Differential control of glucoregulatory hormone response and glucose metabolism by NMDA and kainate

Yousef, Khalil A.; Tepper, Patrick G.; Molina, Patricia E.; Abumrad, Naji N.; Lang, Charles H.

doi:10.1016/0006-8993(94)90266-6

Cited by 24 publications

(8 citation statements)

References 32 publications

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“…In our study, the stimulatory effect was observed 5 min after injection, and the normal TSH levels did not recover at 60 min. Yousef et al [16]confirmed the stimulatory effect of NMDA or KA on corticosterone release. In our experiment conditions, the stimulatory effect of glutamatergic agonist on the release of hormones by peripheral gland (thyroid) was less than that observed with corticosterone, though the increase in serum T4 and T3 levels was induced at 30 min with both types of glutamate agonists.…”

Section: Discussionmentioning

confidence: 57%

Effect of Excitatory Amino Acids on Serum TSH and Thyroid Hormone Levels in Freely Moving Rats

Alfonso

Durán²,

Arufe³

2000

Horm Res Paediatr

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The actions of glutamate (L-Glu), and glutamate receptor agonists on serum thyroid hormones (T4 and T3) and TSH levels have been studied in conscious and freely moving adult male rats. The excitatory amino acids (EAA), L-Glu, N-methyl-D-aspartate (NMDA), kainic acid (KA) and domoic acid (Dom) were administered intraperitoneally. Blood samples were collected through a cannula implanted in the rats jugular 0–60 min after injection. Thyroid hormone concentrations were measured by enzyme immunoassay, and thyrotrophin (TSH) concentrations were determined by radioimmunoassay. The results showed that L-Glu (20 and 25 mg/kg) and NMDA (25 mg/kg) increased serum thyroxine (T4), triiodothyronine (T3) and TSH concentrations. Serum thyroid hormone levels increased 30 min after treatment, while serum TSH levels increased 5 min after i.p. administration, in both cases serum levels remained elevated during one hour. Injection of the non-NMDA glutamatergic agonists KA (30 mg/kg) and Dom (1 mg/kg) produced an increase in serum thyroid hormones and TSH levels. These results suggest the importance of EAAs in the regulation of hormone secretion from the pituitary-thyroid axis, as well as the importance of the NMDA and non-NMDA receptors in this stimulatory effect.

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Section: Discussionmentioning

confidence: 57%

Effect of Excitatory Amino Acids on Serum TSH and Thyroid Hormone Levels in Freely Moving Rats

Alfonso

Durán²,

Arufe³

2000

Horm Res Paediatr

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“…The lower IL-1␤ mRNA expression at 5 hr compared to 2 and 12 hr may reflect an inhibition of expression by sIL-1ra or icIL-1ra (Watson et al, 1995;Dinarello, 1996), or by circulating factors such as corticosteroids (Kern et al, 1988;Yousef et al, 1994;Dinarello, 1996;Kent et al, 1996). I.p.…”

Section: Discussionmentioning

confidence: 96%

“…I.p. administration of NMDA or kainic acid results in elevated levels of circulating ACTH and corticosterone (Yousef et al, 1994;Kent et al, 1996), which may cause an inhibition of IL-1␤ synthesis in a negative feedback fashion (Besedovsky et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

Increased expression of mRNA encoding interleukin-1? and caspase-1, and the secreted isoform of interleukin-1 receptor antagonist in the rat brain following systemic kainic acid administration

