A major quantitative trait locus co-localizing with cholecystokinin type A receptor gene influences poor pancreatic proliferation in a spontaneously diabetogenic rat

Moralejo, Daniel H.; Ogino, Tomoe; Zhu, Mingyan; Toide, Kiyotaka; Wei, Suwen; Wei, Kai; Yamada, Takahisa; Mizuno, Akira; Matsumoto, Kozo; Shima, Kenji

doi:10.1007/s003359900869

Cited by 20 publications

(13 citation statements)

References 35 publications

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“…The essential contribution of CCK1R for pancreatic regeneration following pancreatectomy or pancreatic duct ligation has been demonstrated in OLETF rats as well as in a congenic rat carrying a CCK1R null allele (321,322,332,333). The importance of CCK for normal pancreatic growth has also been reported in this rat strain or in control rats after FIG. 6.…”

Section: Exocrine Pancreasmentioning

confidence: 79%

Cholecystokinin and Gastrin Receptors

Dufresne

Seva²,

Fourmy³

2006

Physiological Reviews

417

418

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Cholecystokinin and gastrin receptors (CCK1R and CCK2R) are G protein-coupled receptors that have been the subject of intensive research in the last 10 years with corresponding advances in the understanding of their functioning and physiology. In this review, we first describe general properties of the receptors, such as the different signaling pathways used to exert short- and long-term effects and the structural data that explain their binding properties, activation, and regulation. We then focus on peripheral cholecystokinin receptors by describing their tissue distribution and physiological actions. Finally, pathophysiological peripheral actions of cholecystokinin receptors and their relevance in clinical disorders are reviewed.

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Section: Exocrine Pancreasmentioning

confidence: 79%

Cholecystokinin and Gastrin Receptors

Dufresne

Seva²,

Fourmy³

2006

Physiological Reviews

417

418

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“…Since genetic and environmental factors can be strictly controlled when inbred animal models are used, such models are invaluable for the dissection of complex diseases. Loci contributing to type 2 diabetes and related traits in diabetic animal models have been reported using quantitative trait locus (QTL) mapping analyses (GK rat [2,3], OLETF rat [2,[4][5][6][7], SDT rat [8], NSY mouse [9], NZO mouse [10,11], TSOD mouse [12], KK mouse [13], KK-Ay mouse [14,15] and TH mouse [16]). …”

Section: Introductionmentioning

confidence: 99%

Major quantitative trait locus on chromosome 2 for glucose tolerance in diabetic SMXA-5 mouse established from non-diabetic SM/J and A/J strains

Kobayashi

Kawai

et al. 2006

Diabetologia

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Aims/hypothesis: The SMXA-5 mouse is one of the SMXA recombinant inbred substrains established from the non-diabetic SM/J and A/J strains, and is a model for polygenic type 2 diabetes, characterised by moderately impaired glucose tolerance and hyperinsulinaemia. These diabetic traits are worsened by feeding a high-fat diet. The aim of this study was to dissect the diabetogenic loci in the A/J regions of the SMXA-5 genome that contribute to diabetes-related traits. Materials and methods: We analysed the quantitative trait loci (QTL) for diabetes-related traits and obesity in (SM/J×SMXA-5)F 2 intercross mice fed a high-fat diet. To verify the function of the responsible locus that was mapped in the present study, we constructed a congenic strain and characterised its diabetes-related traits. Results: A major QTL for glucose tolerance, free-fed blood glucose concentration and BMI was mapped on chromosome 2. This locus existed near D2Mit15, with the highest logarithm of the odds score (12.6) for glucose concentration at 120 min in a glucose tolerance test, and was designated T2dm2sa. The diabetogenic allele of T2dm2sa originated in the A/J strain. SM.A-T2dm2sa, a congenic strain that introgressed the T2dm2sa region of A/J genome into SM/J, exhibited overt impaired glucose tolerance and hyperinsulinaemia. Conclusions/interpretation: The development of impaired glucose tolerance in SM.A-T2dm2sa mice confirmed the results of QTL analysis for diabetes-related traits in F 2 intercross mice. The present results suggest that there are latent diabetogenic loci in the genomes of non-diabetic A/J and SM/J mice, and that the coexistence of these loci, including T2dm2sa, causes impaired glucose tolerance in SMXA-5 and SM.A-T2dm2sa mice.

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“…Many recessive genes on several chromosomes including the X chromosome are involved in the induction of diabetes in OLETF rats. It is also observed that the OLETF rats carry a null allele for the cholecystokinin A receptor which may be related to the regulation of food intake [50, 51]. The pancreatic islets of OLETF rats change progressively, and less than 9 weeks of age, the islets just exhibit mild lymphocyte infiltration, then show hyperplastic alterations and fibrosis in or around islets at around 10 to 40 weeks of age, finally more than 40 weeks, represent atrophy of islets [52].…”

Section: Spontaneous Type 2 Diabetic Rodent Modelsmentioning

confidence: 99%

Spontaneous Type 2 Diabetic Rodent Models

Wang

Sun

et al. 2013

Journal of Diabetes Research

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Diabetes mellitus, especially type 2 diabetes (T2DM), is one of the most common chronic diseases and continues to increase in numbers with large proportion of health care budget being used. Many animal models have been established in order to investigate the mechanisms and pathophysiologic progress of T2DM and find effective treatments for its complications. On the basis of their strains, features, advantages, and disadvantages, various types of animal models of T2DM can be divided into spontaneously diabetic models, artificially induced diabetic models, and transgenic/knockout diabetic models. Among these models, the spontaneous rodent models are used more frequently because many of them can closely describe the characteristic features of T2DM, especially obesity and insulin resistance. In this paper, we aim to investigate the current available spontaneous rodent models for T2DM with regard to their characteristic features, advantages, and disadvantages, and especially to describe appropriate selection and usefulness of different spontaneous rodent models in testing of various new antidiabetic drugs for the treatment of type 2 diabetes.

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A major quantitative trait locus co-localizing with cholecystokinin type A receptor gene influences poor pancreatic proliferation in a spontaneously diabetogenic rat

Cited by 20 publications

References 35 publications

Cholecystokinin and Gastrin Receptors

Cholecystokinin and Gastrin Receptors

Major quantitative trait locus on chromosome 2 for glucose tolerance in diabetic SMXA-5 mouse established from non-diabetic SM/J and A/J strains

Spontaneous Type 2 Diabetic Rodent Models

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