High-fat diet alters the dopamine and opioid systems: effects across development

Reyes, Teresa M.

doi:10.1038/ijosup.2012.18

Cited by 29 publications

(26 citation statements)

References 64 publications

(65 reference statements)

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“…After 3 wks of HFD feeding, however, DA and HVA levels in the brain were similar to those measured in LFD mice. These findings support the contention that a HFD can affect brain reward and impact the DA system which is activated by unexpected rewards and novelty (Reyes 2012). Chronic feeding of a HFD is associated with down-regulation of gene transcripts for the dopamine 1 and 2 receptors and the dopamine transporter, indicating that a HFD may eventually lead to a quieting of the DA system (Reyes 2012).…”

Section: Discussionsupporting

confidence: 86%

Methylphenidate prevents high-fat diet (HFD)-induced learning/memory impairment in juvenile mice

Kaczmarczyk

Machaj

Chiu

et al. 2013

Psychoneuroendocrinology

106

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The prevalence of childhood obesity has risen dramatically and coincident with this upsurge is a growth in adverse childhood psychological conditions including impulsivity, depression, anxiety and attention deficit/hyperactive disorder (ADHD). Due to confounds that exist when determining causality of childhood behavioral perturbations, controversy remains as to whether overnutrition and/or childhood obesity is important. Therefore, we examined juvenile mice to determine if biobehaviors were impacted by a short-term feeding (1–3 wks) of a high-fat diet (HFD). After 1 wk of a HFD feeding, mouse burrowing and spontaneous wheel running were increased while mouse exploration of the open quadrants of a zero maze, perfect alternations in a Y-maze and recognition of a novel object were impaired. Examination of mouse cortex, hippocampus and hypothalamus for dopamine and its metabolites demonstrated increased homovanillic acid (HVA) concentrations in the hippocampus and cortex that were associated with decreased cortical BDNF gene expression. In contrast, pro-inflammatory cytokine gene transcripts and serum IL-1α, IL-1β, TNF-α and IL-6 were unaffected by the short-term HFD feeding. Administration to mice of the psychostimulant methylphenidate prevented HFD-dependent impairment of learning/memory. HFD learning/memory impairment was not inhibited by the anti-depressants desipramine or reboxetine nor was it blocked in IDO or IL-1R1 knockout mice. In sum, a HFD rapidly impacts dopamine metabolism in the brain appearing to trigger anxiety-like behaviors and learning/memory impairments prior to the onset of weight gain and/or pre-diabetes. Thus, overnutrition due to fats may be central to childhood psychological perturbations such as anxiety and ADHD.

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Section: Discussionsupporting

confidence: 86%

Methylphenidate prevents high-fat diet (HFD)-induced learning/memory impairment in juvenile mice

Kaczmarczyk

Machaj

Chiu

et al. 2013

Psychoneuroendocrinology

106

View full text Add to dashboard Cite

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“…This finding would suggest a time-dependent course of chronic diet effects on the fear neurocircuitry, confirming previous studies (Kalyan-Masih et al, 2016;Vega-Torres et al, 2018). Given the robust effects of obesogenic diets on the dopamine system (Reichelt, 2016;Reyes, 2012), and the modulatory actions of this neurotransmitter on mPFC-amygdala circuit function and FPS responses (Fadok et al, 2009;Onozawa et al, 2011), we hypothesized that the obesogenic diet would reduce dopamine receptor expression in the mPFC and amygdala.…”

Section: Introductionsupporting

confidence: 83%

Developmental regulation of fear memories by an obesogenic high-saturated fat/high-sugar diet

Vega-Torres

Reyes-Rivera

Figueroa

2019

Preprint

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Background: Anxiety and stress-related disorders are strongly linked with obesity and the consumption of obesogenic diets. Paralleling clinical findings, we showed that the consumption of an obesogenic diet during adolescence disrupts the structural integrity of amygdalar and prefrontal cortex circuits underlying emotional responses to stress. These abnormalities were associated with a PTSD-like phenotype, including heightened stress reactivity to predator odor trauma, anxietylike behaviors, and profound learning deficits. The present follow-up study investigates how an obesogenic diet alters aversion-related associative memories across adolescence. Methods: Adolescent Lewis rats were fed for eight weeks with an experimentalWestern-like high-saturated fat/high-sugar diet (WD, 41% kcal from fat) or a matched control diet (CD, 13% kcal from fat). Acoustic fear-potentiated startle (FPS) responses were assessed longitudinally at weeks 1, 4, and 8 after commencing the diets to determine the effects of the WD on cued fear conditioning, fear extinction learning, and fear extinction retention. Results:We found that the rats that consumed the WD exhibited substantial attenuation of fear extinction and fear extinction retention when remote memory was tested. One-week WD consumption was sufficient to induce impairments in fear extinction learning. This phenotype was associated with reduced dopamine receptor 1 mRNA levels in the prefrontal cortex. Interestingly, our reconditioning paradigm revealed that early-acquired fear memories were resistant to the disruptive effects of chronic WD consumption on cued fear learning. Vega-Torres et. al., 3Conclusions: Our findings demonstrate that consumption of an obesogenic WD during adolescence heightens behavioral vulnerabilities associated with risk for anxiety and stress-related disorders. Given that fear extinction promotes resilience and that fear extinction principles are the foundation of psychological treatments for PTSD, understanding how obesity and obesogenic diets affect the acquisition and expression of fear extinction memories is of tremendous clinical relevance. HIGHLIGHTS• Acute WD consumption impairs cued fear extinction learning in a fearpotentiated startle paradigm.• WD consumption attenuates fear extinction memory retention • WD consumption during adolescence increases acoustic startle responsivity over time • Chronic WD consumption decreases dopamine receptor D1 mRNA levels in the prefrontal cortex.

