Novel Role of Endogenous Catalase in Macrophage Polarization in Adipose Tissue

Park, Ye Seul; Uddin, Jamal; Piao, Lingjuan; Hwang, Inah; Lee, Jung Hwa; Ha, Hunjoo

doi:10.1155/2016/8675905

Cited by 25 publications

(23 citation statements)

References 47 publications

(54 reference statements)

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“…Ho and colleagues, the originators of the mice used in the present study, showed increased hydrogen peroxide production by tissue from Cat -/- mice [10]. Park and colleagues demonstrated elevated nitrotyrosine expression in epididymal white adipose tissue of Cat -/- mice [47]. Reactive oxygen species are abundantly produced in obesity and metabolic syndrome [5] and adipose tissue proteins of obese patients have been found to be more carbonylated (a marker of oxidative stress) [63].…”

Section: Discussionmentioning

confidence: 95%

“…Notably, crown-like structures, reflective of macrophages surrounding dying or dead adipocytes, are commonly observed in the adipose tissue of ob/ob and db/db mice and are thought to be associated with insulin resistance [46]. A recent study showed higher levels of plasma free fatty acids and triglycerides in Cat -/- mice [47], reaffirming a potential role for catalase in lipid mobilization. The same study also revealed increased numbers of crown-like structures in white adipose tissue in Cat -/- mice, but only under conditions of a high fat diet.…”

Section: Discussionmentioning

confidence: 99%

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Catalase deletion promotes prediabetic phenotype in mice

Heit

Marshall

Singh

et al. 2017

Free Radical Biology and Medicine

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Hydrogen peroxide is produced endogenously and can be toxic to living organisms by inducing oxidative stress and cell damage. However, it has also been identified as a signal transduction molecule. By metabolizing hydrogen peroxide, catalase protects cells and tissues against oxidative damage and may also influence signal transduction mechanisms. Studies suggest that acatalasemic individuals (i.e., those with very low catalase activity) have a higher risk for the development of diabetes. We now report catalase knockout (Cat-/-) mice, when fed a normal (6.5% lipid) chow, exhibit an obese phenotype that manifests as an increase in body weight that becomes more pronounced with age. The mice demonstrate altered hepatic and muscle lipid deposition, as well as increases in serum and hepatic triglycerides (TGs), and increased hepatic transcription and protein expression of PPARγ. Liver morphology revealed steatosis with inflammation. Cat-/- mice also exhibited pancreatic morphological changes that correlated with impaired glucose tolerance and increased fasting serum insulin levels, conditions consistent with pre-diabetic status. RNA-seq analyses revealed a differential expression of pathways and genes in Cat-/- mice, many of which are related to metabolic syndrome, diabetes, and obesity, such as Pparg and Cidec. In conclusion, the results of the present study show mice devoid of catalase develop an obese, pre-diabetic phenotype and provide compelling evidence for catalase (or its products) being integral in metabolic regulation.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Catalase deletion promotes prediabetic phenotype in mice

Heit

Marshall

Singh

et al. 2017

Free Radical Biology and Medicine

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“…In regard to obesity, a mouse model expressing mitochondria specific catalase on a high fat diet displayed attenuated mitochondrial ROS emission, preserved insulin signaling, and no inflammatory response compared to wild type controls [11]. This may be because overexpression of endogenous catalase was shown to regulate the polarization of macrophages within adipose tissue and thereby inhibiting inflammation and insulin resistance [31]. On the other hand, mice devoid of antioxidant catalase developed an obese, prediabetic phenotype that was exacerbated with age [32].…”

Section: Introductionmentioning

confidence: 99%

Catalase overexpression modulates metabolic parameters in a new ‘stress-less’ leptin-deficient mouse model

Amos

Robinson

Massie

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Oxidative stress plays a key role in obesity by modifying the function of important biological molecules, thus altering obesogenic pathways such as glucose and lipid signaling. Catalase, is an important endogenous antioxidant enzyme that catabolizes hydrogen peroxide produced by the dismutation of superoxide. Recent studies have shown knockdown of catalase exacerbates insulin resistance and leads to obesity. We hypothesized that overexpressing catalase in an obese mouse will modulate obesogenic pathways and protect against obesity. Therefore, we bred catalase transgenic ([Tg(CAT)+/−] mice with Ob/Ob mice to generate the hybrid “Bob-Cat” mice. This newly generated “stress-less” mouse model had decreased oxidative stress (oxidized carbonylated proteins). ECHO-MRI showed lower fat mass but higher lean mass in “Bob-Cat” mice. Comprehensive Lab Animal Monitoring System (CLAMS) showed light and dark cycle increase in energy expenditure in Bob-Cat mice compared to wild type controls. Circulating levels of leptin and resistin showed no change. Catalase mRNA expression was increased in key metabolic tissues (adipose, liver, intestinal mucosa, and brain) of the Bob-Cat mouse. Catalase activity, mRNA and protein expression was increased in adipose tissue. Expression of the major adipokines leptin and adiponectin was increased while pro-inflammatory genes, MCP-1/JE and IL-1β were lowered. Interestingly, sexual dimorphism was seen in body composition, energy expenditure, and metabolic parameters in the Bob-Cat mice. Overall, the characteristics of the newly generated “Bob-Cat” mice make it an ideal model for studying the effect of redox modulators (diet/exercise) in obesity.

