Modulation of Plasma Glucose Levels by Thyrotropin-Releasing Hormone Administered Intracerebroventricularly in the Rat

Marubashi, Seijiro; Kunii, Yoshihiko; Tominaga, Makoto; Sasaki, Hideo

doi:10.1159/000125075

Cited by 18 publications

(15 citation statements)

References 17 publications

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“…As reported in other studies [3,4,7], the injection of TRH in intact rats elicited hyperglycemia with an increase in the secre tion of epinephrine and glucagon. The secretion of insulin is a finding which distinguishes it from other substrates such as neostigmine [1], 2-DG [2], bombesin [12], or corticotropin-releasing factor [13], since with each of the substances, insulin secretion is absent in the intact rat.…”

Section: Discussionsupporting

confidence: 79%

“…Therefore, it is not clear whether the relative contribution of each mechanism to CNS-mediated hy perglycemia is independent of neurochemical substances which stimulate the CNS or whether it depends on a specific CNSneuronal activity stimulated by specific neurochemical substan ces. For this study we selected TRH in trying to distinguish be tween these two possibilities, since it has been reported that TRH acts within the CNS to produce hyperglycemia associated with the secretion of glucagon and epinephrine (3,4,7].…”

Section: Discussionmentioning

confidence: 99%

“…In this study we further assessed this hypothesis by using thyrotropin-releasing hormone (TRH), a substance that reported by acts on the CNS to induce hyper glycemia associated with epinephrine and glucagon secretion in rats [3][4][5][6][7]. Since TRH has been reported *o stimulate not only the sympathetic outflow for epinephrine secretion [3,4] but also the parasympathetic outflow for insulin secretion [6][7][8], the mode of action of TRH on the peripheral glucoregulation may differ from that of either neostigmine or 2-DG. Received: April 10, 1990 Accepted after revision: November 6, 1990 We previously reported that brain signals are transmitted to the peripheral organs in hyperglycemia [1,2] by at least three mechanisms: CNS-induced hyperglycemia is mediated (1) via epinephrine secretion; (2) via the secretion of glucagon and the inhibition of insulin secretion, and (3) by a direct signal to the liver which increases the release of glucose.…”

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confidence: 99%

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confidence: 99%

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Relative Contribution of Nervous System and Hormones to Hyperglycemia Induced by Thyrotropin-Releasing Hormone in Fed Rats

Ishiguro¹,

Iguchi²,

Kunoh³

et al. 1991

Neuroendocrinology

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In a continuation of our studies on the mechanism of central nervous system induced hyperglycemia in the rat, we evaluated the relative contribution of a direct neural effect on the liver and of certain hormones to the hyperglycemia induced by administration of thyrotropin-releasing hormone (TRH). The findings were compared with those of a previous investigation using neostigmine or 2-deoxy-D-glucose. In the present study TRH was injected into the third cerebral ventricle of rats, and the concentrations of hepatic venous plasma glucose, immunoreactive glucagon, immunoreactive insulin, epinephrine, and norepinephrine, were measured. Four groups of animals were evaluated: (1) intact rats; (2) rats receiving an infusion of somatostatin with insulin via the femoral vein to inhibit glucagon secretion and to maintain the basal insulin level; (3) rats bilaterally adrenalectomized (ADX) to prevent epinephrine secretion, and (4) ADX rats administered an infusion of somatostatin and insulin. Evaluation of the areas under the glucose curves for the rats receiving somatostatin with insulin, ADX rats, and ADX rats receiving somatostatin with insulin showed values 202, 50, and 79% of those observed in intact animals. These observations suggest that TRH-induced hyperglycemia results from at least two effects: a direct neural effect on the liver including a suppressive effect of epinephrine on insulin secretion (contributing about 79% to the total hyperglycemic effect) and a direct effect of epinephrine on the liver (contributing about 21% to the total hyperglycemic effect). The response of the intact rats was approximately 50% of that seen in rats given an infusion of somatostatin with insulin, suggesting that the parasympathetic outflow affecting insulin secretion or other factors acted to suppress the total hyperglycemia in intact rats. This pattern differs qualitatively from that observed previously with neostigmine or 2-deoxy-D-glucose. These findings do not rule out the contribution of other humoral or neuroactive substances released directly from brain or peripheral nerves that might influence hepatic glucose secretion.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Relative Contribution of Nervous System and Hormones to Hyperglycemia Induced by Thyrotropin-Releasing Hormone in Fed Rats

