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Artykuły w czasopismach na temat „Gotto Kakizaki rat”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 19 lipca 2025

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1

Jin, Yong-Xie, Haeng-Ryan Kim, and So-Young Kim. "Effect of Mineral-rich Salt Intake on Diabetic Goto-Kakizaki Rats." Journal of the Korean Society of Food Science and Nutrition 43, no. 3 (2014): 355–59. http://dx.doi.org/10.3746/jkfn.2014.43.3.355.

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Abd-Elrahman, Khaled S., Olaia Colinas, Emma J. Walsh, et al. "Abnormal myosin phosphatase targeting subunit 1 phosphorylation and actin polymerization contribute to impaired myogenic regulation of cerebral arterial diameter in the type 2 diabetic Goto-Kakizaki rat." Journal of Cerebral Blood Flow & Metabolism 37, no. 1 (2016): 227–40. http://dx.doi.org/10.1177/0271678x15622463.

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The myogenic response of cerebral resistance arterial smooth muscle to intraluminal pressure elevation is a key physiological mechanism regulating blood flow to the brain. Rho-associated kinase plays a critical role in the myogenic response by activating Ca2+ sensitization mechanisms: (i) Rho-associated kinase inhibits myosin light chain phosphatase by phosphorylating its targeting subunit myosin phosphatase targeting subunit 1 (at T855), augmenting 20 kDa myosin regulatory light chain (LC20) phosphorylation and force generation; and (ii) Rho-associated kinase stimulates cytoskeletal actin pol

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3

Zong-Chao, Ling, Suad Efendic, Rolf Wibom, et al. "Glucose Metabolism in Goto-Kakizaki Rat Islets*." Endocrinology 139, no. 6 (1998): 2670–75. http://dx.doi.org/10.1210/endo.139.6.6053.

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Abstract Islets from Goto-Kakizaki (GK) rats from our colony, despite marked impairment of glucose-induced insulin release, used glucose and produced CO2 at a rate 3 times that of islets from control Wistar rats. Almost all glucose used was accounted for in CO2 and lactate production. The percentages of glucose carbon used collected in CO2 and lactate were similar for control and GK islets. GK islets also oxidized 40% more acetate and leucine to CO2 than did control islets. The fraction of carbon leaving the Krebs cycle relative to CO2 production was the same in GK and control islets. The capa

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4

El-Omar, Magdi M., Zhao-Kang Yang, Aled O. Phillips, and Ajay M. Shah. "Cardiac dysfunction in the Goto-Kakizaki rat." Basic Research in Cardiology 99, no. 2 (2004): 133–41. http://dx.doi.org/10.1007/s00395-004-0440-4.

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Rose, Tobias, Suad Efendic, and Marjan Rupnik. "Ca2+–Secretion Coupling Is Impaired in Diabetic Goto Kakizaki rats." Journal of General Physiology 129, no. 6 (2007): 493–508. http://dx.doi.org/10.1085/jgp.200609604.

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The Goto Kakizaki (GK) rat is a widely used animal model to study defective glucose-stimulated insulin release in type-2 diabetes (T2D). As in T2D patients, the expression of several proteins involved in Ca2+-dependent exocytosis of insulin-containing large dense-core vesicles is dysregulated in this model. So far, a defect in late steps of insulin secretion could not be demonstrated. To resolve this apparent contradiction, we studied Ca2+–secretion coupling of healthy and GK rat β cells in acute pancreatic tissue slices by assessing exocytosis with high time-resolution membrane capacitance me

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6

Guest, PC, SM Abdel-Halim, DJ Gross, et al. "Proinsulin processing in the diabetic Goto-Kakizaki rat." Journal of Endocrinology 175, no. 3 (2002): 637–47. http://dx.doi.org/10.1677/joe.0.1750637.

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The biosynthesis and processing of proinsulin was investigated in the diabetic Goto-Kakizaki (GK) rat. Immunofluorescence microscopy comparing GK and Wistar control rat pancreata revealed marked changes in the distribution of alpha-cells and pronounced beta-cell heterogeneity in the expression patterns of insulin, prohormone convertases PC1, PC2, carboxypeptidase E (CPE) and the PC-binding proteins 7B2 and ProSAAS. Western blot analyses of isolated islets revealed little difference in PC1 and CPE expression but PC2 immunoreactivity was markedly lower in the GK islets. The processing of the PC2

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7

Kim, Dae-Jung, Mi-Ja Chung, Jin-Kyoun You, Dong-Joo Seo, Jeong-Mi Kim, and Myeon Choe. "Effect of Medicinal Plant Water Extracts on Glucose-regulating Enzyme Activities in Goto-Kakizaki Rat Liver Cytosol." Journal of the Korean Society of Food Science and Nutrition 38, no. 10 (2009): 1331–35. http://dx.doi.org/10.3746/jkfn.2009.38.10.1331.

