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Journal articles on the topic 'Goto-Kakizaki'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

Abd-Elrahman, Khaled S., Olaia Colinas, Emma J. Walsh, Hai-Lei Zhu, Christine M. Campbell, Michael P. Walsh, and William C. Cole. "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 (July 22, 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 polymerization, enhancing force transmission to the cell membrane. Here, we tested the hypothesis that abnormal Rho-associated kinase-mediated myosin light chain phosphatase regulation underlies the dysfunctional cerebral myogenic response of the Goto-Kakizaki rat model of type 2 diabetes. Basal levels of myogenic tone, LC20, and MYPT1-T855 phosphorylation were elevated and G-actin content was reduced in arteries of pre-diabetic 8–10 weeks Goto-Kakizaki rats with normal serum insulin and glucose levels. Pressure-dependent myogenic constriction, LC20, and myosin phosphatase targeting subunit 1 phosphorylation and actin polymerization were suppressed in both pre-diabetic Goto-Kakizaki and diabetic (18–20 weeks) Goto-Kakizaki rats, whereas RhoA, ROK2, and MYPT1 expression were unaffected. We conclude that abnormal Rho-associated kinase-mediated Ca2+ sensitization contributes to the dysfunctional cerebral myogenic response in the Goto-Kakizaki model of type 2 diabetes.

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2

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 (March 31, 2014): 355–59. http://dx.doi.org/10.3746/jkfn.2014.43.3.355.

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3

Zong-Chao, Ling, Suad Efendic, Rolf Wibom, Samy M. Abdel-Halim, Claes-Göran Östenson, Bernard R. Landau, and Akhtar Khan. "Glucose Metabolism in Goto-Kakizaki Rat Islets*." Endocrinology 139, no. 6 (June 1, 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 capacities of mitochondria from GK islets to generate ATP from glutamate and malate were similar and that to generate ATP from succinate and rotenone was somewhat less from GK islets. The reason for the enhanced utilization of substrates by islets of the GK rat is not apparent. In conclusion, there is no decrease in islet glucose utilization, glucose oxidation, Krebs cycle function, or the electron transport system evident from these measurements to explain the impaired insulin release in islets from GK rats.

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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 (March 1, 2004): 133–41. http://dx.doi.org/10.1007/s00395-004-0440-4.

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5

Zhang, Chengcheng, Weicheng Wu, Xiaoting Xin, Xiaoqiong Li, and Daqun Liu. "Extract of ice plant (Mesembryanthemum crystallinum) ameliorates hyperglycemia and modulates the gut microbiota composition in type 2 diabetic Goto-Kakizaki rats." Food & Function 10, no. 6 (2019): 3252–61. http://dx.doi.org/10.1039/c9fo00119k.

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6

Sugawara, Isamu, Hiroyuki Yamada, and Satoru Mizuno. "Pulmonary Tuberculosis in Spontaneously Diabetic Goto Kakizaki Rats." Tohoku Journal of Experimental Medicine 204, no. 2 (2004): 135–45. http://dx.doi.org/10.1620/tjem.204.135.

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7

Guest, PC, SM Abdel-Halim, DJ Gross, A. Clark, V. Poitout, R. Amaria, CG Ostenson, and JC Hutton. "Proinsulin processing in the diabetic Goto-Kakizaki rat." Journal of Endocrinology 175, no. 3 (December 1, 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-dependent substrate chromogranin A was reduced as evidenced by the appearance of intermediates. No differences were seen in the biosynthesis and post-translational modification of PC1, PC2 or CPE following incubation of islets in 16.7 mM glucose, but incubation in 3.3 mM glucose resulted in decreased PC2 biosynthesis in the GK islets. The rates of biosynthesis, processing and secretion of newly synthesized (pro)insulin were comparable. Circulating insulin immunoreactivity in both Wistar and GK rats was predominantly insulin 1 and 2 in the expected ratios with no (pro)insulin evident. Thus, the marked changes in islet morphology and PC2 expression did not impact the rate or extent of proinsulin processing either in vitro or in vivo in this experimental model.

