High dietary fat induces NADPH oxidase-associated oxidative stress and inflammation in rat cerebral cortex

Zhang, Xiaochun; Dong, Feng; Ren, Jun; Driscoll, Meghan; Culver, Bruce

doi:10.1016/j.expneurol.2004.10.011

Cited by 244 publications

(165 citation statements)

References 54 publications

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“…Cortical COX-2 has also been reported to be markedly increased, and high levels of ROS generated in response to a high fat diet, suggesting a neural inflammatory response [32]. Our results reveal that IL-1␤ and COX-2 mRNA are similarly increased following immobilization stress and that high levels of ROS are generated in the cerebral cortex.…”

supporting

confidence: 67%

Immobilization stress induces cell death through production of reactive oxygen species in the mouse cerebral cortex

Choi

Lee

Choi

et al. 2006

Neuroscience Letters

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supporting

confidence: 67%

Immobilization stress induces cell death through production of reactive oxygen species in the mouse cerebral cortex

Choi

Lee

Choi

et al. 2006

Neuroscience Letters

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“…High dietary fat has, in fact, been reported to induce NADPH oxidase-associated oxidative stress and inflammation in the brain. 34 Thus, the present results might suggest a reason why the metabolic disorder accelerates the risk of salt-sensitive hypertension 35 and why the opposite is true. 32,33 Based on our new insights, a novel strategy, such as an antioxidant factor with a sympathoinhibitory effect, may well be developed to prevent and manage not only the salt-sensitive hypertension but also the metabolic disorder-mediated high-risk state.…”

Section: Perspectivesmentioning

confidence: 94%

Sympathoexcitation by Oxidative Stress in the Brain Mediates Arterial Pressure Elevation in Salt-Sensitive Hypertension

et al. 2007

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Abstract-Central sympathoexcitation is involved in the pathogenesis of salt-sensitive hypertension. We have suggested that oxidative stress in the brain modulates the sympathetic regulation of arterial pressure. Thus, we investigated whether oxidative stress could mediate central sympathoexcitation in salt-sensitive hypertension. Five-to 6-week-old male Dahl salt-sensitive rats and salt-resistant rats were fed with a normal (0.3%) or high-(8%) salt diet for 4 weeks. In urethane-anesthetized and artificially ventilated rats, arterial pressure, renal sympathetic nerve activity, and heart rate decreased in a dose-dependent fashion, when 20 or 40 mol of tempol, a membrane-permeable superoxide dismutase mimetic, was infused into the lateral cerebral ventricle. The same degree of reduction was noted in salt-sensitive and salt-resistant rats without salt loading. Salt loading significantly increased central tempol-induced reductions in arterial pressure (Ϫ29.1Ϯ4.8% versus Ϫ10.6Ϯ3.3% at 40 mol; PϽ0.01), sympathetic nerve activity (Ϫ18.7Ϯ2.0% versus Ϫ7.1Ϯ1.8%; PϽ0.01), and heart rate (Ϫ10.7Ϯ2.8% versus Ϫ2.0Ϯ0.7%; PϽ0.05) in salt-sensitive rats but not in salt-resistant rats. Intracerebroventricular diphenyleneiodonium, a reduced nicotinamide-adenine dinucleotide phosphate oxidase inhibitor, also elicited significantly greater reduction in each parameter in salt-loaded salt-sensitive rats. Moreover, salt loading increased reduced nicotinamide-adenine dinucleotide phosphate-dependent superoxide production in the hypothalamus in salt-sensitive rats but not in salt-resistant rats. In addition, reduced nicotinamide-adenine dinucleotide phosphate oxidase subunits p22 phox , p47 phox , and gp91 phox mRNA expression significantly increased in the hypothalamus of salt-loaded salt-sensitive rats. In conclusion, in salt-sensitive hypertension, increased oxidative stress in the brain, possibly via activation of reduced nicotinamide-adenine dinucleotide phosphate oxidase, may elevate arterial pressure through central sympathoexcitation. Key Words: salt-sensitive hypertension Ⅲ oxidative stress Ⅲ brain Ⅲ hypertension Ⅲ salt Ⅲ sympathetic nervous system Ⅲ Dahl rat S ubstantial findings indicate that abnormal modulation of the sympathetic nervous system may be involved in salt-induced development of hypertension in humans 1 and animals. [2][3][4][5][6] In our previous study, 2 salt loading impaired the arterial baroreceptor reflex associated with abnormal central properties in spontaneously hypertensive rats (SHRs); the sympathetic nerve activity (SNA) was less inhibited by stimulation of the aortic depressor nerve in salt-loaded SHRs. However, salt loading did not affect the SNA in Wistar-Kyoto rats. Similarly, the SNA was augmented with salt loading in Dahl salt-sensitive rats (DSs), but not in Dahl salt-resistant rats (DRs). 3 Intracerebroventricular (ICV) infusion of sodium caused sympathoexcitatory and pressor responses to a greater degree in DSs than in DRs. 4 Thus, central sympathetic activation may be involved in salt-sensitive ...

