Oxidative stress provokes atherogenic changes in adipokine gene expression in 3T3-L1 adipocytes

Kamigaki, Mitsunori; Sakaue, Shinji; Tsujino, Ichizo; Ohira, Hiroshi; Ikeda, Daisuke; Itoh, Naofumi; Ishimaru, Shin’ichi; Ohtsuka, Yoshinori; Nishimura, Masaharu

doi:10.1016/j.bbrc.2005.11.059

Cited by 104 publications

(85 citation statements)

References 29 publications

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“…Hcy also increased intracellular ROS significantly, and Hcy-induced expression of resistin was inhibited by the antioxidants in adipocytes, which is consistent with previous reports that exposure of adipocytes to hyperglycemic conditions reduces insulin sensitivity and increases ROS levels in vitro (41) and that Hcy induces ROS formation in monocytes followed by chemokine formation (16,17) but argues against other results that ROS is not involved in Hcy-induced secretion of chemokines from endothelial cells (38). Moreover, our results do not support the observation that oxidative stress, from either short-term exposure to high concentrations of H 2 O 2 or sustained exposure to low concentrations of H 2 O 2 , significantly decreases resistin expression and secretion in 3T3-L1 adipocytes (42). Increased ROS levels are an important trigger for insulin resistance in numerous settings (43); adipocytes isolated from animals with high-fat dietinduced diabetes display significantly elevated ROS levels, together with reduced insulin-mediated glucose uptake (44).…”

Section: Discussioncontrasting

confidence: 98%

Homocysteine Upregulates Resistin Production From Adipocytes In Vivo and In Vitro

Jiang

Gao

et al. 2008

Diabetes

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OBJECTIVE—Homocysteine (Hcy) is epidemiologically related to insulin resistance, which has been speculated to be a low-grade systemic inflammatory condition. Resistin acts as a critical mediator of insulin resistance associated with inflammatory conditions. We aimed to determine whether Hcy can induce insulin resistance by directly regulating the expression and secretion of resistin from adipose tissue. RESEARCH DESIGN AND METHODS—The effect of Hcy on the expression and secretion of resistin and insulin resistance was investigated using primary rat adipocytes and mice with hyperhomocysteinemia (HHcy). RESULTS—Hcy impaired glucose transport and, particularly, the insulin signaling pathway as shown by decreased insulin-stimulated tyrosine phosphorylation of insulin receptor and insulin receptor substrate (IRS)-1, increased serine phosphorylation of IRS-1, and inhibited Akt phosphorylation both in vitro and in vivo, and these impairments were accompanied by an increase in resistin expression. Compared with normal mice, HHcy mice with a clinically relevant level of plasma Hcy (19 μmol/l) showed significantly increased resistin production from adipose tissue (33.38 ± 3.08 vs. 19.27 ± 1.71 ng/ml, P < 0.01). Hcy (300–1000 μmol/l) also increased mRNA expression of resistin in primary rat adipocytes in a time- and concentration-dependent manner, with maximal induction at 24 h of approximately fourfold with 1,000 μmol/l. In addition, Hcy-induced resistin expression attenuated by treatment with reactive oxygen species (ROS) scavengers, protein kinase C (PKC), and nuclear factor (NF)-κB inhibitors implies a role in the process for ROS, PKC, and NF-κB. CONCLUSIONS—HHcy may promote insulin resistance through the induction of resistin expression and secretion from adipocytes via the activation of the ROS-PKC–NF-κB pathway.

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Section: Discussioncontrasting

confidence: 98%

Homocysteine Upregulates Resistin Production From Adipocytes In Vivo and In Vitro

Jiang

Gao

et al. 2008

Diabetes

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“…Plasma and cardiac APN levels are reduced in patients with diabetes (39) and in STZ-induced diabetic rats (9,40). Moreover, oxidative stress can downregulate APN level (9,41). Thus, reduced APN, in part as a consequence of increased oxidative stress in diabetes, should be responsible for the loss of IPo cardioprotection in diabetes.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia Abrogates Ischemic Postconditioning Cardioprotection by Impairing AdipoR1/Caveolin-3/STAT3 Signaling in Diabetic Rats

Yao

Liu

et al. 2015

Diabetes

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Signal transducer and activator of transcription 3 (STAT3) activation is key for ischemic postconditioning (IPo) to attenuate myocardial ischemia-reperfusion injury (MIRI), but IPo loses cardioprotection in diabetes in which cardiac STAT3 activation is impaired and adiponectin (APN) reduced. We found that IPo increased postischemic cardiomyocyte-derived APN, activated mitochondrial STAT3 (mitoSTAT3), improved mitochondrial function, and attenuated MIRI in wild-type but not in APN knockout (Adipo 2/2 ) mice subjected to 30 min coronary occlusion, followed by 2 or 24 h of reperfusion. Hypoxic postconditioning-induced protection against hypoxia/reoxygenation injury was lost in Adipo 2/2 cardiomyocytes but restored by recombinant APN, but this APN beneficial effect was abolished by specific STAT3 or APN receptor 1 (AdipoR1) gene knockdown, or caveolin-3 (Cav3) disruption. APN activated cardiac STAT3 and restored IPo cardioprotection in 4-week diabetic rats where AdipoR1 and Cav3 were functionally interactive but not in 8-week diabetic rats whose cardiac Cav3 was severely reduced and AdipoR1/Cav3 signaling impaired. We concluded that IPo activates mitoSTAT3 through APN/AdipoR1/Cav3 pathway to confer cardioprotection, whereas in diabetes, IPo loses cardioprotection due to impaired APN/AdipoR1/Cav3 signaling. Therefore, effective means that may concomitantly activate APN and repair APN signaling (i.e., AdipoR1/Cav3) in diabetes may represent promising avenues in the treatment of MIRI in diabetes.

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“…In the same way, other antioxidants such as Vitamin C and resveratrol also inhibit leptin secretion by adipocytes [56,57]. However, prooxidant agents (exposure to H 2 O 2 ) have also been shown to alter adipokine gene expression in adipocytes, including the inhibition of leptin secretion [58]. JNKs are activated by reactive oxygen species, and are well known for regulating transcription factors through phosphorylation.…”

Section: Discussionmentioning

confidence: 99%

Lipoic acid inhibits leptin secretion and Sp1 activity in adipocytes

Prieto-Hontoria

Pérez-Matute

Fernández‐Galilea

et al. 2011

Molecular Nutrition Food Res

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Oxidative stress provokes atherogenic changes in adipokine gene expression in 3T3-L1 adipocytes

Cited by 104 publications

References 29 publications

Homocysteine Upregulates Resistin Production From Adipocytes In Vivo and In Vitro

Homocysteine Upregulates Resistin Production From Adipocytes In Vivo and In Vitro

Hyperglycemia Abrogates Ischemic Postconditioning Cardioprotection by Impairing AdipoR1/Caveolin-3/STAT3 Signaling in Diabetic Rats

Lipoic acid inhibits leptin secretion and Sp1 activity in adipocytes

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