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“…CAT is one of the major endogenous antioxidant enzymes that detoxify the reactive oxygen species (ROS) hydrogen peroxide (H2O2) to water and oxygen. While brain CAT activity is low compared to other tissues and organs [25], this enzyme regulates macrophage polarization in adipose tissue [82]. Overexpression of catalase is beneficial in the context of obesity.…”

Section: Ros-related Gene Expression Between Ptsd Patients and Controlsmentioning

confidence: 99%

Oxidative Stress and Neuroinflammation in a Rat Model of Co-Morbid Obesity and Psychogenic Stress

Santana

Vega-Torres

Ontiveros-Angel

et al. 2020

Preprint

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Contributions: JMS, wrote manuscript, performed Western blot experiments and analyses; JDV, design and performed behavioral experiments, wrote manuscript; YAT, performed Western blot experiments; POA, performed and analyzed ELISA experiments, prepared illustrations, wrote manuscript; JBL, analyzed behavioral data; AYCG and EAB, performed Western blots; DZO and CAC, peformed Western blot analyses; JDF, planned experiments, analyzed data, wrote manuscript. AbstractBackground: There is growing recognition for a reciprocal, bidirectional link between anxiety disorders and obesity. Although the mechanisms linking obesity and anxiety remain speculative, this bidirectionality suggests shared pathophysiological processes. Neuroinflammation and oxidative damage are implicated in both pathological anxiety and obesity. This study investigates the relative contribution of comorbid dietinduced obesity and stress-induced anxiety to neuroinflammation and oxidative stress.Methods: Thirty-six (36) male Lewis rats were divided into four groups based on diet type and stress exposure: 1) control diet unexposed (CDU) and 2) exposed (CDE), 3)Western-like high-saturated fat diet unexposed (WDU) and 4) exposed (WDE).Neurobehavioral tests were performed to assess anxiety-like behaviors. The catalytic concentrations of glutathione peroxidase and reductase were measured from plasma samples, and neuroinflammatory/oxidative stress biomarkers were measured from brain samples using Western blot. Correlations between behavioral phenotypes and biomarkers were assessed with Pearson's correlation procedures. Results:We found that WDE rats exhibited markedly increased levels of glial fibrillary acidic protein (185%), catalase protein (215%), and glutathione reductase (GSR) enzymatic activity (418%) relative to CDU rats. Interestingly, the brain protein levels of glutathione peroxidase (GPx) and catalase were positively associated with body weight and behavioral indices of anxiety. Conclusions:Together, our results support a role for neuroinflammation and oxidative stress in heightened emotional reactivity to obesogenic environments and psychogenic stress. Uncovering adaptive responses to obesogenic environments characterized by 3 high access to high-saturated fat/high-sugar diets and toxic stress has the potential to strongly impact how we treat psychiatric disorders in at-risk populations. Highlights:• Predatory odor stress heightens footshock reactivity and anxiety-like behaviors in Lewis rats.• WD intake increases glutathione reductase activity in plasma.• WD intake and PS exposure acted synergistically to increase the brain protein levels of catalase and the glial fibrillary acidic protein.• The protein levels and activities of some redox/neuroinflammatory biomarkers are closely associated with behavioral proxies related to fear and anxiety in rats. astrocytes use glycolysis for energy production and, as a consequence, have been associated with a higher generation of mitochondrial reactive oxygen species (ROS) [26].It is known that ROS accumula...

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Novel Role of Endogenous Catalase in Macrophage Polarization in Adipose Tissue

Cited by 25 publications

References 47 publications

Catalase deletion promotes prediabetic phenotype in mice

Catalase deletion promotes prediabetic phenotype in mice

Catalase overexpression modulates metabolic parameters in a new ‘stress-less’ leptin-deficient mouse model

Oxidative Stress and Neuroinflammation in a Rat Model of Co-Morbid Obesity and Psychogenic Stress

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