Metabolic markers following beta-adrenoceptor agonist infusion in footshock-stressed rats

Verago, J.L.; Kassisse, Dora Maria Grassi; Spadari-Bratfisch, Regina Célia

doi:10.1590/s0100-879x2001000900014

Cited by 21 publications

(24 citation statements)

References 34 publications

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“…As previously reported [10,11] footshock-stress caused a glucose intolerance and increase corticosterone serum levels, in addition in the present study we demonstrated that the ingestion for 8 weeks of normolipidic diet rich in fish oil prevented these effects.…”

Section: Discussionsupporting

confidence: 90%

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Fish oil consumption prevents glucose intolerance and hypercorticosteronemy in footshock-stressed rats

et al. 2011

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BackgroundEnvironmental stress plays an important role in the development of glucose intolerance influencing lipid and glucose metabolism through sympathetic nervous system, cytokines and hormones such as glucocorticoids, catecholamines and glucagon. Otherwise, fish oil prevents glucose intolerance and insulin resistance. Although the mechanisms involved are not fully understood, it is known that sympathetic and HPA responses are blunted and catecholamines and glucocorticoids concentrations can be modulated by fish consumption. The aim of the present study was to evaluate whether fish oil, on a normal lipidic diet: 1) could prevent the effect of footshock-stress on the development of glucose intolerance; 2) modified adiponectin receptor and serum concentration; and 3) also modified TNF-α, IL-6 and interleukin-10 (IL-10) levels in adipose tissue and liver. The study was performed in thirty day-old male Wistar randomly assigned into four groups: no stressed (C) and stressed (CS) rats fed with control diet, and no stressed (F) and stressed (FS) rats fed with a fish oil rich diet. The stress was performed as a three daily footshock stress sessions.ResultsBody weight, carcass fat and protein content were not different among groups. FS presented a reduction on the relative weight of RET. Basal serum glucose levels were higher in CS and FS but 15 min after glucose load just CS remained with higher levels than other groups. Serum corticosterone concentration was increased in CS, this effect was inhibited in FS. However, 15 min after footshock-stress, corticosterone levels were similar among groups. IL-6 was increased in EPI of CS but fish oil consumption prevented IL-6 increase in FS. Similar levels of TNF-α and IL-10 in RET, EPI, and liver were observed among groups. Adipo R1 protein concentration was not different among groups. Footshock-stress did not modify AdipoR2 concentration, but fish oil diet increases AdipoR2 protein concentration.ConclusionsFootshock-stress promotes glucose intolerance associated to corticosterone serum level and epididymal white adipose tissue IL-6 concentration increase. The fish oil consumption by stressed rats normalized the stress responses. These results suggested that fish oil intake could be useful to minimize or prevent the development of diseases associated to the stress.

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Section: Discussionsupporting

confidence: 90%

“…These results demonstrated that foot-shock stress could be a useful model for studying glucose intolerance and insulin resistance [10,11]. …”

Section: Introductionmentioning

confidence: 99%

Fish oil consumption prevents glucose intolerance and hypercorticosteronemy in footshock-stressed rats

et al. 2011

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“…It is possible that once UV emissions are bound to behavioral responses of stress, both neonatal capsaicin treatment and OVA sensitization probably have no effect on emotional behavior. Furthermore, the high serum corticosterone levels detected on samples collected from stressed rats seem compatible with previously published data [36,37] and also demonstrate the efficiency of the stress model used.…”

Section: Discussionsupporting

confidence: 90%

Effects of Stress and Neuropeptides on Airway Responses in Ovalbumin-Sensitized Rats

Portela¹,

Leick-Maldonado

Kasahara

et al. 2007

Neuroimmunomodulation

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Objective: The aim of this study was to investigate the influence of stress and neuropeptides on airway responses in ovalbumin (OVA)-sensitized rats. Methods: Three experimental conditions were employed: neonatal capsaicin treatment, foot shock stress and OVA sensitization. For neuropeptide depletion, male Wistar rats were neonatally treated with capsaicin (50 mg/kg) or with control solution 2 days after birth. Ninety days later, they were injected with OVA and aluminum hydroxide (ED0) or no injection. Thereafter, rats of the stressed groups were individually placed in a shuttle box where they received 50 mild escapable foot shocks/day; the stressful stimuli were repeated until ED14, when the animals received OVA aerosol. Pulmonary mechanic function was measured before and after OVA challenge in anesthetized and mechanically ventilated rats. Results: Data on ultrasonic vocalizations and corticosterone showed high levels of anxiety in stressed animals. As expected, a significant increment in airway elastance and resistance after the OVA challenge was found in sensitized rats compared to non-sensitized ones. Capsaicin treatment decreased the values of elastance in sensitized and non-stressed rats; however, after the OVA challenge, elastance was increased in stressed animals. No differences were found in the levels of resistance among sensitized and non-stressed rats; however, a reduced increment in resistance was verified in capsaicin-treated, stressed animals. Conclusions: Our results suggest that neurokinin depletion and stress may affect smooth muscle tonus around the airways during an anaphylactic reaction. These data suggest that stress and neuropeptides play a significant role in pulmonary function in OVA-sensitized rats.

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“…The bars indicate the means ± S.E.M. example, it has been reported that blood glucose level is significantly increased in foot shock stress model (Tajima et al, 1996;Verago et al, 2001;Márquez et al, 2002;Amano et al, 2007). On the other hand, the alteration of blood glucose level in emotional stress has not been well characterized.…”

Section: Discussionmentioning

confidence: 96%

The regulation of blood glucose level in physical and emotional stress models: Possible involvement of adrenergic and glucocorticoid systems

Sim¹,

Park²,

Kang³

et al. 2010

Arch. Pharm. Res.

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This study was done to determine the effect of stress on blood glucose regulation in ICR mice. The stress was induced by the electrical foot shock-witness model. Blood glucose level was found to be increased in the electrical foot shock-induced physical stress group. Furthermore, the blood glucose levels were also elevated in the emotional stress group in both physical and emotional stress groups. The blood glucose level reached maximum 30 min after stress stimulation and returned to normal level 2 h after stress stimulation in both physical and emotional stress groups. Subsequently, we observed that intraperitoneal injection of phentolamine (an α1-adrenergic receptor antagonist), yohimbine (an α2-adrenergic receptor antagonist) or RU486 (a glucocorticoid receptor blocker) significantly inhibited blood glucose level induced by both physical and emotional stress. The results of our study suggest that physical and emotional stress increases blood glucose level via activation of adrenergic and glucocorticoid system.

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Metabolic markers following beta-adrenoceptor agonist infusion in footshock-stressed rats

Cited by 21 publications

References 34 publications

Fish oil consumption prevents glucose intolerance and hypercorticosteronemy in footshock-stressed rats

Fish oil consumption prevents glucose intolerance and hypercorticosteronemy in footshock-stressed rats

Effects of Stress and Neuropeptides on Airway Responses in Ovalbumin-Sensitized Rats

The regulation of blood glucose level in physical and emotional stress models: Possible involvement of adrenergic and glucocorticoid systems

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