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8

YOSHINARI, Nobuo, Yukihiko AOYAMA, Morikatsu OHHARA, Hitoshi NISHIYAMA, Kiyomi KOMATSU, Tamaki KUSUZAKI, and Toshihide NOGUCHI. "Experimental Periodontitis in Spontaneous Diabetic (GK: Goto-Kakizaki) Rats." Nihon Shishubyo Gakkai Kaishi (Journal of the Japanese Society of Periodontology) 34, no. 1 (1992): 114–24. http://dx.doi.org/10.2329/perio.34.114.

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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 (July 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 the tibial metaphysis. Notably, the diaphysis in all long bones showed expansion of periosteal and endosteal circumference. In tibia this resulted in increased cortical thickness, whereas in humerus and metatarsal it was unchanged. Areal moment of inertia was increased in all diaphyses suggesting greater bending strength. The most conspicuous finding in diabetic rats pertained to trabecular osteopenia. Thus, trabecular bone mineral density was significantly reduced in all bones examined, by 33-53%. Our pQCT study of axial and appendicular bones suggests that the typical feature of diabetic osteopathy in the GK rat is loss of trabecular bone and expansion of the diaphysis. The loss of metaphyseal trabecular bone if also present in diabetic patients may prove to underlie the susceptibility to periarticular fracture and Charcot arthropathy. The findings suggest that the risk of fracture in diabetes varies according to the specific sub-regions of a bone. The approach described may prove to be useful in the early detection of osteopathy in diabetic patients who may be amenable to preventive treatment.

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10

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 (May 1997): 158–62. http://dx.doi.org/10.1016/s1056-8727(96)00049-9.

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11

Crisóstomo, Joana, Lisa Rodrigues, Paulo Matafome, Carmen Amaral, Elsa Nunes, Teresa Louro, Pedro Monteiro, and Raquel Seiça. "Beneficial effects of dietary restriction in type 2 diabetic rats: the role of adipokines on inflammation and insulin resistance." British Journal of Nutrition 104, no. 1 (February 24, 2010): 76–82. http://dx.doi.org/10.1017/s0007114510000164.

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Inflammation plays an important role in diabetes mellitus and its complications. In this context, the negative cross-talk between adipose tissue and skeletal muscle leads to disturbances in muscle cell insulin signalling and induces insulin resistance. Because several studies have shown that energy restriction brings some benefits to diabetes, the aim of the present study was to evaluate the effects of dietary restriction on systemic and skeletal muscle inflammatory biomarkers, such C-reactive protein, adipokines and cytokines, and in insulin resistance in Goto-Kakizaki rats. This is an animal model of spontaneous non-obese type 2 diabetes with strongly insulin resistance and without dyslipidaemia. Animals were maintained during 2 months of dietary restriction (50 %) and were killed at 6 months of age. Some biochemical determinations were done using ELISA and Western blot. Data from the present study demonstrate that in Goto-Kakizaki rats the dietary restriction improved insulin resistance, NEFA levels and adipokine profile and ameliorated inflammatory cytokines in skeletal muscle. These results indicate that dietary restriction in type 2 diabetes enhances adipose tissue metabolism leading to an improved skeletal muscle insulin sensitivity.

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12

Kim, Kil-Soo, Dae-Ik Kim, Ae-Kyoung Lim, Sung-Ran Yoon, Jung-Ok Kim, and Gee-Dong Lee. "Anti-diabetic Effects of Hemicentrotus pulcherrimus Shells on Non-obese Type 2 Diabetic Goto-Kakizaki Rats." Journal of the Korean Society of Food Science and Nutrition 40, no. 11 (November 30, 2011): 1537–43. http://dx.doi.org/10.3746/jkfn.2011.40.11.1537.

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13

Ferreira, F. M. L., C. M. Palmeira, R. Seiça, and M. S. Santos. "Alterations of liver mitochondrial bioenergetics in diabetic Goto-Kakizaki rats." Metabolism 48, no. 9 (September 1999): 1115–19. http://dx.doi.org/10.1016/s0026-0495(99)90124-5.

