l-Arginine prevents metabolic effects of high glucose in diabetic mice

Matthew B. West; Kota V. Ramana; Karin Kaiserova; Satish K. Srivastava; Aruni Bhatnagar

doi:10.1016/j.febslet.2008.06.039

l-Arginine prevents metabolic effects of high glucose in diabetic mice

Matthew B. West
, Kota V. Ramana
, Karin Kaiserova
, Satish K. Srivastava
, Aruni Bhatnagar

Research output: Contribution to journal › Article › peer-review

28 Scopus citations

Abstract

We tested the hypothesis that activation of the polyol pathway and protein kinase C (PKC) during diabetes is due to loss of NO. Our results show that after 4 weeks of streptozotocin-induced diabetes, treatment with l-arginine restored NO levels and prevented tissue accumulation of sorbitol in mice, which was accompanied by an increase in glutathiolation of aldose reductase. l-Arginine treatment decreased superoxide generation in the aorta, total PKC activity and PKC-β_II phosphorylation in the heart, and the plasma levels of triglycerides and soluble ICAM. These data suggest that increasing NO bioavailability by l-arginine corrects the major biochemical abnormalities of diabetes.

Original language	English (US)
Pages (from-to)	2609-2614
Number of pages	6
Journal	FEBS Letters
Volume	582
Issue number	17
DOIs	https://doi.org/10.1016/j.febslet.2008.06.039
State	Published - Jul 23 2008
Externally published	Yes

Keywords

Cell adhesion molecule
Diabetes mellitus
Inflammation
Nitric oxide
Signal transduction

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/j.febslet.2008.06.039

Cite this

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title = "l-Arginine prevents metabolic effects of high glucose in diabetic mice",

abstract = "We tested the hypothesis that activation of the polyol pathway and protein kinase C (PKC) during diabetes is due to loss of NO. Our results show that after 4 weeks of streptozotocin-induced diabetes, treatment with l-arginine restored NO levels and prevented tissue accumulation of sorbitol in mice, which was accompanied by an increase in glutathiolation of aldose reductase. l-Arginine treatment decreased superoxide generation in the aorta, total PKC activity and PKC-βII phosphorylation in the heart, and the plasma levels of triglycerides and soluble ICAM. These data suggest that increasing NO bioavailability by l-arginine corrects the major biochemical abnormalities of diabetes.",

keywords = "Cell adhesion molecule, Diabetes mellitus, Inflammation, Nitric oxide, Signal transduction",

author = "West, \{Matthew B.\} and Ramana, \{Kota V.\} and Karin Kaiserova and Srivastava, \{Satish K.\} and Aruni Bhatnagar",

note = "Funding Information: This work was supported in part by NIH Grants HL59378 ES1180 (to A.B.), and DK36118 (to S.K.S.) and American Heart Association Grant 0415128B (to M.B.W.).",

year = "2008",

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day = "23",

doi = "10.1016/j.febslet.2008.06.039",

language = "English (US)",

volume = "582",

pages = "2609--2614",

journal = "FEBS Letters",

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publisher = "John Wiley and Sons Inc.",

number = "17",

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TY - JOUR

T1 - l-Arginine prevents metabolic effects of high glucose in diabetic mice

AU - West, Matthew B.

AU - Ramana, Kota V.

AU - Kaiserova, Karin

AU - Srivastava, Satish K.

AU - Bhatnagar, Aruni

N1 - Funding Information: This work was supported in part by NIH Grants HL59378 ES1180 (to A.B.), and DK36118 (to S.K.S.) and American Heart Association Grant 0415128B (to M.B.W.).

PY - 2008/7/23

Y1 - 2008/7/23

N2 - We tested the hypothesis that activation of the polyol pathway and protein kinase C (PKC) during diabetes is due to loss of NO. Our results show that after 4 weeks of streptozotocin-induced diabetes, treatment with l-arginine restored NO levels and prevented tissue accumulation of sorbitol in mice, which was accompanied by an increase in glutathiolation of aldose reductase. l-Arginine treatment decreased superoxide generation in the aorta, total PKC activity and PKC-βII phosphorylation in the heart, and the plasma levels of triglycerides and soluble ICAM. These data suggest that increasing NO bioavailability by l-arginine corrects the major biochemical abnormalities of diabetes.

AB - We tested the hypothesis that activation of the polyol pathway and protein kinase C (PKC) during diabetes is due to loss of NO. Our results show that after 4 weeks of streptozotocin-induced diabetes, treatment with l-arginine restored NO levels and prevented tissue accumulation of sorbitol in mice, which was accompanied by an increase in glutathiolation of aldose reductase. l-Arginine treatment decreased superoxide generation in the aorta, total PKC activity and PKC-βII phosphorylation in the heart, and the plasma levels of triglycerides and soluble ICAM. These data suggest that increasing NO bioavailability by l-arginine corrects the major biochemical abnormalities of diabetes.

KW - Cell adhesion molecule

KW - Diabetes mellitus

KW - Inflammation

KW - Nitric oxide

KW - Signal transduction

UR - https://www.scopus.com/pages/publications/46749157250

UR - https://www.scopus.com/pages/publications/46749157250#tab=citedBy

U2 - 10.1016/j.febslet.2008.06.039

DO - 10.1016/j.febslet.2008.06.039

M3 - Article

C2 - 18586034

AN - SCOPUS:46749157250

SN - 0014-5793

VL - 582

SP - 2609

EP - 2614

JO - FEBS Letters

JF - FEBS Letters

IS - 17

ER -

l-Arginine prevents metabolic effects of high glucose in diabetic mice

Abstract

Keywords

ASJC Scopus subject areas

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