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Cited by 166Metabolism, Diabetes, and CancerNatural Antidiabetic Agents StudiesDiet, Metabolism, and Disease

An insulin sensitizer improves the free radical defense system potential and insulin sensitivity in high fructose-fed rats.

Faure, P, Rossini, E, Wiernsperger, N, Richard, M J, Favier, A, Halimi, S·1999·Diabetes
DOI 10.2337/diabetes.48.2.353
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Abstract

Recently there has been growing interest in the effects of antioxidants on insulin activity. In the present study, we investigated the effect of metformin on free radical activity and insulin sensitivity in high fructose-fed rats, a diet that leads to insulin resistance. The animals were divided into four groups (n = 16 per group; experiment duration = 6 weeks): the control (C) group received a standard diet; the control metformin (CM) group was fed a control diet and received metformin (200 mg x kg(-1) x day(-1) in water); the fructose control (FT) group was fed a diet in which fructose composed 56.8% of the total carbohydrates; and the fructose metformin (FM) group received high-fructose diet and metformin (200 mg x kg(-1) x day(-1) in water). The glucose clamp technique was used to determine insulin sensitivity in eight animals per group. Metabolic and oxidative stress parameters were measured in the remaining rats. In the FT rats, insulin resistance, lower red cell CuZn superoxide dismutase activity and lower blood reduced glutathione were observed. Metformin treatment improved both the insulin activity and the antioxidant defense system. In the CM group, metformin had no effect on metabolic parameters, but improved red cell antioxidant enzyme activities and the blood GSH level, which suggests that it has an antioxidant activity independent of its effect on insulin activity.

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Crossref · 10.2337/diabetes.48.2.353

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  • Metformin has recently been reported to have antioxidant effects in addition to known favorable effects on circulating lipids and FFAs.

    “In fact, metformin has recently been reported to have antioxidant effects (34) in addition to the known favorable effects on circulating lipids (10) and FFAs (35).”

    From Improved Endothelial Function With Metformin in Type 2 Diabetes Mellitus (2001) · cites this paper as [34]

  • Metformin reduces reactive oxygen species by inhibiting mitochondrial respiration and decreases advanced glycosylation end product indirectly through reduction of hyperglycemia and directly through an insulin-dependent mechanism.

    “It reduces reactive oxygen species (ROS) by inhibiting mitochondrial respiration [100] and decreases advanced glycosylation end product (AGE) indirectly through reduction of hyperglycemia and directly through an insulin-dependent mechanism [101].”

    From Metformin: An Old But Still the Best Treatment for Type 2 Diabetes (2013) · cites this paper as [100]

  • Metformin has been proposed to cause a mild and transient inhibition of mitochondrial complex I which decreases ATP levels and activates AMPK-dependent catabolic pathways, increasing lipolysis and beta-oxidation in white adipose tissue and reducing neoglucogenesis.

    “Metformin has been proposed to cause a mild and transient inhibition of mitochondrial complex I which decreases ATP levels and activates AMPK-dependent catabolic pathways [100], increasing lipolysis and ß-oxidation in white adipose tissue [102] and reducing neoglucogenesis [2].”

    From Metformin: An Old But Still the Best Treatment for Type 2 Diabetes (2013) · cites this paper as [100]

  • Metformin can upregulate uncoupled proteins 2 in adipose tissue and can cause an increase in reduced glutathione.

    “It can upregulate uncoupled proteins 2 (UCP2) in adipose tissue [102] and can also cause an increase in reduced glutathione [100].”

    From Metformin: An Old But Still the Best Treatment for Type 2 Diabetes (2013) · cites this paper as [100]

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Authors
Faure, P., Rossini, E., Wiernsperger, N., Richard, M. J., Favier, A., & Halimi, S.
Affiliations
Groupe de Recherché sur les Pathologies Oxydatives, UFR de Pharmacie, La Tronche, France. patrice.faure@ujf-grenoble.fr
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
1999-02-01
Volume
48
Issue
2
Pages
353-357
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/diabetes.48.2.353
OpenAlex
W2150046218
Cited by
166
References
14
Citations by year
2026: 1 · 2025: 1 · 2023: 5 · 2022: 2 · 2021: 5 · 2020: 6 · 2019: 4 · 2018: 5 · 2017: 3 · 2016: 11 · 2015: 10 · 2014: 5 · 2013: 10 · 2012: 6
FWCI
2.18
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Natural Antidiabetic Agents Studies
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
Keywords
metformin, insulin sensitivity, insulin resistance, high-fructose diet, oxidative stress, antioxidant defense, superoxide dismutase, glutathione, free radicals, glucose clamp
MeSH terms
Animals, Dietary Carbohydrates, Fructose, Hypoglycemic Agents, Insulin, Lipid Peroxides, Male, Metformin, Oxidoreductases, Free Radical Scavengers, Rats, Wistar, Rats

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