Deterioration of physical performance and cognitive function in rats with short‐term high‐fat feeding

Murray, Andrew J.; Knight, Nicholas; Cochlin, Lowri E; McAleese, Sara; Deacon, Robert M. J.; Rawlins, J. N. P.; Clarke, Kieran

doi:10.1096/fj.09-139691

Cited by 122 publications

(119 citation statements)

References 36 publications

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“…17,19 However, high-fat diets can also lead to higher levels of mitochondrial uncoupling protein (UCP3), which reduces the efficiency of energy production and, therefore, can impair exercise capacity. 41 Although the precise limitation(s) on endurance exercise performance depend on the intensity and/or duration of the activity, the depletion of energy substrates is a commonly considered cause of fatigue. The ingestion, loading or use of particular dietary macronutrients is important in maintaining muscular activity and delaying fatigue during exercise.…”

Section: Discussionmentioning

confidence: 99%

Western diet increases wheel running in mice selectively bred for high voluntary wheel running

2010

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Objective: Mice from a long-term selective breeding experiment for high voluntary wheel running offer a unique model to examine the contributions of genetic and environmental factors in determining the aspects of behavior and metabolism relevant to body-weight regulation and obesity. Starting with generation 16 and continuing through to generation 52, mice from the four replicate high runner (HR) lines have run 2.5-3-fold more revolutions per day as compared with four non-selected control (C) lines, but the nature of this apparent selection limit is not understood. We hypothesized that it might involve the availability of dietary lipids. Methods: Wheel running, food consumption (Teklad Rodent Diet (W) 8604, 14% kJ from fat; or Harlan Teklad TD.88137 Western Diet (WD), 42% kJ from fat) and body mass were measured over 1-2-week intervals in 100 males for 2 months starting 3 days after weaning. Results: WD was obesogenic for both HR and C, significantly increasing both body mass and retroperitoneal fat pad mass, the latter even when controlling statistically for wheel-running distance and caloric intake. The HR mice had significantly less fat than C mice, explainable statistically by their greater running distance. On adjusting for body mass, HR mice showed higher caloric intake than C mice, also explainable by their higher running. Accounting for body mass and running, WD initially caused increased caloric intake in both HR and C, but this effect was reversed during the last four weeks of the study. Western diet had little or no effect on wheel running in C mice, but increased revolutions per day by as much as 75% in HR mice, mainly through increased time spent running. Conclusion: The remarkable stimulation of wheel running by WD in HR mice may involve fuel usage during prolonged endurance exercise and/or direct behavioral effects on motivation. Their unique behavioral responses to WD may render HR mice an important model for understanding the control of voluntary activity levels.

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Section: Discussionmentioning

confidence: 99%

Western diet increases wheel running in mice selectively bred for high voluntary wheel running

2010

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“…Evidence of a link between food intake and impaired memory performance is accumulating (for a review, see [23]). First, for the case of an overly rich diet, such as the Western diet, it has been shown that feeding rats a high-fat diet alters working memory, even after only 3 [77] or 9 days [110]. This type of memory is impaired both in the short and longterm [77].…”

Section: Hippocampus and Memory For Food Intakementioning

confidence: 99%

The anterior medial temporal lobes: Their role in food intake and body weight regulation

Coppin

2016

Physiology & Behavior

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• The amygdala and hippocampus play a major role in food intake and weight regulation.• These functions are far less known to cognitive and affective scientists.• This review uniquely expands on the interactions between these two brain structures. a b s t r a c t a r t i c l e i n f o The anterior medial temporal lobes are one of the most studied parts of the brain. Classically, their two main structures -the amygdalae and the hippocampi -have been linked to key cognitive and affective functions, related in particular to learning and memory. Based on abundant evidence, we will argue for an alternative but complementary point of view: they may also play a major role in food intake and body weight regulation. First, an overview is given of early clinical evidence in this line of thought. Subsequently, empirical evidence is presented on how food intake, including in the extreme case of obesity, may relate to amygdalian and hippocampal functioning. The focus is on the amygdala's role in processing the relevance of food stimuli, cue-induced feeding, and stress-induced eating and on the hippocampus' involvement in the use of interoceptive signals of hunger and satiety, as well as memory and inhibitory processes related to food intake. Additionally, an elaboration takes place on possible reciprocal links between food intake, body weight, and amygdala and hippocampus functioning. Finally, issues that seemed particularly critical for future research in the field are discussed.

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“…Diets with high saturated fat content impaired cognitive function in a delayed alternation task in young rats, and the percent of saturated fat in the diet correlated positively with behavioral impairment (61). Murray et al showed that only 9 days of a high-fat diet was sufficient to cause physical impairment on a treadmill and cognitive impairment in the water maze (121). When 16-month-old rats were fed diets high in fat and cholesterol they made more errors in a test of working memory especially when memory loads were high, and they also showed altered hippocampal morphology (60).…”

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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Deterioration of physical performance and cognitive function in rats with short‐term high‐fat feeding

Cited by 122 publications

References 36 publications

Western diet increases wheel running in mice selectively bred for high voluntary wheel running

Western diet increases wheel running in mice selectively bred for high voluntary wheel running

The anterior medial temporal lobes: Their role in food intake and body weight regulation

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

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