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  1. Article: Association of reduced red blood cell deformability and diabetic nephropathy.

    Rebsomen, Laurie / Tsimaratos, Michel

    Kidney international

    2005  Volume 67, Issue 5, Page(s) 2066; author reply 2066–7

    MeSH term(s) C-Peptide/blood ; Diabetes Mellitus, Type 2/blood ; Diabetic Nephropathies/blood ; Erythrocyte Deformability ; Humans ; Sodium-Potassium-Exchanging ATPase/blood
    Chemical Substances C-Peptide ; Sodium-Potassium-Exchanging ATPase (EC 3.6.3.9)
    Language English
    Publishing date 2005-05
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1111/j.1523-1755.2005.310_3.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 797: Show issues Location:
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  2. Article ; Online: C-Peptide effects on renal physiology and diabetes.

    Rebsomen, L / Khammar, A / Raccah, D / Tsimaratos, M

    Experimental diabetes research

    2008  Volume 2008, Page(s) 281536

    Abstract: The C-peptide of proinsulin is important for the biosynthesis of insulin and has for a long time been considered to be biologically inert. Animal studies have shown that some of the renal effects of the C-peptide may in part be explained by its ability ... ...

    Abstract The C-peptide of proinsulin is important for the biosynthesis of insulin and has for a long time been considered to be biologically inert. Animal studies have shown that some of the renal effects of the C-peptide may in part be explained by its ability to stimulate the Na,K-ATPase activity. Precisely, the C-peptide reduces diabetes-induced glomerular hyperfiltration both in animals and humans, therefore, resulting in regression of fibrosis. The tubular function is also concerned as diabetic animals supplemented with C-peptide exhibit better renal function resulting in reduced urinary sodium waste and protein excretion together with the reduction of the diabetes-induced glomerular hyperfiltration. The tubular effectors of C-peptide were considered to be tubule transporters, but recent studies have shown that biochemical pathways involving cellular kinases and inflammatory pathways may also be important. The matter theory concerning the C-peptide effects is a metabolic one involving the effects of the C-peptide on lipidic metabolic status. This review concentrates on the most convincing data which indicate that the C-peptide is a biologically active hormone for renal physiology.
    MeSH term(s) Animals ; C-Peptide/metabolism ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Experimental/physiopathology ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/physiopathology ; Diabetic Nephropathies/metabolism ; Diabetic Nephropathies/physiopathology ; Glomerular Filtration Rate ; Humans ; Inflammation/metabolism ; Inflammation/physiopathology ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/physiopathology ; Kidney Tubules/metabolism ; Kidney Tubules/physiopathology ; Lipid Metabolism ; Signal Transduction ; Sodium-Potassium-Exchanging ATPase/metabolism
    Chemical Substances C-Peptide ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13)
    Language English
    Publishing date 2008-05-20
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2465179-5
    ISSN 1687-5303 ; 1687-5214
    ISSN (online) 1687-5303
    ISSN 1687-5214
    DOI 10.1155/2008/281536
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Tubule et diabête. Fonction tubulaire et rein diabétique.

    Rebsomen, Laure / Raccah, Denis / Tsimaratos, Michel

    Nephrologie & therapeutique

    2006  Volume 2 Suppl 1, Page(s) S28–31

    Abstract: Early stages of insulin-dependent diabetes are characterized by silent nephropathy. There are however several tubular events before the onset of glomerular disease. This article focuses on the specific diabetes-induced events that determine the tubular ... ...

    Title translation Diabetes mellitus and renal tubule functions.
    Abstract Early stages of insulin-dependent diabetes are characterized by silent nephropathy. There are however several tubular events before the onset of glomerular disease. This article focuses on the specific diabetes-induced events that determine the tubular injury and their relation with the progression to glomerular disease.
    MeSH term(s) Diabetes Mellitus, Type 1/etiology ; Diabetes Mellitus, Type 1/physiopathology ; Humans ; Kidney Tubules/physiopathology
    Language French
    Publishing date 2006-01
    Publishing country France
    Document type English Abstract ; Journal Article ; Review
    ZDB-ID 2229575-6
    ISSN 1872-9177 ; 1769-7255
    ISSN (online) 1872-9177
    ISSN 1769-7255
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  4. Article ; Online: C-Peptide Effects on Renal Physiology and Diabetes

    L. Rebsomen / A. Khammar / D. Raccah / M. Tsimaratos

    Experimental Diabetes Research, Vol

    2008  Volume 2008

    Keywords Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Language English
    Publishing date 2008-01-01T00:00:00Z
    Publisher Hindawi Publishing Corporation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: C-Peptide Effects on Renal Physiology and Diabetes

    M. Tsimaratos / D. Raccah / A. Khammar / L. Rebsomen

    Experimental Diabetes Research, Vol

    2008  Volume 2008

    Abstract: The C-peptide of proinsulin is important for the biosynthesis of insulin and has for a long time been considered to be biologically inert. Animal studies have shown that some of the renal effects of the C-peptide may in part be explained by its ability ... ...

