Thyrotropin-releasing hormone (TRH) reverses hyperglycemia in rat

Luo, Liqiang; Luo, John Zq; Jackson, Ivor M. D.

doi:10.1016/j.bbrc.2008.06.111

Cited by 10 publications

(3 citation statements)

References 24 publications

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“…Hyperglycemia and decreased β-cell sensitivity to blood glucose level owing to low T3 and T4 levels were reported in TRH-deficient mice (tertiary HT). Insulin deficiency associated with increased insulin resistance and the impairment of glucose utilization in peripheral tissues was identified as the probable mechanism [Luo et al, 2008]. A study on HT females revealed a link between TSH, insulin resistance, and serum lipid concentrations [Singh et al, 2010].…”

Section: Discussionmentioning

confidence: 99%

Bone Marrow-Derived Mesenchymal Stem Cells Ameliorate the Pancreatic Changes of Chemically Induced Hypothyroidism by Carbimazole in Male Rats

Arafa

Gouda

El-naseery

et al. 2018

Cells Tissues Organs

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We induced hypothyroidism (HT) in male rats through chronic oral administration of carbimazole and then tested whether an i.v. injection of rat bone marrow-derived mesenchymal stem cells (BM-MSCs) could ameliorate the HT-induced changes in pancreatic structure and function. The thyroid and pancreatic function tests, as well as total antioxidant capacity (TAC) and malondialdehyde (MDA) were estimated. The pancreatic structure was evaluated by hematoxylin and eosin (H&E) stain. Insulin protein and cleaved caspase-3 were detected immunohistochemically. The degree of apoptosis was assessed by TUNEL assay. The morphometric measurements were done by an image analyzer system and the obtained data were statistically analyzed. HT rats showed hyperglycemia associated with insulin deficiency, decreased TAC and increased MDA levels. H&E-stained sections showed that the pancreatic septa were infiltrated with acidophilic material. Some acini were vacuolated while others showed depleted acidophilia and dilated lumina. Spindle-shaped cells were accumulated within deformed islets in HT rats. The positive reaction with anti-cleaved caspase-3 was exclusively noted in the cytoplasm of islet cells with no immunostaining reaction in the acinar and ductal cells, whereas the positively stained nuclei with TUNEL were demonstrated in the islet and acinar cells. A significant increase in the apoptotic index % of both markers was detected. Injection of BM-MSCs in HT rats restored all biochemical indicators of disturbed pancreatic function to normal level and improved pancreatic structure, resulting in a clear septa and normal appearance of acini and islets. In conclusion, many of the significant structural and func tional pancreatic alterations detected in HT rats were ameliorated after the injection of BM-MSCs. These data demonstrate the ability of BM-MSCs to repair pancreatic disturbances. Further studies on humans are necessary to determine the potential clinical applications of BM-MSCs.

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Section: Discussionmentioning

confidence: 99%

Bone Marrow-Derived Mesenchymal Stem Cells Ameliorate the Pancreatic Changes of Chemically Induced Hypothyroidism by Carbimazole in Male Rats

Arafa

Gouda

El-naseery

et al. 2018

Cells Tissues Organs

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“…This hyperglycemia seen in the TRH-/- mice indicates that TRH is involved in the regulation of glucose homeostasis. Supporting this hypothesis, a recent study showed that TRH was able to reverse STZ-induced hyperglycemia by increasing pancreatic islet insulin content, preventing apoptosis, and potentially inducing islet regeneration [126]. Also, perinatal TRH treatment enhanced basal insulin secretion in STZ-induced animals of both sexes and partially restored the insulin response to glucose stimulation in females [127].…”

Section: Protrh Biosynthesis Processing and Trafficking To The Rementioning

confidence: 98%

Regulation of the hypothalamic Thyrotropin Releasing Hormone (TRH) neuron by neuronal and peripheral inputs