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14

D'Souza, Alicia, Frank C. Howarth, Joseph Yanni, Halina Dobryznski, Mark R. Boyett, Ernest Adeghate, Keshore R. Bidasee, and Jaipaul Singh. "Left ventricle structural remodelling in the prediabetic Goto-Kakizaki rat." Experimental Physiology 96, no. 9 (July 7, 2011): 875–88. http://dx.doi.org/10.1113/expphysiol.2011.058271.

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15

Abdourahman, Aicha, and John G. Edwards. "Chromium supplementation improves glucose tolerance in diabetic Goto‐Kakizaki rats." IUBMB Life 60, no. 8 (August 2008): 541–48. http://dx.doi.org/10.1002/iub.84.

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16

Bitar, M. S., S. Wahid, C. W. Pilcher, E. Al-Saleh, and F. Al-Mulla. "α-lipoic Acid Mitigates Insulin Resistance in Goto-Kakizaki Rats." Hormone and Metabolic Research 36, no. 8 (August 2004): 542–49. http://dx.doi.org/10.1055/s-2004-825760.

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17

Rose, Tobias, Suad Efendic, and Marjan Rupnik. "Ca2+–Secretion Coupling Is Impaired in Diabetic Goto Kakizaki rats." Journal of General Physiology 129, no. 6 (May 29, 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 measurements. We found that β cells of GK rats respond to glucose stimulation with a normal increase in the cytosolic Ca2+ concentration. During trains of depolarizing pulses, the secretory activity from GK rat β cells was defective in spite of upregulated cell size and doubled voltage-activated Ca2+ currents. In GK rat β cells, evoked Ca2+ entry was significantly less efficient in triggering release than in nondiabetic controls. This impairment was neither due to a decrease of functional vesicle pool sizes nor due to different kinetics of pool refilling. Strong stimulation with two successive trains of depolarizing pulses led to a prominent activity-dependent facilitation of release in GK rat β cells, whereas secretion in controls was unaffected. Broad-spectrum inhibition of PKC sensitized Ca2+-dependent exocytosis, whereas it prevented the activity-dependent facilitation in GK rat β cells. We conclude that a decrease in the sensitivity of the GK rat β-cell to depolarization-evoked Ca2+ influx is involved in defective glucose-stimulated insulin secretion. Furthermore, we discuss a role for constitutively increased activity of one or more PKC isoenzymes in diabetic rat β cells.

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18

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 (October 31, 2009): 1331–35. http://dx.doi.org/10.3746/jkfn.2009.38.10.1331.

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19

Pontes Andersen, Carla C., Karsten Buschard, Allan Flyvbjerg, Kaj Stoltze, and Palle Holmstrup. "Periodontitis Deteriorates Metabolic Control in Type 2 Diabetic Goto-Kakizaki Rats." Journal of Periodontology 77, no. 3 (March 2006): 350–56. http://dx.doi.org/10.1902/jop.2006.050184.

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20

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 (January 1, 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 levels were measured. The operated and PFSO groups showed significant weight loss 4 weeks postoperatively compared with the controls. The SG/MJIB and SG groups exhibited a significant improvement in oral glucose tolerance and insulin tolerance compared with the PFSO and control groups. The improved effects in the SG/MJIB group were better than those in the SG group. The SG/MJIB and SG groups showed decreased fasting ghrelin levels and increased levels of GLP-1 secretion 2 and 16 weeks postoperatively. Compared with the SG group, only the SG/MJIB group showed higher glucose-stimulated GLP-1 levels and significantly improved insulin secretion. SG/MJIB may be an effective, steady hypoglycemic surgical model, showing better diabetic control than SG. The hindgut may play a direct role in ameliorating glucose homeostasis.