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“…Second, we reasoned that short-term exposure to an obesogenic diet would reduce the neuronal activation in corticolimbic regions implicated in fear extinction and anxiolytic effects. Finally, given the robust effects of obesogenic diets on the HPA axis and dopamine systems (Boitard et al, 2015;Khazen et al, 2019;Reyes, 2012;Sharma et al, 2013), and the modulatory actions of these factors on mPFC-amygdala circuit function (Fadok et al, 2009b;Jovanovic et al, 2010;2020;Veer et al, 2012;Whittle et al, 2016), we hypothesized that the obesogenic diet would increase the HPA tone while reducing dopamine receptor expression in the mPFC.…”

Section: Introductionmentioning

confidence: 99%

Early maturational emergence of adult-like emotional reactivity and anxiety after brief exposure to an obesogenic diet

Vega-Torres

Azadian

Rios-Orsini

et al. 2020

Preprint

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Background: Emerging evidence demonstrates that diet-induced obesity disrupts corticolimbic circuits underlying emotional regulation. Studies directed at understanding how obesity alters brain and behavior are easily confounded by a myriad of complications related to obesity. This study investigated the early neurobiological stress response triggered by an obesogenic diet. Furthermore, this study directly determined the combined impact of a short-term obesogenic diet and adolescence on critical behavioral and molecular substrates implicated in emotion regulation and stress.Methods: Adolescent (postnatal day 31) or adult (postnatal day 81) Lewis rats were fed for one week with an experimental Western-like high-saturated fat diet (WD, 41% kcal from fat) or a matched control diet (CD, 13% kcal from fat). We used the acoustic fear-potentiated startle (FPS) paradigm to determine the effects of the WD on cued fear conditioning and fear extinction. We used c-Fos mapping to determine the functional influence of the diet and stress on corticolimbic circuits. Results:We report that one-week WD consumption was sufficient to induce fear extinction deficits in adolescent rats, but not in adult rats. We identify fear-induced alterations in corticolimbic neuronal activation and demonstrate increased prefrontal cortex CRHR1 mRNA levels in the rats that consumed the WD. Conclusions:Our findings demonstrate that short-term consumption of an obesogenic diet during adolescence heightens behavioral and molecular vulnerabilities associated with risk for anxiety and stress-related disorders. Given that fear extinction promotes resilience, and that fear extinction principles are the Vega-Torres et. al., 3 foundation of psychological treatments for PTSD, understanding how obesogenic environments interact with the adolescent period to affect the acquisition and expression of fear extinction memories is of tremendous clinical relevance. KEYWORDS PTSD, diet-induced obesity, adolescence, anxiety, fear-potentiated startle, CRHR1 HIGHLIGHTS • Short-term WD consumption during adolescence impairs cued fear extinction memory retention in a fear-potentiated startle paradigm.• Short-term WD consumption during adolescence attenuates neuronal activation to electric footshock stress in the basomedial nuclei of the amygdala.• Short-term WD consumption increases CRHR1 mRNA levels in the medial prefrontal cortex.• Adult LEW rats exhibit increased basal HPA axis tone and heightened emotional reactivity to footshock stress relative to adolescent rats.

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High-fat diet alters the dopamine and opioid systems: effects across development

Cited by 29 publications

References 64 publications

Methylphenidate prevents high-fat diet (HFD)-induced learning/memory impairment in juvenile mice

Methylphenidate prevents high-fat diet (HFD)-induced learning/memory impairment in juvenile mice

Developmental regulation of fear memories by an obesogenic high-saturated fat/high-sugar diet

Early maturational emergence of adult-like emotional reactivity and anxiety after brief exposure to an obesogenic diet

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