Altered behavior of adult obese rats by monosodium l-glutamate neonatal treatment is related to hypercorticosteronemia and activation of hypothalamic ERK1 and ERK2

Guimarães, Ernesto da Silveira Goulart; Júnior, Luiz Carlos de Caires; Musso, Camila Manso; Almeida, Mariana Macedo de; Gonçalves, C. F.; Pettersen, Klaus G.; Paes, Santiago Tavares; García, Raúl; Mathias, Paulo Cézar de Freitas; Torrezan, Rosana; Júnior, Carlos Alberto Mourão; Andreazzi, Ana Eliza

doi:10.1179/1476830515y.0000000004

Cited by 11 publications

(8 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TFA+MSG caused impairment in locating the hidden platform in the Morris Water Maze (MWM), showing a reduction in spatial cognition. Similar results were found by Guimarães et al ( 2017 ) using the novel object recognition memory test in adult rats injected with MSG subcutaneously during the first 5 days of life to induce obesity. In adolescent animals, various authors also evidenced the relationship between juvenile HFD and spatial cognitive deficits (Boitard et al, 2012 ; Wang et al, 2015 ).…”

Section: Effects Of Obesity On Cognitive Functions and Moodsupporting

confidence: 89%

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

et al. 2018

View full text Add to dashboard Cite

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.

show abstract

Section: Effects Of Obesity On Cognitive Functions and Moodsupporting

confidence: 89%

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

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Vagotomy decreased high insulin secretion induced in MSG-obese rats [ 96 ]. Although still widely used in lesion-induced obesity models [ 97 , 98 , 99 , 100 , 101 , 102 ], MSG-induced damage is not limited to distinct hypothalamic nuclei as it also penetrates the brain on other sites of circumventricular organs, e.g., subfornical organ and area prostrema, as well as eyes and pituitary [ 91 , 92 , 103 , 104 , 105 , 106 ]. In addition, MSG-induced obesity is not associated with hyperphagia [ 88 ].…”

Section: Studying Hypothalamic Obesity In Ratsmentioning

confidence: 99%

Hypothalamic Obesity in Craniopharyngioma Patients: Disturbed Energy Homeostasis Related to Extent of Hypothalamic Damage and Its Implication for Obesity Intervention

Roth

2015

JCM

View full text Add to dashboard Cite

Hypothalamic obesity (HO) occurs in patients with tumors and lesions in the medial hypothalamic region. Hypothalamic dysfunction can lead to hyperinsulinemia and leptin resistance. This review is focused on HO caused by craniopharyngiomas (CP), which are the most common childhood brain tumors of nonglial origin. Despite excellent overall survival rates, CP patients have substantially reduced quality of life because of significant long-term sequelae, notably severe obesity in about 50% of patients, leading to a high rate of cardiovascular mortality. Recent studies reported that both hyperphagia and decreased energy expenditure can contribute to severe obesity in HO patients. Recognized risk factors for severe obesity include large hypothalamic tumors or lesions affecting several medial and posterior hypothalamic nuclei that impact satiety signaling pathways. Structural damage in these nuclei often lead to hyperphagia, rapid weight gain, central insulin and leptin resistance, decreased sympathetic activity, low energy expenditure, and increased energy storage in adipose tissue. To date, most efforts to treat HO have shown disappointing long-term success rates. However, treatments based on the distinct pathophysiology of disturbed energy homeostasis related to CP may offer options for successful interventions in the future.

show abstract

“…However, this increased lipid accumulation also depends, in addition to the excess of glucocorticoids, of the state of insulin resistance and decreased growth hormone (GH) levels [73]. In our study, all these changed levels hormones are present in MSG-model [26, 74–76], which could effectively induce to visceral lipid tissue accumulation. In addition, due to a major density of the glucocorticoid receptors are found in visceral than in other adipose tissues, is expected that the lipid-accumulating effect of cortisol would be more pronounced in visceral than in other fat areas [71].…”

Section: Discussionmentioning

confidence: 78%

Lipectomy associated to obesity produces greater fat accumulation in the visceral white adipose tissue of female compared to male rats

Pimenta

Tose

Waichert³

et al. 2019

Lipids Health Dis

View full text Add to dashboard Cite

BackgroundMobility of fat deposited in adipocytes among different fatty territories can play a crucial role in the pathogenesis of obesity-related diseases. Our goal was to investigate which of the remaining fat pads assume the role of accumulating lipids after surgical removal of parietal WAT (lipectomy; LIPEC) in rats of both sexes displaying MSG-induced obesity.MethodsThe animals entered the study straight after birth, being separated according to gender and randomly divided into CON (control, saline-treated) and MSG (monosodium glutamate-treated) groups. Next, the animals underwent LIPEC or sham-operated surgery (SHAM). Obesity was induced by the injection of MSG (4 mg/g/day) during neonatal stage (2nd to 11th day from birth). LIPEC was performed on the 12th week, consisting in the withdrawal of parietal WAT. On the 16th week, the following WATs were isolated and collected: peri-epididymal-WAT (EP-WAT); parametrial-WAT (PM-WAT); omental-WAT (OM-WAT); perirenal-WAT (PR-WAT) and retroperitoneal-WAT (RP-WAT).ResultsThe adiposity index was significantly increased in both male (3.2 ± 0.2** vs 1.8 ± 0.1) and female (4.9 ± 0.7* vs 2.6 ± 0.3) obese rats compared to their respective control groups. LIPEC in obese animals produced fat accumulation in visceral fat sites in a more accentuated manner in female (3.6 ± 0.3** vs 2.8 ± 0.3 g/100 g) rather than in male (1.8 ± 0.2* vs 1.5 ± 0.1 g/100 g) rats compared to obese non-lipectomized animals. Among the visceral WATs, the greater differences were observed between gonadal WATs of obese lipectomized rats, with higher accumulation having been observed in PM-WAT (2.8 ± 0.3* vs 2.1 ± 0.2 g/100 g) rather than in EP-WAT (1.0 ± 0.1 ± 0.9 ± 0.1 g/100 g) when compared to obese non-lipectomized animals.ConclusionsThe results of the present study led us to conclude that obesity induced by MSG treatment occurs differently in male and female rats. When associated with parietal LIPEC, there was a significant increase in the deposition of visceral fat, which was significantly higher in obese female rats than in males, indicating that fat mobility among WATs in lipectomized-obese rats can occur more expressively in particular sites of remaining WATs.

show abstract

Altered behavior of adult obese rats by monosodium l-glutamate neonatal treatment is related to hypercorticosteronemia and activation of hypothalamic ERK1 and ERK2

Abstract: Both treatments induced obesity but only Ob-MSG showed altered behavioral parameters, which is related to increased concentration of corticosterone and hypothalamic ERK1 and 2 activation.

Cited by 11 publications

References 37 publications

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

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

Hypothalamic Obesity in Craniopharyngioma Patients: Disturbed Energy Homeostasis Related to Extent of Hypothalamic Damage and Its Implication for Obesity Intervention

Lipectomy associated to obesity produces greater fat accumulation in the visceral white adipose tissue of female compared to male rats

Contact Info

Product

Resources

About