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“…52). Some of these peripheral effects, such as oxidative stress, also occur in the brain following HF feeding (21,40,58), and HF feeding increases cognitive impairment, tau deposition, MPTP vulnerability, and inflammation in the brain (15,38,44,45). Although specific contributions of other HF diet effects cannot be ruled out, our observation of increased markers of insulin resistance in the absence of increased total cholesterol or LDL-C levels and a positive correlation between HOMA-IR and DA depletion support a role for insulin resistance in mediating increased toxin-induced DA depletion.…”

Section: Discussionmentioning

confidence: 99%

Neurodegeneration in an animal model of Parkinson's disease is exacerbated by a high-fat diet

Morris

Bomhoff

Stanford

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

128

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(PD), the clinical literature remains equivocal. We, therefore, sought to address the relationship between insulin resistance and nigrostriatal dopamine (DA) in a preclinical animal model. High-fat feeding in rodents is an established model of insulin resistance, characterized by increased adiposity, systemic oxidative stress, and hyperglycemia. We subjected rats to a normal chow or high-fat diet for 5 wk before infusing 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle. Our goal was to determine whether a high-fat diet and the resulting peripheral insulin resistance would exacerbate 6-OHDA-induced nigrostriatal DA depletion. Prior to 6-OHDA infusion, animals on the high-fat diet exhibited greater body weight, increased adiposity, and impaired glucose tolerance. Two weeks after 6-OHDA, locomotor activity was tested, and brain and muscle tissue was harvested. Locomotor activity did not differ between the groups nor did cholesterol levels or measures of muscle atrophy. High-fat-fed animals exhibited higher homeostatic model assessment of insulin resistance (HOMA-IR) values and attenuated insulin-stimulated glucose uptake in fast-twitch muscle, indicating decreased insulin sensitivity. Animals in the high-fat group also exhibited greater DA depletion in the substantia nigra and the striatum, which correlated with HOMA-IR and adiposity. Decreased phosphorylation of HSP27 and degradation of IB␣ in the substantia nigra indicate increased tissue oxidative stress. These findings support the hypothesis that a diet high in fat and the resulting insulin resistance may lower the threshold for developing PD, at least following DA-specific toxin exposure. dopamine; diabetes; substantia nigra; striatum; insulin resistance CLINICAL STUDIES SUGGEST A LINK between type 2 diabetes (T2D) and Parkinson's disease (PD) (30,46), and between fat intake or adiposity and PD (1, 31, 34). Moreover, it was reported over 40 years ago that greater than 50% of PD patients exhibit abnormal glucose tolerance (4, 10) or diabetes (36). Despite this information, very little is known regarding the relationship of these diseases and the impact of comorbidity on their pathogenesis. By 2025, T2D is estimated to impact 300 million individuals (47), with the elderly at greatest risk (54), the population also at greatest risk for neurodegenerative diseases like PD. For these reasons, understanding the potential for T2D, obesity, high dietary fat intake, and insulin resistance to contribute to PD is critical. Although the exact cause of PD is unknown, various environmental factors such as aging, diet, and environmental toxin exposure have been implicated in contributing to its development (29, 34, 51). The idea that "multiple hits" play a role in PD degeneration is supported by the fact that 80% of dopamine (DA)-producing neurons must be lost for symptoms to appear (50). While diabetes and PD do not invariably coincide, several studies suggest that obesity may potentiate neuronal dysfunction or even neurodegeneration (reviewed in Ref. 11). High-f...

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High dietary fat induces NADPH oxidase-associated oxidative stress and inflammation in rat cerebral cortex

Cited by 244 publications

References 54 publications

Immobilization stress induces cell death through production of reactive oxygen species in the mouse cerebral cortex

Immobilization stress induces cell death through production of reactive oxygen species in the mouse cerebral cortex

Sympathoexcitation by Oxidative Stress in the Brain Mediates Arterial Pressure Elevation in Salt-Sensitive Hypertension

Neurodegeneration in an animal model of Parkinson's disease is exacerbated by a high-fat diet

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