Effects of high fat diet on Morris maze performance, oxidative stress, and inflammation in rats: Contributions of maternal diet

White, Christy L.; Pistell, Paul J.; Purpera, Megan N.; Gupta, Sunita; Fernandez-Kim, Sun-Ok; Hise, Taylor L.; Keller, Jeffrey N.; Ingram, Donald K.; Morrison, Christopher D.; Bruce‐Keller, Annadora J.

doi:10.1016/j.nbd.2009.04.002

Cited by 210 publications

(177 citation statements)

References 101 publications

(123 reference statements)

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“…These findings are consistent with our previous evidence showing that 12 weeks of HFD consumption in rats caused brain mitochondrial dysfunction (Pipatpiboon et al 2012). Previous studies as well as our findings suggest that the cognitive impairment caused by long-term HFD consumption could be related to brain mitochondrial dysfunction and oxidative stress , Stranahan et al 2008, White et al 2009, Pintana et al 2012. Interestingly, we found that both vildagliptin and sitagliptin completely restored brain mitochondrial function and improved learning and memory behaviors in rats with HFD-induced insulin resistance.…”

Section: Discussionsupporting

confidence: 93%

DPP-4 inhibitors improve cognition and brain mitochondrial function of insulin-resistant rats

Pintana

Apaijai²,

Chattipakorn³

2013

Journal of Endocrinology

169

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Recent evidence has demonstrated that insulin resistance is related to the development of type 2 diabetes mellitus. Our previous study found that high-fat diet (HFD) consumption caused not only peripheral and brain insulin resistance but also brain mitochondrial dysfunction and cognitive impairment. Vildagliptin and sitagliptin, dipeptidyl-peptidase-4 inhibitors, are recently developed anti-diabetic drugs. However, the effects of both drugs on cognitive behaviors and brain mitochondrial function in HFD-induced insulin-resistant rats have not yet been investigated. Sixty male Wistar rats were divided into two groups to receive either normal diet or HFD for 12 weeks. Rats in each group were then further divided into three treatment groups to receive either vehicle, vildagliptin (3 mg/kg per day), or sitagliptin (30 mg/kg per day) for 21 days. The cognitive behaviors of the rats were tested using the Morris Water Maze test. Blood samples were collected to determine metabolic parameters and plasma oxidative stress levels. Upon completion of the study, the animals were killed and the brains were removed to investigate brain and hippocampal mitochondrial function as well as to determine oxidative stress levels. We demonstrated that both drugs significantly improved the metabolic parameters and decreased circulating and brain oxidative stress levels in HFD-induced insulin-resistant rats. In addition, both drugs completely prevented brain and hippocampal mitochondrial dysfunction and equally improved the learning behaviors impaired by the HFD. Our findings suggest that the inhibition of dipeptidyl-peptidase-4 enzymes with vildagliptin or sitagliptin in insulinresistant rats not only increases peripheral insulin sensitivity but also decreases brain dysfunction. Key Words" insulin resistance " high-fat diet " DDP-4 inhibitors " memory decline " brain mitochondrial dysfunction

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Section: Discussionsupporting

confidence: 93%

DPP-4 inhibitors improve cognition and brain mitochondrial function of insulin-resistant rats

Pintana

Apaijai²,

Chattipakorn³

2013

Journal of Endocrinology

169

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“…Studies from our laboratory and others' have demonstrated that HFDs exacerbate tissue dysfunction in aging animals (11,29,46,68,76). Additionally, studies from our laboratory and others' have shown that HFDs promote much greater amounts of adipose gain, and presumably adipose tissue dysfunction, compared with younger animals (46,50,66).…”

Section: Discussionmentioning

confidence: 72%

“…Mice were fasted overnight and euthanized by isoflurane anaesthesia followed by rapid decapitation. Subcutaneous (inguinal) and visceral fat pads (epididymal) were manually dissected as described previously (68).…”

Section: Methodsmentioning

confidence: 99%

Aging is associated with hypoxia and oxidative stress in adipose tissue: implications for adipose function

Zhang

Ebenezer

Dasuri

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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As a part of aging there are known to be numerous alterations which occur in multiple tissues of the body, and the focus of this study was to determine the extent to which oxidative stress and hypoxia occur during adipose tissue aging. In our studies we demonstrate for the first time that aging is associated with both hypoxia (38% reduction in oxygen levels, Po2 21.7 mmHg) and increases reactive oxygen species in visceral fat depots of aging male C57Bl/6 mice. Interestingly, aging visceral fat depots were observed to have significantly less change in the expression of genes involved in redox regulation compared with aging subcutaneous fat tissue. Exposure of 3T3-L1 adipocytes to the levels of hypoxia observed in aging adipose tissue was sufficient to alter multiple aspects of adipose biology inducing increased levels of in insulin-stimulated glucose uptake and decreased lipid content. Taken together, these data demonstrate that hypoxia and increased levels of reactive oxygen species occur in aging adipose tissue, highlighting the potential for these two stressors as potential modulators of adipose dysfunction during aging.

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“…Evidence is emerging that the weight of the pregnant dam can increase dentate gyrus lipid peroxidation and impair neurogenesis in her offspring (160). Rats that were kept on a high-fat diet after being born to dams on high-fat diets had increased susceptibility to memory impairment and increase oxidative stress compared with rats that were either kept on a high-fat diet after being birthed by a dam on a normal diet, or rats kept on a normal fat diet after being birthed by a dam on a high fat (171).…”

Section: Animal Studiesmentioning

confidence: 99%

Impaired Adaptive Cellular Responses to Oxidative Stress and the Pathogenesis of Alzheimer's Disease

Texel

Mattson

2011

Antioxidants & Redox Signaling

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As is generally true with other age-related diseases, Alzheimer's disease (AD) involves oxidative damage to cellular components in the affected tissue, in this case the brain. The causes and consequences of oxidative stress in neurons in AD are not fully understood, but considerable evidence points to important roles for accumulation of amyloid b-peptide upstream of oxidative stress and perturbed cellular Ca 2+ homeostasis and energy metabolism downstream of oxidative stress. The identification of mutations in the b-amyloid precursor protein and presenilin-1 as causes of some cases of early onset inherited AD, and the development of cell culture and animal models based on these mutations has greatly enhanced our understanding of the AD process, and has greatly expanded opportunities for preclinical testing of potential therapeutic interventions. In this regard, and of particular interest to us, is the elucidation of adaptive cellular stress response pathways (ACSRP) that can counteract multiple steps in the AD neurodegenerative cascades, thereby limiting oxidative damage and preserving cognitive function. ACSRP can be activated by factors ranging from exercise and dietary energy restriction, to drugs and phytochemicals. In this article we provide an overview of oxidative stress and AD, with a focus on ACSRP and their potential for preventing and treating AD. Antioxid. Redox Signal. 14, 1519-1534.

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Effects of high fat diet on Morris maze performance, oxidative stress, and inflammation in rats: Contributions of maternal diet

Cited by 210 publications

References 101 publications

DPP-4 inhibitors improve cognition and brain mitochondrial function of insulin-resistant rats

DPP-4 inhibitors improve cognition and brain mitochondrial function of insulin-resistant rats

Aging is associated with hypoxia and oxidative stress in adipose tissue: implications for adipose function

Impaired Adaptive Cellular Responses to Oxidative Stress and the Pathogenesis of Alzheimer's Disease

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