Non-alcoholic fatty liver disease impairs hippocampal-dependent memory in male rats

Ross, Amy P.; Bruggeman, Emily C.; Kasumu, Adebimpe W.; Mielke, John G.; Parent, Marise B.

doi:10.1016/j.physbeh.2012.01.008

Cited by 41 publications

(32 citation statements)

References 82 publications

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“…There is a well-established link between human obesity and cognitive decline [23]. Specific brain functions related to the hippocampus may be particularly vulnerable as evidenced in a large number of studies in rodents linking high-caloric diets with decreased contextual and spatial memory [24][25][26][27][28][29]. Significantly, it has been demonstrated that obese animals whose diet regimen is reversed from HFD back to standard chow, recover memory function [22].…”

Section: Lifestyle and Admentioning

confidence: 99%

The role of leptin in the sporadic form of Alzheimer's disease. Interactions with the adipokines amylin, ghrelin and the pituitary hormone prolactin

et al. 2015

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Section: Lifestyle and Admentioning

confidence: 99%

The role of leptin in the sporadic form of Alzheimer's disease. Interactions with the adipokines amylin, ghrelin and the pituitary hormone prolactin

et al. 2015

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“…The present findings have significant implications for the interpretation of previous research that has tested the effects of HEDs on memory in stressful memory tasks such as the water maze (Darling et al, 2013;Pathan et al, 2008;Ross et al, 2009;Ross et al, 2012;Stranahan et al, 2008). Swimming is an intense Stressor for rats that causes large increases in plasma epinephrine and corticosterone concentrations (Mabry, Gold, & McCarty, 1995;McFadden et al, 2011).…”

Section: Discussionmentioning

confidence: 70%

“…Previous research investigating the effects of HEDs on memory has employed diets in which the nutrients were all presented in one pellet (Greenwood & Winocur, 1990, 1996, 2001Ross et al, 2009;Ross et al, 2012). Compared with these pelleted diets, the cafeteria-style high-energy diet has more relevance to human consumption patterns.…”

Section: Discussionmentioning

confidence: 99%

High energy diets prevent the enhancing effects of emotional arousal on memory.

Ross¹,

Darling²,

Parent³

2013

Behavioral Neuroscience

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Over the past five decades, per capita caloric intake has increased by approximately 28% in the United States. Excessive intake of calories from fats and sugars (high energy diets; HEDs) negatively impacts hippocampal-dependent memory. These deleterious effects of HEDs on hippocampal function involve HED-induced decreases in neuronal growth factors, neurogenesis, and synaptic plasticity. Given that HEDs also alter responses to emotional arousal, the present experiment determined whether the effects of HEDs on memory depend on the emotional arousal produced by the memory task during encoding. Rats were fed a high fat/sugar cafeteria-style diet for 4 weeks and then tested in a low or high emotional arousal version of a spatial object place recognition task. The results demonstrated that the HED prevented the memory-enhancing effects of emotional arousal. Thus, altered responses to emotional arousal likely contribute to HED-induced memory impairments, particularly in stressful memory tasks such as the spatial water maze.

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“…Research also demonstrates that diet-induced obesity impairs hippocampal functions [152-155]. Obesity could compromise hippocampal functioning through increased blood-brain barrier permeability allowing inflammatory cytokines to enter the brain [154, 156], inflammatory processes within the CNS [157, 158], and/or fatty liver inflammatory signals [153, 159]. While altered cytokine signaling in the inflammatory state of obesity may be partially to blame for compromised CNS centers [160-162], tight junctions of the blood-brain barrier likely prevent cytokines from entering most areas of the brain [163].…”

Section: Emotion/memory Systemsmentioning

confidence: 99%

Central nervous system regulation of eating: Insights from human brain imaging

2016

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Appetite and body weight regulation are controlled by the central nervous system (CNS) in a rather complicated manner. The human brain plays a central role in integrating internal and external inputs to modulate energy homeostasis. Although homeostatic control by the hypothalamus is currently considered to be primarily responsible for controlling appetite, most of the available evidence derives from experiments in rodents, and the role of this system in regulating appetite in states of hunger/starvation and in the pathogenesis of overeating/obesity remains to be fully elucidated in humans. Further, cognitive and affective processes have been implicated in the dysregulation of eating behavior in humans, but their exact relative contributions as well as the respective underlying mechanisms remain unclear. We briefly review each of these systems here and present the current state of research in an attempt to update clinicians and clinical researchers alike on the status and future directions of obesity research.

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Non-alcoholic fatty liver disease impairs hippocampal-dependent memory in male rats

Cited by 41 publications

References 82 publications

The role of leptin in the sporadic form of Alzheimer's disease. Interactions with the adipokines amylin, ghrelin and the pituitary hormone prolactin

The role of leptin in the sporadic form of Alzheimer's disease. Interactions with the adipokines amylin, ghrelin and the pituitary hormone prolactin

High energy diets prevent the enhancing effects of emotional arousal on memory.

Central nervous system regulation of eating: Insights from human brain imaging

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