Ishiguro¹,

Iguchi²,

Kunoh³

et al. 1991

Neuroendocrinology

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“…The central thyrotropin-releasing hormone (TRH) system is known to be involved in thermoregulation and glucose metabolism, two important adaptive systems during cold exposure, through both endocrine and neuronal pathways [1,2] . Indeed, TRH administration, either peripherally or centrally, has strong effects on glucose metabolism [3] and body temperature regulation [4][5][6] . In addition, animals with TRH deficiency exhibit impaired cold tolerance [7,8] and glucose metabolism [9] .…”

Section: Introductionmentioning

confidence: 99%

Administration of Thyrotropin-Releasing Hormone in the Hypothalamic Paraventricular Nucleus of Male Rats Mimics the Metabolic Cold Defense Response

et al. 2018

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Background: Cold exposure increases thyrotropin-releasing hormone (TRH) expression primarily in the hypothalamic paraventricular nucleus (PVN). The PVN is a well-known hypothalamic hub in the control of energy metabolism. TRH terminals and receptors are found on PVN neurons. We hypothesized that TRH release in the PVN plays an important role in the control of thermogenesis and energy mobilization during cold exposure. Methods: Male Wistar rats were exposed to a cold environment (4 ° C) or TRH retrodialysis in the PVN for 2 h. We compared the effects of cold exposure and TRH administration in the PVN on plasma glucose, corticosterone, and thyroid hormone concentrations, body temperature, locomotor activity, as well as metabolic gene expression in the liver and brown adipose tissue. Results: Cold exposure increased body temperature, locomotor activity, and plasma corticosterone concentrations, but blood glucose concentrations were similar to that of room temperature control animals. TRH administration in the PVN also promptly increased body temperature, locomotor activity and plasma corticosterone concentrations. However, TRH administration in the PVN markedly increased blood glucose concentrations and endogenous glucose production (EGP) compared to saline controls. Selective hepatic sympathetic or parasympathetic denervation reduced the TRH-induced increase in glucose concentrations and EGP. Gene expression data indicated increased gluconeogenesis in liver and lipolysis in brown adipose tissue, both after cold exposure and TRH administration. Conclusions: We conclude that TRH administration in the rat PVN largely mimics the metabolic and behavioral changes induced by cold exposure indicating a potential link between TRH release in the PVN and cold defense.

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Surgical pathology stage by American Joint Commission on Cancer criteria predicts patient survival after preoperative chemoradiation for localized gastric carcinoma

Rohatgi

Mansfield

Crane

et al. 2006

Cancer

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The JAK2 V617F mutation is responsible for the constitutive activation of the erythropoietin receptor signaling pathway in most cases of polycythemia vera (PV). The mutation has also been described in healthy people. As smoking may result in secondary polycythemia, the goal of this trial was to examine the effect of smoking on the prevalence of the JAK2 mutation and its correlation to erythrocytosis. The study was case–control. Hospitalized smokers (n = 81) and nonsmokers (n = 61) were recruited. Serum was drawn for complete blood count, erythropoietin, ferritin and venous blood gases. JAK2 mutation was analyzed by highly sensitive allele‐specific Quantitative Real Time PCR. The JAK2 mutation was found in 29/81 (35.8%) of smokers in comparison to only 9/61 (14.8%) of the control group (P = 0.007). The frequency of the mutation among smokers who were positive for the JAK2 mutation had a mean of 6.78 × 10−4 ± 1.08 × 10−3 vs. 1.51 × 10−4 ± 2.04 × 10−4 among nonsmokers (P = 0.027). Both frequencies are much lower than those found in PV. There was a medium correlation between older age and mutation frequency in nonsmokers (r= 0.67, P = 0.043). Hematocrit was higher in smokers (47.8 ± 6 vs. 41.7 ± 4.7, P < 0.0001), but no correlation was found to JAK2 mutation. In a cohort of hospitalized smokers and nonsmokers, JAK2 mutation was more prevalent and found in higher frequencies among smokers than nonsmokers. We suggest that accelerated erythropoiesis renders the cells susceptible to JAK2 mutation. Am. J. Hematol., 2011. © 2011 Wiley Periodicals, Inc.

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Modulation of Plasma Glucose Levels by Thyrotropin-Releasing Hormone Administered Intracerebroventricularly in the Rat

Cited by 18 publications

References 17 publications

Relative Contribution of Nervous System and Hormones to Hyperglycemia Induced by Thyrotropin-Releasing Hormone in Fed Rats

Relative Contribution of Nervous System and Hormones to Hyperglycemia Induced by Thyrotropin-Releasing Hormone in Fed Rats

Administration of Thyrotropin-Releasing Hormone in the Hypothalamic Paraventricular Nucleus of Male Rats Mimics the Metabolic Cold Defense Response

Surgical pathology stage by American Joint Commission on Cancer criteria predicts patient survival after preoperative chemoradiation for localized gastric carcinoma

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