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21

Yang, Jian, Jingbo Zhao, and Hans Gregersen. "Su1186 Mechano-Sensory Properties of Diabetic Intestine in Goto-Kakizaki Rats." Gastroenterology 142, no. 5 (May 2012): S—446. http://dx.doi.org/10.1016/s0016-5085(12)61679-5.

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22

Kim, Dong-Sun, Tae-Wha Kim, and Ju-Seop Kang. "Chromium picolinate supplementation improves insulin sensitivity in Goto-Kakizaki diabetic rats." Journal of Trace Elements in Medicine and Biology 17, no. 4 (January 2004): 243–47. http://dx.doi.org/10.1016/s0946-672x(04)80025-7.

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23

Tian, Zhiyan, Ning Ren, Jinghua Wang, Danhong Zhang, and Yuying Zhou. "Ginsenoside Ameliorates Cognitive Dysfunction in Type 2 Diabetic Goto-Kakizaki Rats." Medical Science Monitor 24 (June 10, 2018): 3922–28. http://dx.doi.org/10.12659/msm.907417.

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24

Alán, Lukáš, Tomáš Olejár, Monika Cahová, Jaroslav Zelenka, Zuzana Berková, Magdalena Smětáková, František Saudek, Radoslav Matěj, and Petr Ježek. "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) positivity. Unlike the constant glucose-stimulation index for insulin PI release in Wistar rats, this index declined with GK age, whereas for somatostatin it increased with age. A decrease of GK rat PPY serum levels was found. GK rat body weight decreased with increasing hyperglycemia. Somatostatin analog octreotide completely blocked insulin secretion, impaired proliferation at low autocrine insulin, and decreased PPY secretion and mitochondrial DNA in INS-1E cells. In conclusion, in GK rats PI, significant local delta cell hyperplasia and suspected paracrine effect of somatostatin diminish beta cell viability and contribute to the deterioration of beta cell mass. Altered PPY-secreting cells distribution amends another component of GK PI’s pathophysiology.

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25

Yoshinari, Orie, Asako Takenake, and Kiharu Igarashi. "Trigonelline Ameliorates Oxidative Stress in Type 2 Diabetic Goto-Kakizaki Rats." Journal of Medicinal Food 16, no. 1 (January 2013): 34–41. http://dx.doi.org/10.1089/jmf.2012.2311.

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26

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 (June 3, 2011): 1499–508. http://dx.doi.org/10.1002/mnfr.201000605.

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27

Pinto-Souza, Ana Rosa Wakim, Chiara Firetto, Gonzalo Pérez-Arana, Alfonso María Lechuga-Sancho, and José Arturo Prada-Oliveira. "Differences in the estrous cycles of Goto-Kakizaki and Wistar rats." Lab Animal 45, no. 4 (March 22, 2016): 143–48. http://dx.doi.org/10.1038/laban.980.

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28

Cao, Yanguang, Debra C. DuBois, Hao Sun, Richard R. Almon, and William J. Jusko. "Modeling Diabetes Disease Progression and Salsalate Intervention in Goto-Kakizaki Rats." Journal of Pharmacology and Experimental Therapeutics 339, no. 3 (September 8, 2011): 896–904. http://dx.doi.org/10.1124/jpet.111.185686.

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29

Sener, A., F. Malaisse-Lagae, C. G. Östenson, and W. J. Malaisse. "Metabolism of endogenous nutrients in islets of Goto-Kakizaki (GK) rats." Biochemical Journal 296, no. 2 (December 1, 1993): 329–34. http://dx.doi.org/10.1042/bj2960329.