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8

Agardh, Carl-David, Elisabet Agardh, Hui Zhang, and Claes-Göran Östenson. "Altered endothelial/pericyte ratio in Goto-Kakizaki rat retina." Journal of Diabetes and its Complications 11, no. 3 (1997): 158–62. http://dx.doi.org/10.1016/s1056-8727(96)00049-9.

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9

Ahmad, T., C. Ohlsson, M. Saaf, CG Ostenson, and A. Kreicbergs. "Skeletal changes in type-2 diabetic Goto-Kakizaki rats." Journal of Endocrinology 178, no. 1 (2003): 111–16. http://dx.doi.org/10.1677/joe.0.1780111.

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We characterized appendicular and axial bones in rats with type-2 diabetes in five female Goto-Kakizaki (GK) rats, a strain developed from the Wistar rat showing spontaneous type-2 diabetes, and five age- and sex-matched non-diabetic Wistar rats. The humerus, tibia, metatarsals and vertebral bodies were analysed by peripheral quantitative computerized tomography (pQCT). In diabetic rats, the height of the vertebral bodies and length of the humerus were decreased while the length of the metatarsals was increased. A decreased cross-sectional area was found in the vertebral end-plate region and t

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10

D'Souza, Alicia, Frank C. Howarth, Joseph Yanni, et al. "Left ventricle structural remodelling in the prediabetic Goto-Kakizaki rat." Experimental Physiology 96, no. 9 (2011): 875–88. http://dx.doi.org/10.1113/expphysiol.2011.058271.

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11

Alán, Lukáš, Tomáš Olejár, Monika Cahová, et al. "Delta Cell Hyperplasia in Adult Goto-Kakizaki (GK/MolTac) Diabetic Rats." Journal of Diabetes Research 2015 (2015): 1–16. http://dx.doi.org/10.1155/2015/385395.

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Reduced beta cell mass in pancreatic islets (PI) of Goto-Kakizaki (GK) rats is frequently observed in this diabetic model, but knowledge on delta cells is scarce. Aiming to compare delta cell physiology/pathology of GK to Wistar rats, we found that delta cell number increased over time as did somatostatin mRNA and delta cells distribution in PI is different in GK rats. Subtle changes in 6-week-old GK rats were found. With maturation and aging of GK rats, disturbed cytoarchitecture occurred with irregular beta cells accompanied by delta cell hyperplasia and loss of pancreatic polypeptide (PPY)

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12

Kowluru, Anjaneyulu. "Defective protein histidine phosphorylation in islets from the Goto-Kakizaki diabetic rat." American Journal of Physiology-Endocrinology and Metabolism 285, no. 3 (2003): E498—E503. http://dx.doi.org/10.1152/ajpendo.00121.2003.

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We recently described novel regulatory roles for protein histidine phosphorylation of key islet proteins (e.g., nucleoside diphosphate kinase and succinyl thiokinase) in insulin secretion from the islet β-cell (Kowluru A. Diabetologia 44: 89-94, 2001; Kowluru A, Tannous M, and Chen HQ. Arch Biochem Biophys 398: 160-169, 2002). In this context, we also characterized a novel, ATP- and GTP-sensitive protein histidine kinase in isolated β-cells that catalyzed the histidine phosphorylation of islet (endogenous) proteins as well as exogenously added histone 4, and we implicated this kinase in the ac

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13

Kattla, Jayesh J., Rosemarie M. Carew, Mediha Heljić, Catherine Godson та Derek P. Brazil. "Protein kinase B/Akt activity is involved in renal TGF-β1-driven epithelial-mesenchymal transition in vitro and in vivo". American Journal of Physiology-Renal Physiology 295, № 1 (2008): F215—F225. http://dx.doi.org/10.1152/ajprenal.00548.2007.