Nillni

2010

Frontiers in Neuroendocrinology

171

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The hypothalamic pituitary thyroid (HPT) axis plays a critical role in mediating changes in metabolism and thermogenesis. Thus, the central regulation of the thyroid axis by Thyrotropin Releasing Hormone (TRH) neurons in the paraventricular nucleus of the hypothalamus (PVN) is of key importance for the normal function of the axis under different physiological conditions including cold stress and changes in nutritional status. Before the TRH peptide becomes biologically active, a series of tightly regulated processes occur including the proper folding of the prohormone for targeting to the secretory pathway, its post-translational processing, and targeting of the processed peptides to the secretory granules near the plasma membrane of the cell ready for secretion. Multiple inputs coming from the periphery or from neurons present in different areas of the brain including the hypothalamus are responsible for the activation or inhibition of the TRH neuron and in turn affect the output of TRH and the set point of the axis.

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“…KN93 obtained from Calbiochem was dissolved in sterile DMSO 20 μl and injected intrathecally on 15, 17, 19 days after the STZ administration respectively. The dose of KN93 was chosen based on previous publications [ 14 ].…”

Section: Methodsmentioning

confidence: 99%

Inhibition of CaMKIV relieves streptozotocin-induced diabetic neuropathic pain through regulation of HMGB1

Zhao

Shen

et al. 2015

BMC Anesthesiol

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BackgroundThe pathogenesis of diabetic neuropathic pain is complicated and its underlying mechanisms remain unclear. Calmodulin-dependent protein kinases (CaMKs) IV (CaMKIV), one of CaMKs, regulates several transcription factors in pain mechanisms. High-mobility group box 1 (HMGB1) is a key mediator in diabetic neuropathic pain. This study aims to find the roles and mechanisms of CaMIV in diabetic neuropathic pain.MethodsDiabetic animal models were constructed by injecting with streptozotocin (STZ) intraperitoneally. They were randomly divided into seven groups (n = 6 per group): Naive, Normal Saline, STZ, STZ + Sham, STZ + DMSO and STZ + KN93 (an inhibitor of CaMKIV) (50 μg), STZ + KN93 (100 μg), which received KN93 (50 or 100 μg) intrathecally after the administration of STZ. Phospho-CaMKIV (pCaMKIV) and HMGB1 expression in rat dorsal root ganglion (DRG) and RAW264.7 cell line were measured by western blot. Distribution of pCaMKIV immune reactivity in different subpopulations of DRG neurons was measured by double-immunofluorescence staining.ResultsThe pCaMKIV and HMGB1 in DRG significantly increased after STZ administration, and pCaMKIV can regulate the expression of HMGB1 based on both cellular and animal models. Pretreatment with CaMKIV inhibitor attenuated STZ-induced mechanical allodynia and thermal hyperalgesia, as well as reduced HMGB1 expression in the DRG.ConclusionsThis study demonstrates that CaMKIV can relieve STZ-induced diabetic neuropathic pain. The mechanism of this function depended on the process: pCaMKIV localized in the nuclei of DRG neurons and regulated HMGB1 which was an important mediator of neuropathic pain. These findings reported CaMKIV may be a potential target or important node in relieving diabetic neuropathic pain.

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Thyrotropin-releasing hormone (TRH) reverses hyperglycemia in rat

Cited by 10 publications

References 24 publications

Bone Marrow-Derived Mesenchymal Stem Cells Ameliorate the Pancreatic Changes of Chemically Induced Hypothyroidism by Carbimazole in Male Rats

Bone Marrow-Derived Mesenchymal Stem Cells Ameliorate the Pancreatic Changes of Chemically Induced Hypothyroidism by Carbimazole in Male Rats

Regulation of the hypothalamic Thyrotropin Releasing Hormone (TRH) neuron by neuronal and peripheral inputs

Inhibition of CaMKIV relieves streptozotocin-induced diabetic neuropathic pain through regulation of HMGB1

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