACT: We evaluated the expression of glucose transporter (glut) isoforms and its function in RD cells, human rhabdomyosarcoma, which retain the potential to differentiate into muscle. Gluts 1, 3, and 4 were expressed in RD cells, as detected by reverse-transcription polymerase chain reaction and immunocytochemistry. Supraphysiological concentration (1 microM) of insulin treatment increased 2-deoxy glucose transport by up to 1.68-fold together with concomitant tyrosine phosphorylation of the insulin receptor beta subunit and of insulin receptor substrate 1. Suppression of glut 1 mRNA by 38% by antisense oligonucleotide transfection led to a reduction of basal and insulin-stimulated 2-deoxy glucose transport by 38 and 55%, respectively. Suppression of gluts 3 and 4 by antisense oligonucleotide transfection did not affect both basal and insulin-stimulated 2-deoxy glucose transport. Thus, glut 1 accounts for the major part of basal and insulin-stimulated glucose transport in RD cells. Next, we transfected expression vectors carrying human gluts 1 and 4 cDNAs into RD cells to add further support for the role of glut 1 in glucose transport. Overexpression of glut 1 stimulated basal and insulin-stimulated 2-deoxy glucose transport by 1.66- and 1.43-fold, respectively. Glut 4 overexpression did not affect basal and insulin-stimulated 2-deoxy glucose transport. Western blot analysis using glut 1 antibody showed that glut 1 was redistributed from intracellular membrane to plasma membrane. These observations support the notion that RD cells, with the potential to differentiate into muscle, retain insulin responsiveness. As human muscle cell lines are not available at this point, RD cells can serve as a useful alternative to human muscle for studies related to insulin signal transduction and glucose transport.
    Archives of Biochemistry and Biophysics 02/2000; 373(1):72-82. · 3.37 Impact Factor
  • Endocrine Journal - ENDOCR J. 01/2000; 47(6):799-804.

Publication Stats

3k Citations
267.25 Total Impact Points

Institutions

  • 2013
    • Shonan Fujisawa Tokushukai Hospital
      Fujisawa, Kanagawa, Japan
  • 2004–2013
    • Chigasaki Municipal Hospital
      Chigaraki, Kanagawa, Japan
  • 1991–2003
    • Yokohama City University
      • Department of Medicine
      Yokohama, Kanagawa, Japan
  • 1997–2001
    • The University of Tokyo
      • • Faculty & Graduate School of Medicine
      • • Department of Diabetes and Metabolic Diseases
      Tokyo, Tokyo-to, Japan
  • 1988–1997
    • Kyoto Prefectural University of Medicine
      • Department of Surgery
      Kioto, Kyōto, Japan
  • 1994
    • Universiteit Twente
      Enschede, Overijssel, Netherlands
  • 1993
    • National Institutes of Health
      • National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
      Bethesda, MD, United States
    • Universitair Medisch Centrum Groningen
      Groningen, Groningen, Netherlands