The effects of high fat diet on the basal activity of the hypothalamus–pituitary–adrenal axis in mice

Auvinen, Hanna E.; Romijn, Johannes A.; Biermasz, Nienke R.; Pijl, Hanno; Havekes, Louis M.; Smit, Johannes W. A.; Rensen, Patrick C.N.; Pereira, Alberto M.

doi:10.1530/joe-12-0056

Cited by 53 publications

(48 citation statements)

References 38 publications

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“…model) suggests a similar habituation to the SSS effect in rodents (Auvinen et al, 2011;Ryan et al, 2012). Moreover, rats submitted to footshock stress decreased the intake of commercial chow, but kept unaltered the intake of comfort food (Ortolani et al, 2011).…”

Section: Q4mentioning

confidence: 77%

Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis

Бажан¹,

Zelena²

2013

Brain Research Bulletin

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a b s t r a c tThe prevalence of obesity is increasing worldwide with serious consequences such as diabetes mellitus type 2 and cardiovascular diseases. Emotional stress is considered to be one of the main reasons of obesity development in humans. However, there are some contradictory results, which should be addressed. First of all stress induces anorexia, but not overeating in laboratory animals. Glucocorticoids, the effector molecules of the hypothalamo-pituitary-adrenocortical (HPA) axis stimulate and stress inhibits food intake. It is also not clear if stress is diabetogenic or an antidiabetogenic factor. The review will discusses these issues and the involvement of the whole HPA axis and its separate molecules (glucocorticoids, adrenocorticotropin, corticotropin-releasing hormone) in food intake regulation under stress.

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Section: Q4mentioning

confidence: 77%

Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis

Бажан¹,

Zelena²

2013

Brain Research Bulletin

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“…Reduced CRF-R1 levels in the amygdala may be a compensatory response to increased amygdalar CRF levels that are reportedly elevated by long-term high-fat feeding. 56 Indeed, increased CRF mRNA and protein levels are associated with loss of CRF-R1 function. 57,58 Although amygdalar CRF-R1 is implicated in the anxiogenic effects of intermittent HFD withdrawal, 19 we did not see any effect of withdrawal on CRF-R1 protein levels and speculate that this may be due to the later time point (Day 3) tissue was analyzed following withdrawal.…”

Section: Discussionmentioning

confidence: 99%

Adaptations in brain reward circuitry underlie palatable food cravings and anxiety induced by high-fat diet withdrawal

2012

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OBJECTIVE:To identify the emotional and motivational processes that reinstate palatable food intake following removal of high-fat diet (HFD) and associated neuroadaptations tied to neurochemical and behavioural changes underlying dopaminergic function. METHODS: Adult male C57Bl6 mice were placed on a HFD (58% kcal fat) or ingredient-matched, low-fat diet (LFD; 11% kcal fat) for 6 weeks. At the end of diet-regimen mice were either maintained on their respective diets, or HFD and LFD were replaced with normal chow (withdrawal). Effort-based operant responding for sucrose and high-fat food rewards was measured along with basal and stress-induced corticosterone levels and anxiety (elevated-plus maze). Protein levels for tyrosine hydroxylase (TH), corticosterone releasing factor type 1 receptor (CRF-R1), brain-derived neurotrophic factor (BDNF), phospho-CREB (pCREB) and DFosB (truncated splice variant of FosB) were assessed in the amygdala, nucleus accumbens (NAc) and ventral tegmental area (VTA) via western immunoblotting. RESULTS: Six weeks of HFD resulting in significant weight gain elicited sucrose anhedonia, anxiety-like behaviour and hypothalamic-pituitary-adrenocortical axis (HPA) hypersensitivity to stress. Withdrawal from HFD but not LFD-potentiated anxiety and basal corticosterone levels and enhanced motivation for sucrose and high-fat food rewards. Chronic high-fat feeding reduced CRF-R1 and increased BDNF and pCREB protein levels in the amygdala and reduced TH and increased DFosB protein in NAc and VTA. Heightened palatable food reward in mice withdrawn from HFD coincided with increased BDNF protein levels in NAc and decreased TH and pCREB expression in the amygdala. CONCLUSION: Anhedonia, anxiety and sensitivity to stressors develops during the course of HFD and may have a key role in a vicious cycle that perpetuates high-fat feeding and the development of obesity. Removal of HFD enhances stress responses and heightens vulnerability for palatable foods by increasing food-motivated behaviour. Lasting changes in dopamine and plasticityrelated signals in reward circuitry may promote negative emotional states, overeating and palatable food relapse.

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“…Data on high fat diet-induced corticosterone concentrations are highly controversial: there are reports on increase, decrease or unchanged levels (see [29] for review). Here we found a tendency for FatED-induced adrenocortical hyperactivity in both genotypes.…”

Section: Discussionmentioning

confidence: 99%

The fractalkine/Cx3CR1 system is implicated in the development of metabolic visceral adipose tissue inflammation in obesity

Polyák

Ferenczi

Dénes

et al. 2014

Brain, Behavior, and Immunity

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Diet-induced obesity and related peripheral and central inflammation are major risk factors for metabolic, neurological and psychiatric diseases. The chemokine fractalkine (Cx3CL1) and its receptor Cx3CR1 play a pivotal role in recruitment, infiltration and proinflammatory polarization of leukocytes and micoglial cells, however, the role of fractalkine signaling in the development of metabolic inflammation is not fully resolved. To address this issue, fractalkine receptor deficient (Cx3CR1 gfp/gfp) mice were exposed to normal or fat-enriched diet (FatED) for 10 weeks and physiological-, metabolic-and immune parameters were compared to those animals in which the fractalkine signaling is maintained by the presence of one functioning allele (Cx3CR1 +/gfp). Mice with intact fractalkine signaling develop obesity characterized by increased epididymal white fat depots and mild glucose intolerance, recruit leukocytes into the visceral adipose tissue and display increased expression of subset of pro-and anti-inflammatory cytokines when exposed to fat-enriched diet. By contrast, Cx3CR1-deficient (gfp/gfp) mice gain significantly less weight on fat-enriched diet and have smaller amount of white adipose tissue (WAT) in the visceral compartment than heterozygote controls. Furthermore, Cx3CR1 gfp/gfp mice fed a fat-enriched diet do not develop glucose intolerance, recruit proportionally less number of gfp-positive cells and express significantly less MCP-1, IL-1a and TNFa in the WAT than control animals with fat-enriched diet induced obesity. Furthermore, heterozygote obese, but not fractalkine receptor deficient mice express high levels of anti-inflammatory IL-10 and arginase1 markers in the visceral fat. The effect of fat-enriched diet on cytokine expression pattern was specific for the WAT, as we did not detect significant elevation of interleukin-1, tumor necrosis factor-alpha and monocyte chemoatracting protein (MCP-1) expression in the liver or in the hypothalamus in either genotype. These results highlight the importance of fractalkine signaling in recruitment and polarization of adipose tissue immune cells and identify fractalkine as a target to fight obesity-induced inflammatory complications.

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The effects of high fat diet on the basal activity of the hypothalamus–pituitary–adrenal axis in mice

Cited by 53 publications

References 38 publications

Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis

Food-intake regulation during stress by the hypothalamo-pituitary-adrenal axis

Adaptations in brain reward circuitry underlie palatable food cravings and anxiety induced by high-fat diet withdrawal

The fractalkine/Cx3CR1 system is implicated in the development of metabolic visceral adipose tissue inflammation in obesity

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