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The molecular pathogenesis of diabetic nephropathy (DN), the leading cause of end-stage renal disease worldwide, is complex and not fully understood. Transforming growth factor-β (TGF-β1) plays a critical role in many fibrotic disorders, including DN. In this study, we report protein kinase B (PKB/Akt) activation as a downstream event contributing to the pathophysiology of DN. We investigated the potential of PKB/Akt to mediate the profibrotic bioactions of TGF-β1 in kidney. Treatment of normal rat kidney epithelial cells (NRK52E) with TGF-β1 resulted in activation of phosphatidylinositol 3-ki

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14

KASHIBA, Misato, Jun OKA, Rumi ICHIKAWA, et al. "Impaired reductive regeneration of ascorbic acid in the Goto–Kakizaki diabetic rat." Biochemical Journal 351, no. 2 (2000): 313–18. http://dx.doi.org/10.1042/bj3510313.

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Ascorbic acid (AA) is a naturally occurring major antioxidant that is essential for the scavenging of toxic free radicals in both plasma and tissues. AA levels in plasma and tissues have been reported to be significantly lower than normal in diabetic animals and humans, and might contribute to the complications found at the late stages of diabetes. In this study, plasma and hepatic AA levels and AA regeneration were studied in the Goto–Kakizaki diabetic rat (GK rat) to elucidate the mechanism of decreasing plasma and hepatic AA levels in diabetes. AA concentrations in the plasma and liver were

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15

Sena, C. M., C. Barosa, E. Nunes, R. Seiça, and J. G. Jones. "Sources of endogenous glucose production in the Goto–Kakizaki diabetic rat." Diabetes & Metabolism 33, no. 4 (2007): 296–302. http://dx.doi.org/10.1016/j.diabet.2007.03.002.

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16

Ahmad, Tashfeen, Anna Ugarph-Morawski, Moira S. Lewitt, Jian Li, Maria Sääf, and Kerstin Brismar. "Diabetic osteopathy and the IGF system in the Goto–Kakizaki rat." Growth Hormone & IGF Research 18, no. 5 (2008): 404–11. http://dx.doi.org/10.1016/j.ghir.2008.02.003.

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Keller, Amy C., Leslie A. Knaub, Matthew W. Miller, Nicholas Birdsey, Dwight J. Klemm, and Jane E. B. Reusch. "Saxagliptin Restores Vascular Mitochondrial Exercise Response in the Goto-Kakizaki Rat." Journal of Cardiovascular Pharmacology 65, no. 2 (2015): 137–47. http://dx.doi.org/10.1097/fjc.0000000000000170.

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18

Shen, Li, Michael J. Keenan, Anne Raggio, Cathy Williams, and Roy J. Martin. "Dietary-resistant starch improves maternal glycemic control in Goto-Kakizaki rat." Molecular Nutrition & Food Research 55, no. 10 (2011): 1499–508. http://dx.doi.org/10.1002/mnfr.201000605.

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Lokman, Ezarul Faradianna, Siti Mastura Abdul Aziz, Aina Shafiza Ibrahim, Nurleyna Yunus, Awang Zulfikar Rizal Awang Seruji, and Sal Hazreen Bugam. "Hepatic Glucose Regulations by Sago (Metroxylon sagu) Resistant Starch in Diabetic Goto Kakizaki Rat." International Journal of Biomedical Science 17, no. 3 (2021): 28–33. http://dx.doi.org/10.59566/ijbs.2021.17028.

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Resistant starch (RS) Sago (Metroxylon sagu) intake has been linked with the improvement in postprandial hyperglycemia and diabetes management via several modes of action including delayed glucose absorption and inhibition of carbohydrate digestion in the gastrointestinal tract. However, to our knowledge, studies on local Malaysian sago RS associated with hepatic glucose production has not been reported elsewhere. Thus, this study was done to identify the underlying mechanisms of local Malaysian RS sago native and modified known as sago RS type 2 (sago RS2) and type 4 (sago RS4) respectively i

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20

Al Kury, L., M. Smail, M. A. Qureshi, et al. "Calcium Signaling in the Ventricular Myocardium of the Goto-Kakizaki Type 2 Diabetic Rat." Journal of Diabetes Research 2018 (2018): 1–15. http://dx.doi.org/10.1155/2018/2974304.

