Hypercaloric diet modulates effects of chronic stress: a behavioral and biometric study on rats

Oliveira, Carla de; Oliveira, Cristiano Aguiar de; Macedo, Isabel Cristina de; Quevedo, Alexandre Silva de; Filho, Paulo Ricardo Marques; Silva, Fernanda Ribeiro da; Vercelino, Rafael; Souza, Izabel Cristina Custodio de; Caumo, Wolnei; Torres, Iraci Lucena da Silva

doi:10.3109/10253890.2015.1079616

Cited by 23 publications

(12 citation statements)

References 55 publications

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“…We also observed reduced corticosterone levels in sickle mice with sickle diet and/or companionship. Since corticosterone is involved in stress response, this observation is consistent with reported stress-relieving effects of satisfying food 84 , 85 and social bonding 86 , 87 . Stress has been known for decades to enhance pain perception, especially in patients having chronic pain 88 – 91 .…”

Section: Discussionsupporting

confidence: 89%

Diet and companionship modulate pain via a serotonergic mechanism

Tran

Sagi

Jarrett

et al. 2021

Sci Rep

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Treatment of severe chronic and acute pain in sickle cell disease (SCD) remains challenging due to the interdependence of pain and psychosocial modulation. We examined whether modulation of the descending pain pathway through an enriched diet and companionship could alleviate pain in transgenic sickle mice. Mechanical and thermal hyperalgesia were reduced significantly with enriched diet and/or companionship. Upon withdrawal of both conditions, analgesic effects observed prior to withdrawal were diminished. Serotonin (5-hydroxytryptamine, 5-HT) was found to be increased in the spinal cords of mice provided both treatments. Additionally, 5-HT production improved at the rostral ventromedial medulla and 5-HT accumulated at the dorsal horn of the spinal cord of sickle mice, suggesting the involvement of the descending pain pathway in the analgesic response. Modulation of 5-HT and its effect on hyperalgesia was also investigated through pharmaceutical approaches. Duloxetine, a serotonin-norepinephrine reuptake inhibitor, showed a similar anti-nociceptive effect as the combination of diet and companionship. Depletion of 5-HT through p-chlorophenylalanine attenuated the anti-hyperalgesic effect of enriched diet and companionship. More significantly, improved diet and companionship enhanced the efficacy of a sub-optimal dose of morphine for analgesia in sickle mice. These findings offer the potential to reduce opioid use without pharmacological interventions to develop effective pain management strategies.

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Section: Discussionsupporting

confidence: 89%

Diet and companionship modulate pain via a serotonergic mechanism

Tran

Sagi

Jarrett

et al. 2021

Sci Rep

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“…ethological) circumstances, whereas the latter determines drug activity under stress-induced anxiety conditions. Although different types of stress trigger anxiety- and depression-like behaviours (Oliveira et al, 2015), the NSF method is designed to induce animal anxiety. Since the NSF test was conducted after an acute treatment, no depression should be developed in the animals (Harmer et al, 2017), ruling out the possibility that the observed different efficacy of PAM-2 is due to its antidepressant-like activity (Arias et al, 2015; Targowska-Duda et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

3-Furan-2-yl-N-p-tolyl-acrylamide, a highly selective positive allosteric modulator of α7 nicotinic receptors, produces anxiolytic-like activity in mice