    Abstract The C-peptide of proinsulin is important for the biosynthesis of insulin and has for a long time been considered to be biologically inert. Animal studies have shown that some of the renal effects of the C-peptide may in part be explained by its ability to stimulate the Na,K-ATPase activity. Precisely, the C-peptide reduces diabetes-induced glomerular hyperfiltration both in animals and humans, therefore, resulting in regression of fibrosis. The tubular function is also concerned as diabetic animals supplemented with C-peptide exhibit better renal function resulting in reduced urinary sodium waste and protein excretion together with the reduction of the diabetes-induced glomerular hyperfiltration. The tubular effectors of C-peptide were considered to be tubule transporters, but recent studies have shown that biochemical pathways involving cellular kinases and inflammatory pathways may also be important. The matter theory concerning the C-peptide effects is a metabolic one involving the effects of the C-peptide on lipidic metabolic status.This review concentrates on the most convincing data which indicate that the C-peptide is a biologically active hormone for renal physiology.
    Keywords Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; Specialties of internal medicine ; RC581-951
    Subject code 571
    Language English
    Publishing date 2008-05-01T00:00:00Z
    Publisher Hindawi Publishing Corporation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: C-Peptide Effects on Renal Physiology and Diabetes

    L. Rebsomen / A. Khammar / D. Raccah / M. Tsimaratos

    Experimental Diabetes Research, Vol

    2008  Volume 2008

    Abstract: The C-peptide of proinsulin is important for the biosynthesis of insulin and has for a long time been considered to be biologically inert. Animal studies have shown that some of the renal effects of the C-peptide may in part be explained by its ability ... ...

    Abstract The C-peptide of proinsulin is important for the biosynthesis of insulin and has for a long time been considered to be biologically inert. Animal studies have shown that some of the renal effects of the C-peptide may in part be explained by its ability to stimulate the Na,K-ATPase activity. Precisely, the C-peptide reduces diabetes-induced glomerular hyperfiltration both in animals and humans, therefore, resulting in regression of fibrosis. The tubular function is also concerned as diabetic animals supplemented with C-peptide exhibit better renal function resulting in reduced urinary sodium waste and protein excretion together with the reduction of the diabetes-induced glomerular hyperfiltration. The tubular effectors of C-peptide were considered to be tubule transporters, but recent studies have shown that biochemical pathways involving cellular kinases and inflammatory pathways may also be important. The matter theory concerning the C-peptide effects is a metabolic one involving the effects of the C-peptide on lipidic metabolic status.This review concentrates on the most convincing data which indicate that the C-peptide is a biologically active hormone for renal physiology.
    Keywords Medicine ; R ; Internal medicine ; RC31-1245 ; Specialties of internal medicine ; RC581-951 ; Diseases of the endocrine glands. Clinical endocrinology ; RC648-665
    Subject code 571
    Language English
    Publishing date 2008-01-01T00:00:00Z
    Publisher Hindawi Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article: C-peptide replacement improves weight gain and renal function in diabetic rats.

    Rebsomen, L / Pitel, S / Boubred, F / Buffat, C / Feuerstein, J M / Raccah, D / Vague, P / Tsimaratos, M

    Diabetes & metabolism

    2006  Volume 32, Issue 3, Page(s) 223–228

    Abstract: Aim: Recent experimental and clinical data suggest that C-peptide replacement during type 1 diabetes exerts beneficial effects on diabetic nephropathy. The aim of this study was to determine if physiological C-peptide administration in replacement dose ... ...