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The metabolism of endogenous nutrients was examined in pancreatic islets of control and Goto-Kakizaki (GK) rats. At the ultrastructural level, no glycogen was found in the islet cells of GK rats, a situation similar to that prevailing in normal islets. Likewise, by measuring the output of L-lactate from islets first incubated at 16.7 mM D-glucose and then at 2.8 mM D-glucose, no evidence of glycogenolysis was found in the islets of GK rats. The production of NH4+ and that of 14CO2 from islets prelabelled with either L-[U-14C]glutamine or [U-14C]palmitate were higher, however, in GK than in control rats. The changes in NH4+ and 14CO2 production evoked by D-glucose, by a non-metabolized analogue of L-leucine (2-amino-bicyclo[2,2,1]heptane-2-carboxylic acid; BCH) and by 3-phenylpyruvate were qualitatively comparable in control and GK rats. The secretory response to these three secretagogues was severely decreased in the islets of GK rats. This coincided with an impaired enhancing action of D-glucose on the conversion of [2-3H]glycerol into 3HOH. It is concluded that the catabolism of endogenous amino and fatty acids in islets is greater in GK than in control rats, especially at low D-glucose concentration. This may account, in part at least, for the altered secretory response to BCH and 3-phenylpyruvate. For glucose-induced insulin release, however, an impaired acceleration of the glycerol phosphate shuttle apparently also participates in the secretory defect.

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30

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 (February 2015): 137–47. http://dx.doi.org/10.1097/fjc.0000000000000170.

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31

Xue, Bai, Siddharth Sukumaran, Jing Nie, William J. Jusko, Debra C. DuBois, and Richard R. Almon. "Adipose Tissue Deficiency and Chronic Inflammation in Diabetic Goto-Kakizaki Rats." PLoS ONE 6, no. 2 (February 25, 2011): e17386. http://dx.doi.org/10.1371/journal.pone.0017386.

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32

Feng, Su. "Modified billiopancreatic diversion surgery improves glucose levels in Goto-Kakizaki rats." World Chinese Journal of Digestology 22, no. 6 (2014): 766. http://dx.doi.org/10.11569/wcjd.v22.i6.766.

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33

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 (September 2007): 296–302. http://dx.doi.org/10.1016/j.diabet.2007.03.002.

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34

Miura, Yuri, Atsuko Hayakawa, Shohei Kikuchi, Hiroki Tsumoto, Keitaro Umezawa, Yuko Chiba, Yurie Soejima, et al. "Fumarate accumulation involved in renal diabetic fibrosis in Goto-Kakizaki rats." Archives of Biochemistry and Biophysics 678 (December 2019): 108167. http://dx.doi.org/10.1016/j.abb.2019.108167.

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35

Giroix, Marie-Hélène, Karim Louchami, Yvon A. Carpentier, Abdullah Sener, and Willy J. Malaisse. "Fatty acid pattern of pancreatic islet lipids in Goto-Kakizaki rats." Endocrine 37, no. 1 (November 24, 2009): 173–79. http://dx.doi.org/10.1007/s12020-009-9286-8.

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36

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 (October 2008): 404–11. http://dx.doi.org/10.1016/j.ghir.2008.02.003.

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37

Szkudelska, Katarzyna, Marzanna Deniziak, Maciej Sassek, Ignacy Szkudelski, Wojciech Noskowiak, and Tomasz Szkudelski. "Resveratrol Affects Insulin Signaling in Type 2 Diabetic Goto-Kakizaki Rats." International Journal of Molecular Sciences 22, no. 5 (February 28, 2021): 2469. http://dx.doi.org/10.3390/ijms22052469.

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Resveratrol is a biologically active diphenolic compound exerting multiple beneficial effects in the organism, including anti-diabetic properties. This action is, however, not fully elucidated. In the present study, we examined effects of resveratrol on some parameters related to insulin signaling, and also on diabetes-associated dysregulation in Goto-Kakizaki (GK) rats with congenital type 2 diabetes. Resveratrol was given at the dose of 20 mg/kg b.w. for 10 weeks. It was shown that the expression and phosphorylation levels of insulin receptor in the skeletal muscle of GK rats were significantly decreased, compared with control animals. However, these changes were totally prevented by resveratrol. Liver expression of the insulin receptor was also reduced, but in this case, resveratrol was ineffective. Resveratrol was also demonstrated to significantly influence parameters of insulin binding (dissociation constant and binding capacity) in the skeletal muscle and liver. Moreover, it was shown that the expression levels of proteins related to intracellular glucose transport (GLUT4 and TUG) in adipose tissue of GK rats were significantly decreased. However, treatment with resveratrol completely abolished these changes. Resveratrol was found to induce normalization of TUG expression in the skeletal muscle. Blood levels of insulin and GIP were elevated, whereas proinsulin and GLP-1 diminished in GK rats. However, concentrations of these hormones were not affected by resveratrol. These results indicate that resveratrol partially ameliorates diabetes-associated dysregulation in GK rats. The most relevant finding covers the normalization of the insulin receptor expression in the skeletal muscle and also GLUT4 and TUG in adipose tissue.

