Relationship between Immunological Abnormalities in Rat Models of Diabetes Mellitus and the Amplification Circuits for Diabetes.

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hyperglycemia 5 endocrinologydiseases
obesity 5 endocrinologydiseases
type 1 diabetes mellitus 1 endocrinologydiseases
type 2 diabetes mellitus 1 endocrinologydiseases
Insulin 1 endocrinologydiseasesdrugs
diabetes mellitus 8 endocrinologydiseases

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Insulin 11976 rats were used for establishing Zucker lean (ZL) rats and Zucker diabetic fatty (ZDF) rats [[35]]. Insulin secretion is impaired in ZDF rats. Furthermore, ZDF rats were used for breeding with Wister rats and
Select Disease Character Offset Disease Term Instance
diabetes mellitus 587 understanding of pathogenic mechanisms is required in order to treat diseases. However, the mechanisms of diabetes mellitus and diabetic complications are extremely complex. Immune reactions are involved in the pathogenesis
diabetes mellitus 2038 structure of amplification circuits for diabetes in future studies.1. IntroductionThe prevalence of diabetes mellitus (DM) is increasing in developed countries, including Japan. Obesity, which is caused by abnormalities
diabetes mellitus 2266 lifestyles, such as diet, nutrition, and physical activity, is the most important risk factor for type 2 diabetes mellitus . Obesity, a determinant in the pathogenesis of diabetes and diabetic complications, is also associated
diabetes mellitus 8758 responses [[13]]. Other pathological processes, such as slowly progressive insulin-dependent (type 1) diabetes mellitus (SPIDDM), or latent autoimmune diabetes in adults (LADA), which result from gradual distraction of islets
diabetes mellitus 23990 red, G-K. The bubble charts were drawn using Graph-R software, version 2.19.Figure 2Pathogenesis of diabetes mellitus in rat models. Dash lines and gray squares indicate the pathogenesis of diabetes in each rat model.
diabetes mellitus 24112 rat models. Dash lines and gray squares indicate the pathogenesis of diabetes in each rat model. DM, diabetes mellitus ; Ig, immunoglobulin; TCR, T cell receptor.Figure 3Difference in phosphorylation of signal transducers
diabetes mellitus 25440 with post hoc test using Bonferroni).Table 1Summary of immunological abnormalities in rat models of diabetes mellitus .Cell type (subset)AbnormalityEffectAlloxan-induced diabetic rats (type 1 diabetes mellitus) T cellsReduced
diabetes mellitus 25531 models of diabetes mellitus.Cell type (subset)AbnormalityEffectAlloxan-induced diabetic rats (type 1 diabetes mellitus ) T cellsReduced T cell proliferationDownregulation of cellular immunity and humoral immunityMonocyte/macrophageImpaired
hyperglycemia 4463 STZ-induced diabetes, provides a useful model for evaluating immunological changes associated with hyperglycemia and diabetes [[4]]. Therefore, we focus on the alloxan-induced diabetes model in relation to immunity
hyperglycemia 5899 function.In alloxan-induced diabetic rats, both cellular immunity and humoral immunity are impaired by hyperglycemia [[4], [8]]. Phagocytosis by alveolar macrophages from alloxan-DM rats is also impaired [[9]]. These
hyperglycemia 12874 individuals exhibiting reduced glucose tolerance in Wistar rats [[41], [42]]. G-K rats already exhibit mild hyperglycemia and impaired insulin secretion in response to a glucose load at 4 weeks of age. In G-K rats, reduction
hyperglycemia 15869 saturated during 15 to 24 weeks old (350~450 g). After 16 weeks old, ZDF exhibited the most severe hyperglycemia (>600 mg/dL) among the Zucker rat strains. The blood glucose levels of G-K rats (200~300 mg/dL)
hyperglycemia 22109 acid-bound fetuin-A has been shown to be an endogenous ligand for toll-like receptor 4 (TLR4) [[76]], and hyperglycemia has been shown to enhance IL-1β secretion [[77]]. Furthermore, increasing knowledge of IL-1 family
obesity 3753 diabetes are useful for investigating the effect of high glucose conditions on immune responses without obesity , they are not suitable for investigation of autoimmune reactivity to β cells, which is known to be
obesity 12387 complications.4.2. Type 2 DM without ObesitySeveral type 2 DM model rats exhibit glucose tolerance without obesity . These model rats exhibit mild hyposecretion (impaired secretion) of insulin from birth. Thus, energy
obesity 13783 neuropathy [[47]]. Spontaneously Diabetic Torii (SDT) rats have severe diabetic complications without obesity [[48]–[51]]. Recently, mating of ZF rats with SDT rats has also been carried out: the mated rats exhibited
obesity 13952 also been carried out: the mated rats exhibited an increased risk of hypertension caused by DM with obesity [[52], [53]]. To our knowledge, there have been no reports on immunological abnormality in SDT rats.
obesity 22475 contributes to dysfunction of β cells in islets [[75]]. These findings reveal the pathogenetic cascade, from obesity to DM, mediated by inflammation.Reduction and dysplasia of β cells in the islets are already observed
type 1 diabetes mellitus 25524 in rat models of diabetes mellitus.Cell type (subset)AbnormalityEffectAlloxan-induced diabetic rats ( type 1 diabetes mellitus ) T cellsReduced T cell proliferationDownregulation of cellular immunity and humoral immunityMonocyte/macrophageImpaired
type 2 diabetes mellitus 2259 in lifestyles, such as diet, nutrition, and physical activity, is the most important risk factor for type 2 diabetes mellitus . Obesity, a determinant in the pathogenesis of diabetes and diabetic complications, is also associated

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