Cited by 80Nitric Oxide and Endothelin EffectsPancreatic function and diabetesNatural Antidiabetic Agents Studies

Effect of l-arginine-nitric oxide system on chemical-induced diabetes mellitus

Mohan, I.Krishna, Das, U.N.·1998·Free Radical Biology and Medicine

Abstract

Several in vitro studies have suggested that nitric oxide may be the mediator of cytokine-induced beta-cell destruction. On the other hand, in vivo studies have given conflicting results: some studies suggesting that nitric oxide synthase inhibitors do not suppress streptozotocin-induced diabetes in mice, while others revealed that nitric oxide synthase inhibitors can reduce the incidence of insulin-dependent diabetes mellitus in rats. The results of the present study indicate that alloxan-induced diabetes in the male Wistar rats can be abrogated to a large extent by prior and simultaneous administration of the precursor of nitric oxide, L-arginine, where as NG-monomethy-L-arginine (L-NMMA), a specific inhibitor of nitric oxide synthase, can completely block the beneficial action of L-arginine. Sodium nitroprusside, a nitric oxide donor, also showed significant inhibitory effect on the severity of diabetes induced by alloxan. Alloxan treatment reduced nitric oxide generation, whereas L-arginine and sodium nitroprusside, when given along with alloxan, enhanced nitric oxide production to control values. Induction of diabetes by alloxan in the experimental animals was associated with a marked elevation in plasma lactate, ketone body, and lipid peroxide levels with a simultaneous fall in plasma insulin and nitric oxide levels. Alloxan-induced diabetes also induced a fall in the levels of anti-oxidant enzymes such as superoxide dismutase, glutathione reductase, and total glutathione, and antioxidants: vitamin E and ceruloplasmin, and an increase in glutathione peroxidase and glutathione-S-transferase. All these biochemical abnormalities and antioxidant levels have improved to near normal levels in animals treated with insulin, L-arginine, and sodium nitroprusside. From the results of the present study, it is apparent that L-arginine and nitric oxide can prevent alloxan-induced beta-cell damage, and the development of diabetes, and restore the antioxidant status to near normal levels.

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Crossref · 10.1016/s0891-5849(98)00129-4

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  • Increased intake of long-chain n-3 PUFA results in increased proportions of those fatty acids in inflammatory cell phospholipids.

    “Increased intake of long-chain n-3 PUFA results in increased proportions of those fatty acids in inflammatory cell phospholipids (610 -614) .”

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Authors
Mohan, I. K., & Das, U. N.
Affiliations
L V Prasad Eye Institute (IN)
Corresponding author
Das, U.N.
Venue
Free Radical Biology and Medicine
Publisher
Elsevier BV
Published
1998-11
Volume
25
Issue
7
Pages
757-765
ISSN
0891-5849 (ISSN-L)
OpenAlex
W2064244878
Cited by
80
References
26
Citations by year
2025: 1 · 2024: 3 · 2022: 1 · 2020: 4 · 2018: 2 · 2017: 1 · 2016: 3 · 2015: 1 · 2014: 4 · 2013: 1 · 2012: 8
FWCI
1.64
Type
journal article
Language
en
Open access
closed
Locations
  • Free Radical Biology and Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
Keywords
L-arginine, nitric oxide, alloxan-induced diabetes, nitric oxide synthase inhibition, L-NMMA, sodium nitroprusside, beta cell destruction, antioxidant enzymes, lipid peroxidation, ketone bodies, plasma insulin, type 1 diabetes prevention
MeSH terms
Alloxan, Animals, Antioxidants, Arginine, Diabetes Mellitus, Experimental, Enzyme Inhibitors, Insulin, Ketone Bodies, Lipid Peroxides, Male, Nitric Oxide, Nitroprusside, Rats, Wistar, Nitric Oxide Synthase, omega-N-Methylarginine, Lactic Acid, Nitric Oxide Donors, Rats

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