Increased intake of energy-dense diet and negative energy balance in a mouse model of chronic psychosocial defeat

Coccurello, Roberto; Romano, Adele; Giacovazzo, Giacomo; Tempesta, Bianca; Fiore, M.; Giudetti, Anna Maria; Marrocco, Ilaria; Altieri, Fabio; Moles, Anna; Gaetani, Silvana

doi:10.1007/s00394-017-1434-y

Cited by 17 publications

(25 citation statements)

References 78 publications

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“…Here, the increase of expression of mitochondrial UCP-1 proteins found in CPD mice (Fig. 4) provides the molecular basis for the increased thermogenesis previously observed in defeated animals (18).…”

Section: Discussionsupporting

confidence: 60%

“…Nevertheless, type and duration of stress can determine different stress-induced consequences on energy balance. We recently described a murine model of chronic psychosocial stress associated with the overconsumption of a fat-enriched diet (18). In this model, stress exposure with a concomitant HFD intake did not induce body-weight gain or eWAT accumulation but rather induced an increased iBAT depot and higher energy expenditure (18).…”

Section: Discussionmentioning

confidence: 99%

“…UCP-1 is an important protein able to regulate thermogenesis through the dissipation of the proton gradient that is generated across the inner mitochondrial membrane during the respiratory processes (43). Our previous study on CPD mice demonstrated an increase of iBAT pad in CPD mice consuming either the CD or the HFD and a concomitant increase of their resting energy expenditure, both aspects under a sympathetic regulatory tone (18). Here, the increase of expression of mitochondrial UCP-1 proteins found in CPD mice (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…Animals, diets, and the chronic psychosocial stress model Sexually naive, 60-d-old, male C57/BL6 mice were purchased from Charles River Laboratories (Calco, Italy). NMR1 mice, born and reared at the Institute of Cell Biology and Neurobiology (IBCN-CNR) of Rome, were used as intruders in the stress model of chronic psychosocial defeat (18). The experiments were conducted in accordance with Italian National Laws (DL 116/92), with the European Communities Council Directive of November 24, 1986 (86/609/EEC) and the Guide for the Care and Use of Laboratory Animals (National Institutes of Health, Bethesda, MD, USA).…”

Section: Methodsmentioning

confidence: 99%

“…The CPD model was based on a previously described protocol (18), in which C57BL/6J mice from both diet groups were randomly assigned to the unstressed (Un) mice or to the stressed (CPD) group. Un mice were housed in pairs and left undisturbed in their home cage for 24 d. Each CPD mouse was forced, for the same period, to daily sessions of physical interaction and to constant olfactory, auditory, and visual contact with a dominant NMR1 mouse.…”

Section: Methodsmentioning

confidence: 99%

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Chronic psychosocial defeat differently affects lipid metabolism in liver and white adipose tissue and induces hepatic oxidative stress in mice fed a high‐fat diet

et al. 2018

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It is widely accepted that chronic stress may alter the homeostatic mechanisms of body weight control. In this study, we followed the metabolic changes occurring in mice when chronic stress caused by psychosocial defeat (CPD) is associated with ad libitum exposure to a palatable high-fat diet (HFD). In this model, CPD mice consumed more HFD than unstressed (Un) mice without gaining body weight. We focused on metabolic processes involved in weight control, such as de novo lipogenesis (DNL), fatty acid β-oxidation (FAO), and thermogenesis. The activity and expression of DNL enzymes were reduced in the liver and white adipose tissue of mice consuming the HFD. Such effects were particularly evident in stressed mice. In both CPD and Un mice, HFD consumption increased the hepatic expression of the mitochondrial FAO enzyme carnitine palmitoyltransferase-1. In the liver of mice consuming the HFD, stress exposure prevented accumulation of triacylglycerols; however, accumulation of triacylglycerols was observed in Un mice under the same dietary regimen. In brown adipose tissue, stress increased the expression of uncoupling protein-1, which is involved in energy dissipation, both in HFD and control diet-fed mice. We consider increased FAO and energy dissipation responsible for the antiobesity effect seen in CPD/HFD mice. However, CPD associated with HFD induced hepatic oxidative stress.-Giudetti, A. M., Testini, M., Vergara, D., Priore, P., Damiano, F., Gallelli, C. A., Romano, A., Villani, R., Cassano, T., Siculella, L., Gnoni, G. V., Moles, A., Coccurello, R., Gaetani, S. Chronic psychosocial defeat differently affects lipid metabolism in liver and white adipose tissue and induces hepatic oxidative stress in mice fed a high-fat diet.

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Section: Discussionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Chronic psychosocial defeat differently affects lipid metabolism in liver and white adipose tissue and induces hepatic oxidative stress in mice fed a high‐fat diet

et al. 2018

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Measures of Food Intake, Body Weight Gain, and Energy Efficiency in Mice

Ballard,

Cazarin

2022

Basic Protocols in Foods and Nutrition

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Loss of P2X7 receptor function dampens whole body energy expenditure and fatty acid oxidation

Giacovazzo

Apolloni

Coccurello

2018

Purinergic Signalling

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The established role of ATP-responsive P2X7 receptor in inflammatory, neurodegenerative, and immune diseases is now expanding to include several aspects of metabolic dysregulation. Indeed, P2X7 receptors are involved in β cell function, insulin secretion, and liability to diabetes, and loss of P2X7 function may increase the risk of hepatic steatosis and disrupt adipogenesis. Recently, body weight gain, abnormal lipid accumulation, adipocyte hyperplasia, increased fat mass, and ectopic fat distribution have been found in P2X7 KO mice. Here, we hypothesized that such clinical picture of dysregulated lipid metabolism might be the result of altered in vivo energy metabolism. By indirect calorimetry, we assessed 24 h of energy expenditure (EE) and respiratory exchange ratio (RER) as quotient of carbohydrate to fat oxidation in P2X7 KO mice. Moreover, we assessed the same parameters in aged-matched WT counterparts that underwent a 7-day treatment with the P2X7 antagonist A804598. We found that loss of P2X7 function elicits a severe decrease of EE that was less pronounced in A804598-treated mice. In parallel, P2X7KO mice show a drastic increase of RER, thus indicating the occurrence of a greater ratio of carbohydrate to fat oxidation. Decreased EE and fat oxidation is predictive of body weight gain, which was here confirmed. Taken together, our data provide evidence that P2X7 loss of function produces defective energy homeostasis that, together with disrupted adipogenesis, might help to explain accumulation of adipose tissue and contribute to disclose the potential role of P2X7 in metabolic diseases.

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Increased intake of energy-dense diet and negative energy balance in a mouse model of chronic psychosocial defeat

Cited by 17 publications

References 78 publications

Chronic psychosocial defeat differently affects lipid metabolism in liver and white adipose tissue and induces hepatic oxidative stress in mice fed a high‐fat diet

Chronic psychosocial defeat differently affects lipid metabolism in liver and white adipose tissue and induces hepatic oxidative stress in mice fed a high‐fat diet

Measures of Food Intake, Body Weight Gain, and Energy Efficiency in Mice

Loss of P2X7 receptor function dampens whole body energy expenditure and fatty acid oxidation

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