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38

Wachal, Zita, Mariann Bombicz, Dániel Priksz, Csaba Hegedűs, Diána Kovács, Adrienn Mónika Szabó, Rita Kiss, 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 (March 19, 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 diseased animal model (Goto-Kakizaki rats). The used methods include weight measurement, glucose-related measurements—like fasting blood sugar analysis, oral glucose tolerance test, hyperinsulinemic euglycemic glucose clamp (HEGC), and calculations of different indices from HEGC results—electroretinography and Western Blot. Beside its apparent insulin sensitization, BGP-15 was also able to counteract the retina-damaging effect of Type II diabetes comparable to the aforementioned anti-diabetics. The mechanism of retinoprotective action may include sirtuin 1 (SIRT1) and matrix metalloproteinase 9 (MMP9) enzymes, as BGP-15 was able to elevate SIRT1 and decrease MMP9 expression in the eye. Based on our results, this emerging hydroximic acid derivative might be a future target of pharmacological developments as a potential drug against the harmful consequences of diabetes, such as diabetic retinopathy.

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Howarth, FC, EM Gaber, P. Jayaprakash, MA Qureshi, and M. Oz. "Well-preserved ventricular myocyte shortening in Goto–Kakizaki type 2 diabetic rats." Hamdan Medical Journal 7, no. 2 (2014): 211. http://dx.doi.org/10.7707/hmj.v7i2.311.

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Li, Xian-Hui, Xin Xin, Yan Wang, Jian-zhao Wu, Zhen-dong Jin, Li-na Ma, Chun-jie Nie, Xiao Xiao, Yan Hu, and Man-wen Jin. "Pentamethylquercetin Protects Against Diabetes-Related Cognitive Deficits in Diabetic Goto-Kakizaki Rats." Journal of Alzheimer's Disease 34, no. 3 (March 4, 2013): 755–67. http://dx.doi.org/10.3233/jad-122017.

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Jin, Ming, Ming-hua Shen, Mei-hua Jin, Ai-hua Jin, Xue-zhe Yin, and Ji-shu Quan. "Hypoglycemic property of soy isoflavones from hypocotyl in Goto-Kakizaki diabetic rats." Journal of Clinical Biochemistry and Nutrition 62, no. 2 (2018): 148–54. http://dx.doi.org/10.3164/jcbn.17-68.

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TAKITA, Satoru, Yukari WAKAMOTO, Ichirou KUNITSUGU, Shinichi SUGIYAMA, Masayuki OKUDA, and Tatsuya HOUBARA. "ALTERED TISSUE CONCENTRATION OF MINERALS IN SPONTANEOUS DIABETIC RATS (Goto-Kakizaki rats)." Journal of Toxicological Sciences 29, no. 3 (2004): 195–99. http://dx.doi.org/10.2131/jts.29.195.

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LI, ZHAO, JIAN HU, and GUOXIAN QI. "Effects of ghrelin on systolic blood pressure in Goto–Kakizaki Wistar rats." International Journal of Cardiology 137 (October 2009): S44. http://dx.doi.org/10.1016/j.ijcard.2009.09.144.

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Frese, Thomas, Andreas Gunter Bach, Eckhard Mühlbauer, Klaus Pönicke, Hans-Jürgen Brömme, André Welp, and Elmar Peschke. "Pineal melatonin synthesis is decreased in type 2 diabetic Goto–Kakizaki rats." Life Sciences 85, no. 13-14 (September 2009): 526–33. http://dx.doi.org/10.1016/j.lfs.2009.08.004.