et al. 2019

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Background: Several lines of investigations support the idea that nicotinic acetylcholine receptors modulate neuronal pathways involved in anxiety and depression. Aims: The purpose of this study was to determine whether 3-furan-2-yl-N-p-tolyl-acrylamide, a highly selective positive allosteric modulator of α7 nicotinic acetylcholine receptors, influences anxiety-like behaviour in mice, and to determine the modulatory activity of 3-furan-2-yl-N-p-tolyl-acrylamide on mice pretreated with either nicotine or selective α7-agonists (i.e. PNU-282987 or (2.4)-dimethoxybenzylidene anabaseine dihydrochloride). Methods: The elevated plus maze and novelty suppressed feeding tests were selected to evaluate 3-furan-2-yl-N-p-tolyl-acrylamide and other nicotinic ligands on anxiety-like behaviour in mice. Results: The results indicated that: (a) 3-furan-2-yl-N-p-tolyl-acrylamide induces anxiolytic-like activity at 0.5 (elevated plus maze) and 1.0 (novelty suppressed feeding) mg/kg, respectively, after acute treatment, whereas its efficacy is increased after chronic treatments (i.e. active at 0.1 mg/kg; elevated plus maze). This is the first time showing anxiolytic-like activity elicited by 3-furan-2-yl-N-p-tolyl-acrylamide, contrary to the lack of activity for PNU-120596 (0.1 mg/kg); (b) the anxiolytic-like activity of 0.5 mg/kg 3-furan-2-yl-N-p-tolyl-acrylamide is inhibited by methyllycaconitine, a selective α7-antagonist, suggesting that α7 nicotinic acetylcholine receptors are involved in this process; (c) 0.5 mg/kg 3-furan-2-yl-N-p-tolyl-acrylamide reverses the anxiogenic effects induced by 0.1 mg/kg nicotine but not by 10.0 mg/kg PNU-282987; and (d) inactive doses of both 3-furan-2-yl-N-p-tolyl-acrylamide (0.1 mg/kg) and (2.4)-dimethoxybenzylidene anabaseine dihydrochloride (1.0 mg/kg) produce anxiolytic-like effects, suggesting drug interactions, probably synergistic. Conclusions: Our findings indicated that anxiolytic-like activity is mediated by α7 nicotinic acetylcholine receptors, supporting the concept that these receptors modulate anxiety processes. The results indicating that the chronic treatment with 3-furan-2-yl-N-p-tolyl-acrylamide is more efficient than the acute treatment in eliciting anxiolytic-like activity, and that 3-furan-2-yl-N-p-tolyl-acrylamide reverses the anxiogenic effects induced by nicotine, might be of therapeutic importance during smoking cessation.

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“…Santos et al ( 2016 ) demonstrated that a high carbohydrate-containing diet administered for 12 weeks was anxiogenic and induced depressive symptoms after exposure to different stress paradigms. Chronic stress can also increase the consumption of food containing sugar and fat ingredients as a compensatory mechanism (comfort food) to reduce stress-related anxiety, which could lead to overeating and obesity long-term (Oliveira et al, 2015 ). In support of this hypothesis, other studies have shown that HFD administration to adult rats reduced anxiety (Leffa et al, 2015 ; McNeilly et al, 2015 ).…”

Section: Effects Of Obesity On Cognitive Functions and Moodmentioning

confidence: 99%

Interplay Between the Gut-Brain Axis, Obesity and Cognitive Function

et al. 2018

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Obesity continues to be one of the major public health problems due to its high prevalence and co-morbidities. Common co-morbidities not only include cardiometabolic disorders but also mood and cognitive disorders. Obese subjects often show deficits in memory, learning and executive functions compared to normal weight subjects. Epidemiological studies also indicate that obesity is associated with a higher risk of developing depression and anxiety, and vice versa. These associations between pathologies that presumably have different etiologies suggest shared pathological mechanisms. Gut microbiota is a mediating factor between the environmental pressures (e.g., diet, lifestyle) and host physiology, and its alteration could partly explain the cross-link between those pathologies. Westernized dietary patterns are known to be a major cause of the obesity epidemic, which also promotes a dysbiotic drift in the gut microbiota; this, in turn, seems to contribute to obesity-related complications. Experimental studies in animal models and, to a lesser extent, in humans suggest that the obesity-associated microbiota may contribute to the endocrine, neurochemical and inflammatory alterations underlying obesity and its comorbidities. These include dysregulation of the HPA-axis with overproduction of glucocorticoids, alterations in levels of neuroactive metabolites (e.g., neurotransmitters, short-chain fatty acids) and activation of a pro-inflammatory milieu that can cause neuro-inflammation. This review updates current knowledge about the role and mode of action of the gut microbiota in the cross-link between energy metabolism, mood and cognitive function.

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Hypercaloric diet modulates effects of chronic stress: a behavioral and biometric study on rats

Cited by 23 publications

References 55 publications

Diet and companionship modulate pain via a serotonergic mechanism

Diet and companionship modulate pain via a serotonergic mechanism

3-Furan-2-yl-N-p-tolyl-acrylamide, a highly selective positive allosteric modulator of α7 nicotinic receptors, produces anxiolytic-like activity in mice

Interplay Between the Gut-Brain Axis, Obesity and Cognitive Function

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