scholarly journals A Protective Role of Arecoline Hydrobromide in Experimentally Induced Male Diabetic Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Indraneel Saha ◽  
Joydeep Das ◽  
Biswaranjan Maiti ◽  
Urmi Chatterji
Keyword(s):  
Glucose Transporter ◽  
Serum Insulin ◽  
Diabetic Rats ◽  
Receptor Expression ◽  
Cell Regeneration ◽  
Sialic Acid Content ◽  
Glucose Transporter 2 ◽  
Experimentally Induced

Objectives.Arecoline, the most potent and abundant alkaloid of betel nut, causes elevation of serum testosterone and androgen receptor expression in rat prostate, in addition to increase in serum insulin levels in rats, leading to insulin resistance and type 2 diabetes-like conditions. This study investigated the role of arecoline on the reproductive status of experimentally induced type 1 diabetic rats.Methods.Changes in the cellular architecture were analyzed by transmission electron microscopy. Blood glucose, serum insulin, testosterone, FSH, and LH were assayed. Fructose content of the coagulating gland and sialic acid content of the seminal vesicles were also analyzed.Results.Arecoline treatment for 10 days at a dose of 10 mg/kg of body weight markedly facilitatedβ-cell regeneration and reversed testicular and sex accessory dysfunctions by increasing the levels of serum insulin and gonadotropins in type 1 diabetic rats. Critical genes related toβ-cell regeneration, such as pancreatic and duodenal homeobox 1 (pdx-1) and glucose transporter 2 (GLUT-2), were found to be activated by arecoline at the protein level.Conclusion.It can thus be suggested that arecoline is effective in ameliorating the detrimental effects caused by insulin deficiency on gonadal and male sex accessories in rats with type 1 diabetes.

scholarly journals Role of peripheral 5-HT5A receptors in 5-HT-induced cardiac sympatho-inhibition in type 1 diabetic rats

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
José Ángel García-Pedraza ◽  
Oswaldo Hernández-Abreu ◽  
Asunción Morán ◽  
José Carretero ◽  
Mónica García-Domingo ◽  
...  
Keyword(s):  
Sympathetic Innervation ◽  
Stellate Ganglion ◽  
Receptor Activation ◽  
Diabetic Rats ◽  
Receptor Expression ◽  
Cardiac Sympathetic Innervation ◽  
Group I ◽  
Male Wistar Rats

Abstract 5-HT inhibits cardiac sympathetic neurotransmission in normoglycaemic rats, via 5-HT1B, 5-HT1D and 5-HT5A receptor activation. Since type 1 diabetes impairs the cardiac sympathetic innervation leading to cardiopathies, this study aimed to investigate whether the serotonergic influence on cardiac noradrenergic control is altered in type 1 diabetic rats. Diabetes was induced in male Wistar rats by streptozotocin (50 mg/kg, i.p.). Four weeks later, the rats were anaesthetized, pithed and prepared for producing tachycardic responses by electrical preganglionic stimulation (C7-T1) of the cardioaccelerator sympathetic outflow or i.v. noradrenaline bolus injections. Immunohistochemistry was performed to study 5-HT1B, 5-HT1D and 5-HT5A receptor expression in the stellate ganglion from normoglycaemic and diabetic rats. In the diabetic group, i) i.v. continuous infusions of 5-HT induced a cardiac sympatho-inhibition that was mimicked by the 5-HT1/5A agonist 5-carboxamidotryptamine (without modifying noradrenaline-induced tachycardia), but not by the agonists indorenate (5-HT1A), CP 93,129 (5-HT1B), PNU 142633 (5-HT1D), or LY344864 (5-HT1F); ii) SB 699551 (5-HT5A antagonist; i.v.) completely reversed 5-CT-induced cardiac sympatho-inhibition; and iii) 5-HT5A receptors were more expressed in the stellate ganglion compared to normoglycaemic rats. These results show the prominent role of the peripheral 5-HT5A receptors prejunctionally inhibiting the cardiac sympathetic drive in type 1 diabetic rats.

scholarly journals AMPK activation restores ischemic post-conditioning cardioprotection in STZ-induced type 1 diabetic rats: Role of autophagy