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The association between diabetes mellitus (DM) and high mortality linked to cardiovascular disease (CVD) is a major concern worldwide. Clinical and preclinical studies have demonstrated a variety of diastolic and systolic dysfunctions in patients with type 2 diabetes mellitus (T2DM) with the severity of abnormalities depending on the patients’ age and duration of diabetes. The cellular basis of hemodynamic dysfunction in a type 2 diabetic heart is still not well understood. The aim of this review is to evaluate our current understanding of contractile dysfunction and disturbances of Ca2+transp

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21

Wachal, Zita, Mariann Bombicz, Dániel Priksz, et al. "Retinoprotection by BGP-15, a Hydroximic Acid Derivative, in a Type II Diabetic Rat Model Compared to Glibenclamide, Metformin, and Pioglitazone." International Journal of Molecular Sciences 21, no. 6 (2020): 2124. http://dx.doi.org/10.3390/ijms21062124.

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High blood glucose and the consequential ischemia-reperfusion (I/R) injury damage vessels of the retina, deteriorating its function, which can be clearly visualized by electroretinography (ERG). The aim of the present study was to evaluate the possible retinoprotective effects of systemic BGP-15, an emerging drug candidate, in an insulin resistant animal model, the Goto-Kakizaki rat, and compare these results with well-known anti-diabetics such as glibenclamide, metformin, and pioglitazone, which even led to some novel conclusions about these well-known agents. Experiments were carried out on

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22

Zhou, Huarong, Shigeru Saito, Guanying Piao, et al. "Network screening of Goto-Kakizaki rat liver microarray data during diabetic progression." BMC Systems Biology 5, Suppl 1 (2011): S16. http://dx.doi.org/10.1186/1752-0509-5-s1-s16.

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KASHIBA, Misato, Jun OKA, Rumi ICHIKAWA, et al. "Impaired reductive regeneration of ascorbic acid in the Goto‒Kakizaki diabetic rat." Biochemical Journal 351, no. 2 (2000): 313. http://dx.doi.org/10.1042/0264-6021:3510313.

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Hachana, Soumaya, Mylène Pouliot, Réjean Couture, and Elvire Vaucher. "Diabetes-Induced Inflammation and Vascular Alterations in the Goto–Kakizaki Rat Retina." Current Eye Research 45, no. 8 (2020): 965–74. http://dx.doi.org/10.1080/02713683.2020.1712730.

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Oger-Roussel, Stephanie, Delphine Behr-Roussel, Stephanie Caisey, et al. "Bladder and erectile dysfunctions in the Type 2 diabetic Goto-Kakizaki rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 306, no. 2 (2014): R108—R117. http://dx.doi.org/10.1152/ajpregu.00033.2013.

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Despite the fact that urogenito-sexual complications significantly impact the quality of life of diabetic patients, a robust in vivo experimental model is lacking. Bladder and erectile function in the Type 2 diabetic Goto-Kakizaki (GK) rat and responses to standard-of-care treatments for each disorder have been assessed. GK rats ( n = 25, 18-wk-old, GK/Par colony) and age-matched Wistar rats ( n = 23), characterized for their metabolic parameters, were used. Bladder function was assessed by cystometry in conscious rats treated by intravenous solifenacin (1 mg/kg). Subsequently, erectile functi

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Matsubara, Hisashi, Manami Kuze, Mikio Sasoh, Ning Ma, Motoyasu Furuta, and Yukitaka Uji. "Time-Dependent Course of Electroretinograms in the Spontaneous Diabetic Goto-Kakizaki Rat." Japanese Journal of Ophthalmology 50, no. 3 (2006): 211–16. http://dx.doi.org/10.1007/s10384-005-0315-8.

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Nie, Jing, Debra C. DuBois, William J. Jusko, and Richard R. Almon. "Mechanistic population modeling of diabetes disease progression in Goto-Kakizaki rat muscle." Biopharmaceutics & Drug Disposition 32, no. 1 (2010): 50–63. http://dx.doi.org/10.1002/bdd.738.

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Camacho-Ramírez, Alonso, J. Arturo Prada-Oliveira, Antonio Ribelles-García, David Almorza-Gomar, and Gonzalo M. Pérez-Arana. "The Leading Role of Peptide Tyrosine Tyrosine in Glycemic Control After Roux-en-Y Gastric Bypass in Rats." Obesity Surgery 30, no. 2 (2019): 697–706. http://dx.doi.org/10.1007/s11695-019-04239-y.

