scholarly journals Determination of gastric emptying in nonobese diabetic mice

2007 ◽  
Vol 293 (5) ◽  
pp. G1039-G1045 ◽  
Author(s):  
Kyoung Moo Choi ◽  
Jin Zhu ◽  
Gary J. Stoltz ◽  
Steven Vernino ◽  
Michael Camilleri ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Animal Studies ◽  
Time Course ◽  
Breath Test ◽  
Octanoic Acid ◽  
Nonobese Diabetic ◽  
Onset Of Diabetes ◽  
Nonobese Diabetic Mice

Animal studies on diabetic gastroparesis are limited by inability to follow gastric emptying changes in the same mouse. The study aim was to validate a nonlethal gastric emptying method in nonobese diabetic (NOD) LtJ mice, a model of type 1 diabetes, and study sequential changes with age and early diabetic status. The reliability and responsiveness of a [13C]octanoic acid breath test in NOD LtJ mice was tested, and the test was used to measure solid gastric emptying in NOD LtJ mice and nonobese diabetes resistant (NOR) LtJ mice. The 13C breath test produced results similar to postmortem recovery of a meal. Bethanechol accelerated gastric emptying [control: 92 ± 9 min; bethanechol: 53 ± 3 min, mean half emptying time ( T1/2) ± SE], and atropine slowed gastric emptying (control: 92 ± 9 min; atropine: 184 ± 31 min, mean T1/2 ± SE). Normal gastric emptying ( T1/2) in nondiabetic NOD LtJ mice (8–12 wk) was 91 ± 2 min. Aging had differing effects on gastric emptying in NOD LtJ and NOR LtJ mice. Onset of diabetes was accompanied by accelerated gastric emptying during weeks 1–2 of diabetes. Gastric emptying returned to normal by weeks 3–5 with no delay. The [13C]octanoic acid breath test accurately measures gastric emptying in NOD LtJ mice, is useful to study the time course of changes in gastric emptying in diabetic NOD LtJ mice, and is able to detect acceleration in gastric emptying early in diabetes. Opposing changes in gastric emptying between NOD LtJ and NOR LtJ mice suggest that NOR LtJ mice are not good controls for the study of gastric emptying in NOD LtJ mice.

scholarly journals The IL-1βReceptor Antagonist SER140 Postpones the Onset of Diabetes in Female Nonobese Diabetic Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Helena Cucak ◽  
Gitte Hansen ◽  
Niels Vrang ◽  
Torben Skarsfeldt ◽  
Eva Steiness ◽  
...  
Keyword(s):  
Immune Responses ◽  
Cell Function ◽  
Interleukin 1 ◽  
Nod Mice ◽  
Small Peptide ◽  
Nonobese Diabetic ◽  
Onset Of Diabetes ◽  
Diabetes Progression ◽  
Nonobese Diabetic Mice

The cytokine interleukin-1β(IL-1β) is known to stimulate proinflammatory immune responses and impairβ-cell function and viability, all critical events in the pathogenesis of type 1 diabetes (T1D). Here we evaluate the effect of SER140, a small peptide IL-1βreceptor antagonist, on diabetes progression and cellular pancreatic changes in female nonobese diabetic (NOD) mice. Eight weeks of treatment with SER140 reduced the incidence of diabetes by more than 50% compared with vehicle, decreased blood glucose, and increased plasma insulin. Additionally, SER140 changed the endocrine and immune cells dynamics in the NOD mouse pancreas. Together, the data suggest that SER140 treatment postpones the onset of diabetes in female NOD mice by interfering with IL-1βactivated pathways.

scholarly journals Insulin-independent reversal of type 1 diabetes in nonobese diabetic mice with brown adipose tissue transplant

2015 ◽  
Vol 308 (12) ◽  
pp. E1043-E1055 ◽  
Author(s):  
Subhadra C. Gunawardana ◽  
David W. Piston
Keyword(s):  
Type 1 Diabetes ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Nod Mice ◽  
Nonobese Diabetic ◽  
Brown Adipose ◽  
Igf I ◽  
Onset Of Diabetes ◽  
Nonobese Diabetic Mice

Traditional therapies for type 1 diabetes (T1D) involve insulin replacement or islet/pancreas transplantation and have numerous limitations. Our previous work demonstrated the ability of embryonic brown adipose tissue (BAT) transplants to establish normoglycemia without insulin in chemically induced models of insulin-deficient diabetes. The current study sought to extend the technique to an autoimmune-mediated T1D model and document the underlying mechanisms. In nonobese diabetic (NOD) mice, BAT transplants result in complete reversal of T1D associated with rapid and long-lasting euglycemia. In addition, BAT transplants placed prior to the onset of diabetes on NOD mice can prevent or significantly delay the onset of diabetes. As with streptozotocin (STZ)-diabetic models, euglycemia is independent of insulin and strongly correlates with decrease of inflammation and increase of adipokines. Plasma insulin-like growth factor-I (IGF-I) is the first hormone to increase following BAT transplants. Adipose tissue of transplant recipients consistently express IGF-I compared with little or no expression in controls, and plasma IGF-I levels show a direct negative correlation with glucose, glucagon, and inflammatory cytokines. Adipogenic and anti-inflammatory properties of IGF-I may stimulate regeneration of new healthy white adipose tissue, which in turn secretes hypoglycemic adipokines that substitute for insulin. IGF-I can also directly decrease blood glucose through activating insulin receptor. These data demonstrate the potential for insulin-independent reversal of autoimmune-induced T1D with BAT transplants and implicate IGF-I as a likely mediator in the resulting equilibrium.

13C-octanoic acid breath test (OBT) with a new test meal (EXPIROGer®): Toward standardization for testing gastric emptying of solids

2010 ◽  
Vol 42 (8) ◽  
pp. 549-553 ◽  
Author(s):  
Francesco Perri ◽  
Massimo Bellini ◽  
Piero Portincasa ◽  
Andrea Parodi ◽  
Patrizia Bonazzi ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Test Meal ◽  
Breath Test ◽  
Octanoic Acid

scholarly journals Rodent Models for Investigating the Dysregulation of Immune Responses in Type 1 Diabetes

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Feng-Cheng Chou ◽  
Heng-Yi Chen ◽  
Shyi-Jou Chen ◽  
Mei-Cho Fang ◽  
Huey-Kang Sytwu
Keyword(s):  
Type 1 Diabetes ◽  
Animal Studies ◽  
Genetic Manipulation ◽  
Nod Mice ◽  
Environmental Parameters ◽  
Conditional Knockout ◽  
Therapeutic Approaches ◽  
Nonobese Diabetic ◽  
Genetically Manipulated

Type 1 diabetes (T1D) is an autoimmune disease mediated by T cells that selectively destroy the insulin-producingβcells. Previous reports based on epidemiological and animal studies have demonstrated that both genetic factors and environmental parameters can either promote or attenuate the progression of autoimmunity. In recent decades, several inbred rodent strains that spontaneously develop diabetes have been applied to the investigation of the pathogenesis of T1D. Because the genetic manipulation of mice is well developed (transgenic, knockout, and conditional knockout/transgenic), most studies are performed using the nonobese diabetic (NOD) mouse model. This paper will focus on the use of genetically manipulated NOD mice to explore the pathogenesis of T1D and to develop potential therapeutic approaches.

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