Aspects of Inflammation and Oxidative Stress in Pediatric Obesity and Type 1 Diabetes: An Overview of Ten Years of Studies

Tran, Brian D.; Oliver, Stacy R.; Rosa, Jaime S.; Galassetti, Pietro

doi:10.1155/2012/683680

Cited by 46 publications

(32 citation statements)

References 32 publications

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“…Juvenile overweight and obesity have been linked to high levels of oxidative stress [12,13]; obese subjects show higher oxLDL, AAOPs and TBARs levels than control subjects [52]. In adults, BMI, total body fat, and waist circumference have been shown to be positively correlated with urinary F2-isoprostane levels and inversely correlated with PON1 activity [53–55].…”

Section: Redox Balance In Obesitymentioning

confidence: 99%

Obesity-Associated Oxidative Stress: Strategies Finalized to Improve Redox State

Savini

Catani

Evangelista

et al. 2013

IJMS

411

310

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Obesity represents a major risk factor for a plethora of severe diseases, including diabetes, cardiovascular disease, non-alcoholic fatty liver disease, and cancer. It is often accompanied by an increased risk of mortality and, in the case of non-fatal health problems, the quality of life is impaired because of associated conditions, including sleep apnea, respiratory problems, osteoarthritis, and infertility. Recent evidence suggests that oxidative stress may be the mechanistic link between obesity and related complications. In obese patients, antioxidant defenses are lower than normal weight counterparts and their levels inversely correlate with central adiposity; obesity is also characterized by enhanced levels of reactive oxygen or nitrogen species. Inadequacy of antioxidant defenses probably relies on different factors: obese individuals may have a lower intake of antioxidant- and phytochemical-rich foods, such as fruits, vegetables, and legumes; otherwise, consumption of antioxidant nutrients is normal, but obese individuals may have an increased utilization of these molecules, likewise to that reported in diabetic patients and smokers. Also inadequate physical activity may account for a decreased antioxidant state. In this review, we describe current concepts in the meaning of obesity as a state of chronic oxidative stress and the potential interventions to improve redox balance.

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Section: Redox Balance In Obesitymentioning

confidence: 99%

Obesity-Associated Oxidative Stress: Strategies Finalized to Improve Redox State

Savini

Catani

Evangelista

et al. 2013

IJMS

411

310

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show abstract

“…Although the pathogenesis of autoimmune disorders are still not understood fully, oxidative stress has been identified as one of the major contributors to tissue damage in the secretory glands affected by autoimmune reactions (2–5). A role for oxidative stress in SS has been implicated by chemical signatures for reactive oxygen species (ROS) damage to DNA, lipids and proteins observed in labial salivary gland ductal cells from patients with SS, but not in healthy controls (6).…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-gallate modulates anti-oxidant defense enzyme expression in murine submandibular and pancreatic exocrine gland cells and human HSG cells

Dickinson

DeRossi²,

et al. 2014

Autoimmunity

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Sjogren’s syndrome (SS) and type 1 diabetes are prevalent autoimmune diseases in the United States. We reported previously that Epigallocatechin-3-gallate (EGCG) prevented and delayed the onset of autoimmune disease in NOD mice, a model for both Sjogren’s syndrome (SS) and type 1 diabetes. EGCG also normalized the levels of proteins related to DNA repair and antioxidant activity in NOD.B10.Sn-H2 mice, a model for primary SS, prior to disease onset. The current study examined the effect of EGCG on the expression of antioxidant enzymes in the submandibular salivary gland and the pancreas of NOD mice and cultured human salivary gland acinar cells. NOD mice consuming 0.2% EGCG daily dissolved in water showed higher protein levels of peroxiredoxin 6 (PRDX6), a major antioxidant defense protein, and catalase, while the untreated NOD mice exhibited significantly lowered levels of PRDX6. Similarly, pancreas samples from water-fed NOD mice were depleted in PRDX6 and superoxide dismutase, while EGCG-fed mice showed high levels of these antioxidant enzymes. In cultured HSG cells EGCG increased PRDX6 levels significantly, and this was inhibited by p38 and JNK inhibitors, suggesting the EGCG-mediated increase in protective antioxidant capacity is regulated in part through MAPK pathway signaling. This mechanism may explain the higher levels of PRDX6 found in EGCG-fed NOD mice. These preclinical observations warrant future preclinical and clinical studies to determine whether EGCG or green tea polyphenols could be used in novel preventive and therapeutic approaches against autoimmune diseases and salivary dysfunction involving oxidative stress.

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“…Inflammation is the primary cause of T1DM as well as a direct cause of a number of diabetic complications (34). An acute, intense inflammatory response triggers T1DM It has therefore been hypothesized that anti-inflammatory agents may be an effective clinical treatment for patients with T1DM.…”

Section: Discussionmentioning

confidence: 99%

Icariin prevents cytokine‑induced β‑cell death by inhibiting NF‑κB signaling

Zhong

2018

Exp Ther Med

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Abstract. The loss of insulin secretion in type I diabetes mellitus (T1DM) is caused by autoimmune-mediated destruction of insulin-producing pancreatic β-cells. Inflammatory cytokines and immune cell infiltration activate oxidative and endoplasmic reticulum (ER) stress, resulting in reduced β-cell viability. The current pharmacological agents used to control blood glucose have a limited effective duration and are accompanied by strong side effects. Blocking the inflammatory and immune responses that cause the β-cell damage has been investigated as a novel therapeutic approach to control T1DM. Icariin is a flavonoid component of Chinese medicinal herbs that has anti-inflammatory effects in vitro and in vivo. The results of the present study revealed that icariin abrogates the pro-apoptotic effect of inflammatory cytokines and significantly suppresses the activation of nuclear factor (NF)-κB in rat pancreatic β-cell lines. The present study may provide a basis for the potential use of icariin as a therapeutic agent for T1DM.

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Aspects of Inflammation and Oxidative Stress in Pediatric Obesity and Type 1 Diabetes: An Overview of Ten Years of Studies

Cited by 46 publications

References 32 publications

Obesity-Associated Oxidative Stress: Strategies Finalized to Improve Redox State

Obesity-Associated Oxidative Stress: Strategies Finalized to Improve Redox State

Epigallocatechin-3-gallate modulates anti-oxidant defense enzyme expression in murine submandibular and pancreatic exocrine gland cells and human HSG cells

Icariin prevents cytokine‑induced β‑cell death by inhibiting NF‑κB signaling

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