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Abstract Aims Roux-en-Y gastric bypass (RYGB) is one of the most effective surgical therapies for the rapid resolution of type 2 diabetes. However, the mechanisms underlying the entero-hormonal response after surgery and the role of peptide tyrosine tyrosine (PYY) in the restoration of normoglycemia are still not clear. Methods We reproduced the RYGB technique in Wistar and Goto–Kakizaki rats and performed serum hormonal, histological, and hormonal-infusion test. Results Using the diabetic Goto–Kakizaki (GK) rat model, we demonstrated that PYY plasma levels showed a remarkable peak approximate

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Wallace, Karin J., Robert H. Wallis, Stephan C. Collins, et al. "Quantitative trait locus dissection in congenic strains of the Goto-Kakizaki rat identifies a region conserved with diabetes loci in human chromosome 1q." Physiological Genomics 19, no. 1 (2004): 1–10. http://dx.doi.org/10.1152/physiolgenomics.00114.2004.

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Genetic studies in human populations and rodent models have identified regions of human chromosome 1q21–25 and rat chromosome 2 showing evidence of significant and replicated linkage to diabetes-related phenotypes. To investigate the relationship between the human and rat diabetes loci, we fine mapped the rat locus Nidd/ gk2 linked to hyperinsulinemia in an F2 cross derived from the diabetic (type 2) Goto-Kakizaki (GK) rat and the Brown Norway (BN) control rat, and carried out its genetic and pathophysiological characterization in BN.GK congenic strains. Evidence of glucose intolerance and enh

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Zhu, Zhanyong, Xilin Yang, Zhong Wang, Yueqiang Zhao, Mosheng Yu, and Huajun Fan. "Sleeve Gastrectomy With Modified Jejunoileal Bypass Model in Goto-Kakizaki Rats." International Surgery 101, no. 1-2 (2016): 89–97. http://dx.doi.org/10.9738/intsurg-d-15-00162.1.

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The objective of this study was to develop a nonobese diabetic rat model for sleeve gastrectomy with modified jejunoileal bypass (SG/MJIB) and to investigate its effectiveness and safety for inducing diabetic control. Thirty-five 13-week-old male Goto-Kakizaki rats were randomly assigned to the pair-fed to sham-operated SG/MJIB (PFSO-SG/MJIB), SG/MJIB, PFSO-SG, SG, and control groups. The experimental period was 16 weeks postoperatively. Body weight; food intake; glycemic control outcomes; and ghrelin, glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic peptide, and insulin level

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Oliveira, Paulo J., Anabela P. Rolo, R. Seiça, Carlos M. Palmeira, M. S. Santos, and António J. M. Moreno. "Decreased Susceptibility of Heart Mitochondria from Diabetic GK Rats to Mitochondrial Permeability Transition Induced by Calcium Phosphate." Bioscience Reports 21, no. 1 (2001): 45–53. http://dx.doi.org/10.1023/a:1010482017540.

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Type 2 diabetes (or non-insulin dependent diabetes mellitus, NIDDM) is a common metabolic disease in man. The Goto–Kakizaki (GK) rat has been designed as a NIDDM model. Previous studies with this strain have shown differences at the mitochondrial level. The mitochondrial permeability transition (MPT) is a widely studied phenomenon but yet poorly understood, that leads to mitochondrial dysfunction and cell death. The aim of this work was to compare the differences in susceptibility of induction of the MPT with calcium phosphate in GK and Wistar rats. Our results show that heart mitochondria fro

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Efanov, Alexander M., Ioulia B. Appelskog, Samy M. Abdel-Halim, et al. "Insulinotropic activity of the imidazoline derivative RX871024 in the diabetic GK rat." American Journal of Physiology-Endocrinology and Metabolism 282, no. 1 (2002): E117—E124. http://dx.doi.org/10.1152/ajpendo.000031.2001.

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The insulinotropic activity of the imidazoline derivative RX871024 was compared in pancreatic islets from nondiabetic Wistar rats and spontaneously diabetic Goto-Kakizaki (GK) rats. RX871024 significantly stimulated insulin secretion in islets from both animal groups. The insulinotropic activity of RX871024 was higher than that of the sulfonylurea glibenclamide. This difference was more pronounced in islets from GK rats compared with Wistar rat islets. More importantly, RX871024 substantially improved glucose sensitivity in diabetic β-cells, whereas glibenclamide stimulated insulin secretion a

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OHARA-IMAIZUMI, Mica, Chiyono NISHIWAKI, Toshiteru KIKUTA, Shintaro NAGAI, Yoko NAKAMICHI та Shinya NAGAMATSU. "TIRF imaging of docking and fusion of single insulin granule motion in primary rat pancreatic β-cells: different behaviour of granule motion between normal and Goto–Kakizaki diabetic rat β-cells". Biochemical Journal 381, № 1 (2004): 13–18. http://dx.doi.org/10.1042/bj20040434.