    Abstract Aim: Recent experimental and clinical data suggest that C-peptide replacement during type 1 diabetes exerts beneficial effects on diabetic nephropathy. The aim of this study was to determine if physiological C-peptide administration in replacement dose during 28 days had beneficial effects on metabolic status and renal functions in type-1 diabetic rats.
    Methods: Four groups of rats were investigated: a non diabetic group treated with buffer (C group, n=6), three streptozotocin diabetic-induced groups treated with either buffer (D group, n=6), insulin (D-I group, n=6) or rat homologous C-peptide (D-C group, n=6). Weight gain was measured every week. All animals were housed in metabolic cages on day 28 for assessment of metabolic data. Blood and urine samples were collected to allow measurement of plasmatic osmolality, C-peptide concentration, sodium, and glucose losses and proteinuria. Glomerular filtration rate (GFR) was determined by creatinine clearance.
    Results: All streptozotocin-treated animals were diabetic. Glycaemic control (mg/dl), was markedly improved in D-I (133+/-65) when compared with either D (547+/-49, P<0.05) or D-C (520+/-48, P<0.05) groups. Conversely, weight gain during the study, was improved in D-I and D-C as compared with D animals (135+/-13 and 41+/-18 vs 18+/-21 respectively), despite different glycaemic control. Diabetes-induced glomerular hyperfiltration (ml/min/kg), urinary protein leakage (g/kg/day), and Na urinary losses (mmol/100 g/day) respectively, were significantly (P<0.05) reduced in D-C (3.95+/-0.6; 0.08+/-0.06; 1.5+/-0.9) in comparison with D (4.95+/-0.8; 0.18+/-0.16; 3.7+/-2.1) and D-I (5+/-0.9; 0.19+/-0.11; 2.7+/-0.8) animals. Plasmatic osmolality was significantly increased in D group whereas there were no differences between C group and D-C group. Food and water intakes, urinary volume as well as urinary glucose losses were not significantly different between D-C and D groups.
    Conclusions: C-peptide administration in replacement dose to streptozotocin diabetic rats induces weight gain regardless hyperglycaemia or glycosuria. Diabetic animals supplemented with C-peptide exhibit better renal function resulting in reduced urinary sodium waste and protein excretion together with reduction of the diabetes-induced glomerular hyperfiltration.
    MeSH term(s) Animals ; Blood Glucose/drug effects ; Blood Glucose/metabolism ; C-Peptide/blood ; C-Peptide/therapeutic use ; Diabetes Mellitus, Experimental/blood ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/physiopathology ; Diabetic Angiopathies/prevention & control ; Insulin/blood ; Kidney/drug effects ; Kidney/physiopathology ; Male ; Proteinuria ; Rats ; Rats, Sprague-Dawley ; Sodium/urine ; Weight Gain/drug effects
    Chemical Substances Blood Glucose ; C-Peptide ; Insulin ; Sodium (9NEZ333N27)
    Language English
    Publishing date 2006-02-16
    Publishing country France
    Document type Journal Article
    ZDB-ID 1315751-6
    ISSN 1262-3636 ; 0338-1684
    ISSN 1262-3636 ; 0338-1684
    DOI 10.1016/s1262-3636(07)70272-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1267: Show issues Location:
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  8. Article: The shedding activity of ADAM17 is sequestered in lipid rafts.

    Tellier, Edwige / Canault, Matthias / Rebsomen, Laure / Bonardo, Bernadette / Juhan-Vague, Irène / Nalbone, Gilles / Peiretti, Franck

    Experimental cell research

    2006  Volume 312, Issue 20, Page(s) 3969–3980

    Abstract: The tumor necrosis factor-alpha (TNF) converting enzyme (ADAM17) is a metalloprotease-disintegrin responsible for the cleavage of several biologically active transmembrane proteins. However, the substrate specificity of ADAM17 and the regulation of its ... ...

    Abstract The tumor necrosis factor-alpha (TNF) converting enzyme (ADAM17) is a metalloprotease-disintegrin responsible for the cleavage of several biologically active transmembrane proteins. However, the substrate specificity of ADAM17 and the regulation of its shedding activity are still poorly understood. Here, we report that during its transport through the Golgi apparatus, ADAM17 is included in cholesterol-rich membrane microdomains (lipid rafts) where its prodomain is cleaved by furin. Consequently, ADAM17 shedding activity is sequestered in lipid rafts, which is confirmed by the fact that metalloproteinase inhibition increases the proportion of ADAM17 substrates (TNF and its receptors TNFR1 and TNFR2) in lipid rafts. Membrane cholesterol depletion increases the ADAM17-dependent shedding of these substrates demonstrating the importance of lipid rafts in the control of this process. Furthermore, ADAM17 substrates are present in different proportions in lipid rafts, suggesting that the entry of each of these substrates in these particular membrane microdomains is specifically regulated. Our data support the idea that one of the mechanisms regulating ADAM17 substrate cleavage involves protein partitioning in lipid rafts.
    MeSH term(s) ADAM Proteins/metabolism ; ADAM17 Protein ; Animals ; COS Cells ; Cell Line ; Cercopithecus aethiops ; Cholesterol/metabolism ; Cytoskeleton/metabolism ; Furin/metabolism ; Humans ; Membrane Microdomains/enzymology ; Rats ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Receptors, Tumor Necrosis Factor, Type II/metabolism ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances Receptors, Tumor Necrosis Factor, Type I ; Receptors, Tumor Necrosis Factor, Type II ; Tumor Necrosis Factor-alpha ; Cholesterol (97C5T2UQ7J) ; Furin (EC 3.4.21.75) ; ADAM Proteins (EC 3.4.24.-) ; ADAM17 Protein (EC 3.4.24.86) ; ADAM17 protein, human (EC 3.4.24.86) ; Adam17 protein, rat (EC 3.4.24.86)
    Language English
    Publishing date 2006-12-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1493-x
    ISSN 1090-2422 ; 0014-4827
    ISSN (online) 1090-2422
    ISSN 0014-4827
    DOI 10.1016/j.yexcr.2006.08.027
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    Zs.A 563: Show issues Location:
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