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Oger-Roussel, Stephanie, Delphine Behr-Roussel, Stephanie Caisey, Micheline Kergoat, Christine Charon, Annick Audet, Jacques Bernabé, Laurent Alexandre, and Francois Giuliano. "Bladder and erectile dysfunctions in the Type 2 diabetic Goto-Kakizaki rat." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 306, no. 2 (January 15, 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 function was assessed under anesthesia following electrical stimulation of the cavernous nerve in presence of intravenous sildenafil (0.3 mg/kg). GK rats displayed detrusor overactivity with a significant increase in frequency/amplitude of nonvoiding contractions during the filling phase, together with an increase in bladder capacity, intercontraction interval, voided volume, and maximal pressure of voiding contraction. Solifenacin significantly decreased parameters characterizing voiding contractions without modifying voiding efficiency. Erectile function in GK rats was markedly impaired and remained so after sildenafil treatment despite a significant improvement. GK rats display both bladder and erectile dysfunctions and respond at least partially to standard-of-care treatments for each disorder, thus representing a suitable model to investigate the pathophysiology and assess the efficacy of new therapeutic agents for Type 2 diabetes-associated bladder and erectile complications.

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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 (January 20, 2020): 965–74. http://dx.doi.org/10.1080/02713683.2020.1712730.

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Weng, Shan-Geng, Bin Zhang, Zhao-Qi Liu, and Zheng Shi. "Improved gastric bypass surgery decreases blood glucose levels in Goto-Kakizaki rats." World Chinese Journal of Digestology 18, no. 35 (2010): 3778. http://dx.doi.org/10.11569/wcjd.v18.i35.3778.

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KASHIBA, Misato, Jun OKA, Rumi ICHIKAWA, Asako KAGEYAMA, Takayo INAYAMA, Haruaki KAGEYAMA, Takahiro ISHIKAWA, Morimitsu NISHIKIMI, Masayasu INOUE, and Shuji INOUE. "Impaired reductive regeneration of ascorbic acid in the Goto‒Kakizaki diabetic rat." Biochemical Journal 351, no. 2 (October 15, 2000): 313. http://dx.doi.org/10.1042/0264-6021:3510313.

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KASHIBA, Misato, Jun OKA, Rumi ICHIKAWA, Asako KAGEYAMA, Takayo INAYAMA, Haruaki KAGEYAMA, Takahiro ISHIKAWA, Morimitsu NISHIKIMI, Masayasu INOUE, and Shuji INOUE. "Impaired reductive regeneration of ascorbic acid in the Goto–Kakizaki diabetic rat." Biochemical Journal 351, no. 2 (October 10, 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 significantly lower in GK than in control rats. AA levels in primary cultured hepatocytes derived from GK rats were lower than those derived from control Wistar rats with or without dehydroascorbic acid (DHA) in the medium. Among various enzyme activities that reduce DHA to AA, the NADPH-dependent regeneration of AA in the liver was significantly suppressed in GK rats. Northern blot analysis revealed that only the expression of 3-α-hydroxysteroid dehydrogenase (AKR) was significantly suppressed in these rats. These results suggest that decreased AA-regenerating activity, probably through decreased expression of AKR, contributes to the decreased AA levels and increased oxidative stress in GK rats.

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Cheng, Zhong Jian, Timo Vaskonen, Ilkka Tikkanen, Kaisa Nurminen, Heikki Ruskoaho, Heikki Vapaatalo, Dominik Muller, Joon-Keun Park, Friedrich C. Luft, and Eero M. A. Mervaala. "Endothelial Dysfunction and Salt-Sensitive Hypertension in Spontaneously Diabetic Goto-Kakizaki Rats." Hypertension 37, no. 2 (February 2001): 433–39. http://dx.doi.org/10.1161/01.hyp.37.2.433.

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