2017 ◽  
Vol 16 (3) ◽  
pp. 3648-3656 ◽  
Author(s):  
Bin Zhou ◽  
Yan Leng ◽  
Shao-Qing Lei ◽  
Zhong-Yuan Xia
Keyword(s):  
Diabetic Rats ◽  
Ampk Activation

scholarly journals Interleukin-1 Receptors Are Differentially Expressed in Normal and Psoriatic T Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Attila Bebes ◽  
Ferenc Kovács-Sólyom ◽  
Judit Prihoda ◽  
Róbert Kui ◽  
Lajos Kemény ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Interleukin 1 ◽  
Effector T Cells ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Healthy Control

This study was carried out to examine the possible role of interleukin-1 (IL-1) in the functional insufficiency of regulatory T cells in psoriasis, by comparing the expression of IL-1 receptors on healthy control and psoriatic T cells. Patients with moderate-to-severe chronic plaque psoriasis and healthy volunteers, matched in age and sex, were selected for all experiments. CD4+CD25−effector and CD4+CD25+CD127lowregulatory T cells were separated and used for the experiments. Expression of the mRNA of IL-1 receptors (IL-1R1, IL-1R2, and sIL-1R2) was determined by quantitative real-time RT-PCR. Cell surface IL-1 receptor expression was assessed by flow cytometry. Relative expression of the signal transmitting IL-1 receptor type 1 (IL-1R1) mRNA is higher in resting psoriatic effector and regulatory T cells, and activation induces higher IL-1R1 protein expression in psoriatic T cells than in healthy cells. Psoriatic regulatory and effector T cells express increased mRNA levels of the decoy IL-1 receptors (IL-1R2 and sIL-1R2) upon activation compared to healthy counterparts. Psoriatic T cells release slightly more sIL-1R2 into their surrounding than healthy T cells. In conclusion, changes in the expression of IL-1 receptors in psoriatic regulatory and effector T cells could contribute to the pathogenesis of psoriasis.

scholarly journals Deletion of theMen1Gene Prevents Streptozotocin-Induced Hyperglycemia in Mice

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Yuqing Yang ◽  
Haoren Wang ◽  
Xianxin Hua
Keyword(s):  
Mouse Model ◽  
Beta Cells ◽  
Multiple Endocrine Neoplasia ◽  
Glucose Transporter ◽  
Multiple Endocrine Neoplasia Type ◽  
Brdu Incorporation ◽  
Loss Of Function ◽  
Glucose Transporter 2 ◽  
Islet Size

Diabetes ultimately results from an inadequate number of functional beta cells in the islets of Langerhans. Enhancing proliferation of functional endogenous beta cells to treat diabetes remains underexplored. Here, we report that excision of theMen1gene, whose loss-of-function mutation leads to inherited multiple endocrine neoplasia type 1 (MEN1), rendered resistant to streptozotocin-induced hyperglycemia in a tamoxifen-inducible and temporally controlledMen1excision mouse model as well as in a tissue-specificMen1excision mouse model.Men1excision prevented mice from streptozotocin-induced hyperglycemia mainly through increasing the number of functional beta cells. BrdU incorporation by beta cells, islet size, and circulating insulin levels were significantly increased inMen1-excised mice. Membrane localization of glucose transporter 2 was largely preserved inMen1-excised beta cells, but not inMen1-expressing beta cells. Our findings suggest that repression of menin, a protein encoded by theMen1gene, might be a valuable means to maintain or increase the number of functional endogenous beta cells to prevent or ameliorate diabetes.

scholarly journals Functional role of sodium glucose transporter in high glucose-mediated angiotensin type 1 receptor downregulation in human proximal tubule cells

2012 ◽  
Vol 303 (5) ◽  
pp. F766-F774 ◽  
Author(s):  
Rekha Yesudas ◽  
Russell Snyder ◽  
Thomas Abbruscato ◽  
Thomas Thekkumkara
Keyword(s):  
Proximal Tubule ◽  
Glucose Uptake ◽  
High Glucose ◽  
Glucose Transporter ◽  
Glucose Transporters ◽  
Ang Ii ◽  
Angiotensin Type ◽  
Human Proximal Tubule