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We imaged and analysed the motion of single insulin secretory granules near the plasma membrane in live pancreatic β-cells, from normal and diabetic Goto–Kakizaki (GK) rats, using total internal reflection fluorescence microscopy (TIRFM). In normal rat primary β-cells, the granules that were fusing during the first phase originate from previously docked granules, and those during the second phase originate from ‘newcomers’. In diabetic GK rat β-cells, the number of fusion events from previously docked granules were markedly reduced, and, in contrast, the fusion from newcomers was still preserv

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Szkudelska, Katarzyna, Marzanna Deniziak, Iwona Hertig, et al. "Effects of Resveratrol in Goto-Kakizaki Rat, a Model of Type 2 Diabetes." Nutrients 11, no. 10 (2019): 2488. http://dx.doi.org/10.3390/nu11102488.

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Resveratrol exhibits a pleiotropic, favorable action under various pathological conditions, including type 2 diabetes. However, its anti-diabetic effects in animal models and human trials have not been fully elucidated. The aim of the present study was to determine whether resveratrol is capable of inducing beneficial changes in the Goto-Kakizaki rat, a spontaneous model of diabetes, which in several aspects is similar to type 2 diabetes in humans. Goto-Kakizaki (GK) rats and control Sprague–Dawley (SD) rats were treated intragastrically with resveratrol (20 mg/kg b.w./day) for 10 weeks. Then,

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Behr-Roussel, D., S. Oger, S. Caisey, et al. "449 Bladder and erectile dysfunctions in the type 2 Diabetic goto-kakizaki rat." European Urology Supplements 12, no. 1 (2013): e449. http://dx.doi.org/10.1016/s1569-9056(13)60933-1.

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Richardson, Janell R., Laura E. O’Dell, and Arbi Nazarian. "Examination of nicotine and saccharin reward in the Goto-Kakizaki diabetic rat model." Neuroscience Letters 721 (March 2020): 134825. http://dx.doi.org/10.1016/j.neulet.2020.134825.

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Riley, Stephen George, Rachel Anna Evans, Malcolm Davies, Jürgen Floege, and Aled Owain Phillips. "Goto-Kakizaki rat is protected from proteinuria after induction of anti-Thy1 nephritis." American Journal of Kidney Diseases 39, no. 5 (2002): 985–1000. http://dx.doi.org/10.1053/ajkd.2002.32772.

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Yuasa, Izumi, Ning Ma, Hisashi Matsubara, Yoshihiro Fukui, and Yukitaka Uji. "Inducible nitric oxide synthase mediates retinal DNA damage in Goto-Kakizaki rat retina." Japanese Journal of Ophthalmology 52, no. 4 (2008): 314–22. http://dx.doi.org/10.1007/s10384-008-0542-x.

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Howarth, Frank Christopher, and M. A. Qureshi. "Myofilament sensitivity to Ca2+ in ventricular myocytes from the Goto–Kakizaki diabetic rat." Molecular and Cellular Biochemistry 315, no. 1-2 (2008): 69–74. http://dx.doi.org/10.1007/s11010-008-9790-9.

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Saito, Motoaki, Emi Kazuyama, Shogo Shimizu, et al. "Muscarinic receptors and their mRNAs in type 2 Goto-Kakizaki diabetic rat prostate." Prostate 70, no. 14 (2010): 1533–39. http://dx.doi.org/10.1002/pros.21188.

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Cao, Shenghao, Linting Wang, Yance Feng, Xiao-ding Peng, and Lei M. Li. "A data integration approach unveils a transcriptional signature of type 2 diabetes progression in rat and human islets." PLOS ONE 18, no. 10 (2023): e0292579. http://dx.doi.org/10.1371/journal.pone.0292579.