et al. 2000

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Kainic acid, an analogue of glutamate, injected systemically to rats evokes seizures that are accompanied by nerve cell damage primarily in the limbic system. In the present study, we have analyzed the temporal profile of the expression of the cytokines interleukin-1beta (IL-1beta) and IL-1 receptor antagonist (IL-1ra), and the related IL-1beta-converting enzyme (ICE/caspase-1), in different regions of the rat brain in response to peripheral kainic acid administration (10 mg/kg, i.p.). In situ hybridization histochemistry experiments revealed that IL-1beta mRNA-expressing cells, morphologically identified as microglial cells, were mainly localized to regions showing pronounced neuronal degeneration; hippocampus, thalamus, amygdala, and certain cortical regions. The strongest expression of IL-1beta mRNA was observed after 12 hr in these regions. A weak induction of the IL-1beta mRNA expression was observed already at 2 hr. Similar results were obtained by RT-PCR analysis, showing a significantly increased expression of IL-1beta mRNA in the hippocampus and amygdala after 12 hr. In addition, RT-PCR analysis revealed that IL-1ra mRNA, and specifically mRNA encoding the secreted isoform of IL-1ra (sIL-1ra), was strongly induced in the hippocampus and amygdala at 12 and 24 hr post-injection. RT-PCR analysis of mRNA encoding caspase-1 showed a significantly increased expression in the amygdala after 12 hr. In conclusion, in response to systemic kainic acid injection IL-1beta mRNA is rapidly induced and followed by induction of IL-1ra mRNA and caspase-1 mRNA, supporting a role of the IL-1 system in the inflammatory response during excitotoxic damage.

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“…7 In the present study, the levels of circulating insulin, glucagon, and corticosterone were manipulated by the administration of specific agonists, blockers, and antagonists in order to suppress the induction of hepatic and renal Glu-6-Pase and Phentolamine and propranolol as adrenergic blockers, cyclic somatostatin as a glucagon blocker, and exogenous insulin were used prior to hemorrhage or along with fluid resuscitation to accomplish this objective. It has been reported that adrenergic and glucagon blockers are effective in preventing the glucose production in endotoxic 8,9 and septic 10 rats, and insulin is known to suppress the Glu-6-Pase gene expression. 3 In this regard, our hypothesis is that fluid optimization, per se, following hemorrhage will not prevent the induction of Glu-6-Pase gene expression and hyperglycemia and, thus, pharmacologic agents will still be needed to correct the problem.…”

mentioning

confidence: 99%

Regulation of Liver and Kidney Glucose‐6‐phosphatase Gene Expression in Hemorrhage and Resuscitation

Maitra

Wang

el-Maghrabi

et al. 2000

Academic Emergency Medicine

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Abstract.The authors have recently demonstrated that increased gene expression of glucose-6-phosphatase (Glu-6-Pase) in hemorrhagic hypotension (HH) and following lactated Ringer's resuscitation (LR) is associated with a decrease in insulin and an increase in corticosterone concentrations. Objective: To evaluate the in-vivo role of hormones the authors used insulin (IN), phentolamine and propranolol (PP) as an adrenergic blocker, and cyclic somatostatin (CS) as a glucagon blocker to prevent the induction of Glu-6-Pase gene expression in liver and kidney following HH and LR. Methods: Hemorrhage was induced in fasted anesthetized rats, and the reduction of blood pressure to 40 mm Hg for a duration of 30 minutes was accomplished by withdrawal or infusion of shed blood. The resuscitated group underwent hemorrhage followed by fluid resuscitation with lactated Ringer's solution. Results: Neither PP nor CS treatment could block the induction of Glu-6-Pase messenger ribonucleic acid (mRNA) following either HH or LR. However, the administration of IN significantly prevented the increase of Glu-6-Pase mRNA level and activity in both liver and kidney following HH and LR. This was associated with a normalization of plasma glucose, corticosterone, and glucagon levels and glucose-6-phosphate concentrations in liver and kidney toward prehemorrhage levels. Conclusions: These results indicate that in-vivo treatment with insulin during hemorrhagic hypotension and resuscitation is capable of preventing the increase in Glu-6-Pase gene expression in liver and kidney responsible for the observed hyperglycemia.

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Differential control of glucoregulatory hormone response and glucose metabolism by NMDA and kainate

Cited by 24 publications

References 32 publications

Effect of Excitatory Amino Acids on Serum TSH and Thyroid Hormone Levels in Freely Moving Rats

Effect of Excitatory Amino Acids on Serum TSH and Thyroid Hormone Levels in Freely Moving Rats

Increased expression of mRNA encoding interleukin-1? and caspase-1, and the secreted isoform of interleukin-1 receptor antagonist in the rat brain following systemic kainic acid administration

Regulation of Liver and Kidney Glucose‐6‐phosphatase Gene Expression in Hemorrhage and Resuscitation

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