Previously, we have demonstrated human angiotensin type 1 receptor (hAT1R) promoter architecture with regard to the effect of high glucose (25 mM)-mediated transcriptional repression in human proximal tubule epithelial cells (hPTEC; Thomas BE, Thekkumkara TJ. Mol Biol Cell 15: 4347–4355, 2004). In the present study, we investigated the role of glucose transporters in high glucose-mediated hAT1R repression in primary hPTEC. Cells were exposed to normal glucose (5.5 mM) and high glucose (25 mM), followed by determination of hyperglycemia-mediated changes in receptor expression and glucose transporter activity. Exposure of cells to high glucose resulted in downregulation of ANG II binding (4,034 ± 163.3 to 1,360 ± 154.3 dpm/mg protein) and hAT1R mRNA expression (reduced 60.6 ± 4.643%) at 48 h. Under similar conditions, we observed a significant increase in glucose uptake (influx) in cells exposed to hyperglycemia. Our data indicated that the magnitude of glucose influx is concentration and time dependent. In euglycemic cells, inhibiting sodium-glucose cotransporters (SGLTs) with phlorizin and facilitative glucose transporters (GLUTs) with phloretin decreased glucose influx by 28.57 ± 0.9123 and 54.33 ± 1.202%, respectively. However, inhibiting SGLTs in cells under hyperglycemic conditions decreased glucose influx by 53.67 ± 2.906%, while GLUT-mediated glucose uptake remained unaltered (57.67 ± 3.180%). Furthermore, pretreating cells with an SGLT inhibitor reversed high glucose-mediated downregulation of the hAT1R, suggesting an involvement of SGLT in high glucose-mediated hAT1R repression. Our results suggest that in hPTEC, hyperglycemia-induced hAT1R downregulation is largely mediated through SGLT-dependent glucose influx. As ANG II is an important modulator of hPTEC transcellular sodium reabsorption and function, glucose-mediated changes in hAT1R gene expression may participate in the pathogenesis of diabetic renal disease.

scholarly journals Nutrient Induced Type 2 and Chemical Induced Type 1 Experimental Diabetes Differently Modulate Gastric GLP-1 Receptor Expression

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Olga Bloch ◽  
Efrat Broide ◽  
Gilad Ben-Yehudah ◽  
Dror Cantrell ◽  
Haim Shirin ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Experimental Diabetes ◽  
High Energy ◽  
Diabetic Rats ◽  
Receptor Expression ◽  
Glandular Stomach ◽  
Gastric Glands ◽  
Sd Rats ◽  
Neck Area

T2DM patients demonstrate reduced GLP-1 receptor (GLP-1R) expression in their gastric glands. Whether induced T2DM and T1DM differently affect the gastric GLP-1R expression is not known. This study assessed extrapancreatic GLP-1R system in glandular stomach of rodents with different types of experimental diabetes. T2DM and T1DM were induced inPsammomys obesus(PO) by high-energy (HE) diet and by streptozotocin (STZ) in Sprague Dawly (SD) rats, respectively. GLP-1R expression was determined in glandular stomach by RT PCR and immunohistomorphological analysis. The mRNA expression and cellular association of the GLP-1R in principal glands were similar in control PO and SD rats. However, nutrient and chemical induced diabetes resulted in opposite alterations of glandular GLP-1R expression. Diabetic PO demonstrated increased GLP-1R mRNA expression, intensity of cellular GLP-1R immunostaining, and frequency of GLP-1R positive cells in the neck area of principal glands compared with controls. In contrast, SD diabetic rats demonstrated decreased GLP-1 mRNA, cellular GLP-1R immunoreactivity, and frequency of GLP-1R immunoreactive cells in the neck area compared with controls. In conclusion, nutrient and chemical induced experimental diabetes result in distinct opposite alterations of GLP-1R expression in glandular stomach. These results suggest that induced T1DM and T2DM may differently modulate GLP-1R system in enteropancreatic axis.

scholarly journals THE ROLE OF STEM CELL INJECTION IN AMELIORATION OF DIABETIC NEPHROPATHY IN EXPERIMENTALLY INDUCED DIABETIC RATS.

2016 ◽  
Vol 4 (10) ◽  
pp. 1412-1419
Author(s):  
MohammedSamy Fawzy ◽  
◽  
AmalFathy Gharib ◽  
SallyMahmoud Shalaby ◽  
HanimMagdy Abdel-Nour ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Stem Cell ◽  
Diabetic Rats ◽  
Cell Injection ◽  
Stem Cell Injection ◽  
Experimentally Induced
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