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Pancreatic islet failure is a key characteristic of type 2 diabetes besides insulin resistance. To get molecular insights into the pathology of islets in type 2 diabetes, we developed a computational approach to integrating expression profiles of Goto-Kakizaki and Wistar rat islets from a designed experiment with those of the human islets from an observational study. A principal gene-eigenvector in the expression profiles characterized by up-regulated angiogenesis and down-regulated oxidative phosphorylation was identified conserved across the two species. In the case of Goto-Kakizaki versus W

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Meagher, Patrick, Robert Civitarese, Xavier Lee, et al. "The Goto Kakizaki rat: Impact of age upon changes in cardiac and renal structure, function." PLOS ONE 16, no. 6 (2021): e0252711. http://dx.doi.org/10.1371/journal.pone.0252711.

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Background Patients with diabetes are at a high risk for developing cardiac dysfunction in the absence of coronary artery disease or hypertension, a condition known as diabetic cardiomyopathy. Contributing to heart failure is the presence of diabetic kidney disease. The Goto-Kakizaki (GK) rat is a non-obese, non-hypertensive model of type 2 diabetes that, like humans, shares a susceptibility locus on chromosome 10. Herein, we perform a detailed analysis of cardio-renal remodeling and response to renin angiotensin system blockade in GK rats to ascertain the validity of this model for further in

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Brøndum, E., H. Nilsson, and C. Aalkjær. "Functional Abnormalities in Isolated Arteries from Goto-Kakizaki and Streptozotocin-treated Diabetic Rat Models." Hormone and Metabolic Research 37 (April 2005): 56–60. http://dx.doi.org/10.1055/s-2005-861370.

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Santos, Maria S., Ana I. Duarte, Manuel J. Matos, Teresa Proença, Raquel Seiça, and Catarina R. Oliveira. "Synaptosomes isolated from Goto-Kakizaki diabetic rat brain exhibit increased resistance to oxidative stress." Life Sciences 67, no. 25 (2000): 3061–73. http://dx.doi.org/10.1016/s0024-3205(00)00892-4.

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Adams, Deborah, Rachael J. Gill-Randall, Kerry Housler, and John C. Alcolado. "Excessive maternal transmission of type 3 diabetes not apparent in the goto kakizaki rat." Diabetes Research and Clinical Practice 50 (September 2000): 185. http://dx.doi.org/10.1016/s0168-8227(00)82087-2.

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Matsuura, Bunzo, Sakiko Kanno, Hisaka Minami, et al. "Effects of antihyperlipidemic agents on hepatic insulin sensitivity in perfused Goto-Kakizaki rat liver." Journal of Gastroenterology 39, no. 4 (2004): 339–45. http://dx.doi.org/10.1007/s00535-003-1300-y.

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Jeppesen, P. B., S. Gregersen, S. E. D. Rolfsen, et al. "Antihyperglycemic and blood pressure-reducing effects of stevioside in the diabetic Goto-Kakizaki rat." Metabolism 52, no. 3 (2003): 372–78. http://dx.doi.org/10.1053/meta.2003.50058.

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Seiça, Raquel, Dario L. Santos, Carlos M. Palmeira, et al. "Mitochondrial Function Is Not Affected by Renal Morphological Changes in Diabetic Goto-Kakizaki Rat." Toxicology Mechanisms and Methods 15, no. 4 (2005): 253–61. http://dx.doi.org/10.1080/15376520590968806.

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Fu, Shuying, Yuhuan Meng, Shudai Lin, et al. "Transcriptomic responses of hypothalamus to acute exercise in type 2 diabetic Goto-Kakizaki rats." PeerJ 7 (September 24, 2019): e7743. http://dx.doi.org/10.7717/peerj.7743.

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The hypothalamus has an integral role in energy homeostasis regulation, and its dysfunctions lead to the development of type 2 diabetes (T2D). Physical activity positively affects the prevention and treatment of T2D. However, there is not much information on the adaptive mechanisms of the hypothalamus. In this study, RNA sequencing was used to determine how acute exercise affects hypothalamic transcriptome from both type 2 diabetic Goto-Kakizaki (GK) and control Wistar rats with or without a single session of running (15 m/min for 60 min). Through pairwise comparisons, we identified 957 differ

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Portha, Bernard, G. Lacraz, M. Dolz, F. Homo-Delarche, M.-H. Giroix та J. Movassat. "Defective functional β-cell mass and Type 2 diabetes in the Goto–Kakizaki rat model". Expert Review of Endocrinology & Metabolism 2, № 6 (2007): 785–95. http://dx.doi.org/10.1586/17446651.2.6.785.

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