Genetic analysis of the LEW.1AR1-iddm rat: an animal model for spontaneous diabetes mellitus

The temperament of cattle is believed to affect the profitability of the herd through impacting production costs, meat quality, reproduction, maternal behaviour and the welfare of the animals and their handlers. As part of the national beef cattle genetic evaluation in Australia by BREEDPLAN, 50 935 Angus and 50 930 Limousin calves were scored by seedstock producers for temperament using docility score. Docility score is a subjective score of the animal’s response to being restrained and isolated within a crush, at weaning, and is scored on a scale from 1 to 5 with 1 representing the quiet and 5 the extremely nervous or anxious calves. Genetic parameters for docility score were estimated using a threshold animal model with four thresholds (five categories) from a Bayesian analysis carried out using Gibbs sampling in THRGIBBS1F90 with post-Gibbs analysis in POSTGIBBSF90. The heritability of docility score on the observed scale was 0.21 and 0.39 in Angus and Limousin, respectively. Since the release of the docility breeding value to the Australian Limousin population there has been a favourable trend within the national herd towards more docile cattle. Weak but favourable genetic correlations between docility score and the production traits indicates that docility score is largely independent of these traits and that selection to improve temperament can occur without having an adverse effect on growth, fat, muscle and reproduction.

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Melatonin-Pretreated Mesenchymal Stem Cells Improved Cognition in a Diabetic Murine Model

Frontiers in Physiology ◽

10.3389/fphys.2021.628107 ◽

2021 ◽

Vol 12 ◽

Author(s):

Shaimaa Nasr Amin ◽

Nivin Sharawy ◽

Nashwa El Tablawy ◽

Dalia Azmy Elberry ◽

Mira Farouk Youssef ◽

...

Keyword(s):

Diabetes Mellitus ◽

Stem Cells ◽

Animal Model ◽

Mesenchymal Stem Cells ◽

Synaptic Plasticity ◽

Object Recognition ◽

Ex Vivo ◽

Type I ◽

Positive Effects ◽

Tnf Α

Diabetes mellitus (DM) is a multisystem endocrine disorder affecting the brain. Mesenchymal stem cells (MSCs) pretreated with Melatonin have been shown to increase the potency of MSCs. This work aimed to compare Melatonin, stem cells, and stem cells pretreated with Melatonin on the cognitive functions and markers of synaptic plasticity in an animal model of type I diabetes mellitus (TIDM). Thirty-six rats represented the animal model; six rats for isolation of MSCs and 30 rats were divided into five groups: control, TIDM, TIDM + Melatonin, TIDM + Stem cells, and TIDM + Stem ex vivo Melatonin. Functional assessment was performed with Y-maze, forced swimming test and novel object recognition. Histological and biochemical evaluation of hippocampal Neuroligin 1, Sortilin, Brain-Derived Neurotrophic Factor (BDNF), inducible nitric oxide synthase (iNOS), toll-like receptor 2 (TLR2), Tumor necrosis factor-alpha (TNF-α), and Growth Associated Protein 43 (GAP43). The TIDM group showed a significant decrease of hippocampal Neuroligin, Sortilin, and BDNF and a significant increase in iNOS, TNF-α, TLR2, and GAP43. Melatonin or stem cells groups showed improvement compared to the diabetic group but not compared to the control group. TIDM + Stem ex vivo Melatonin group showed a significant improvement, and some values were restored to normal. Ex vivo melatonin-treated stem cells had improved spatial working and object recognition memory and depression, with positive effects on glucose homeostasis, inflammatory markers levels and synaptic plasticity markers expression.

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Prevention of diabetes in the BB rat by essential fatty acid deficiency. Relationship between physiological and biochemical changes.

Journal of Experimental Medicine ◽

10.1084/jem.171.3.729 ◽

1990 ◽

Vol 171 (3) ◽

pp. 729-743 ◽

Cited By ~ 43

Author(s):

J Lefkowith ◽

G Schreiner ◽

J Cormier ◽

E S Handler ◽

H K Driscoll ◽

...

Keyword(s):

Fatty Acids ◽

Animal Model ◽

Fatty Acid ◽

Protective Effect ◽

Essential Fatty Acid ◽

Autoimmune Diabetes ◽

Spontaneous Diabetes ◽

Bb Rat ◽

Deficiency State ◽

Bb Rats

Essential fatty acid (EFA) deficiency exerts a striking protective effect in several animal models of autoimmune disease. We now report that EFA deprivation prevents diabetes in the BB rat, an animal model of human insulin-dependent diabetes mellitus. In diabetes-prone (DP)-BB rats, the incidences of spontaneous diabetes and insulitis (the pathological substrate of autoimmune diabetes) were greatly reduced by EFA deficiency. This beneficial effect of the deficiency state was also seen in diabetes-resistant (DR)-BB rats that, after treatment with antibody to eliminate RT6+ T cells, would otherwise have become diabetic. The susceptibility of EFA-deprived DP-BB rats to spontaneous diabetes was restored when they were given dietary supplements of linoleate at 70 d of age (during the usual period of susceptibility), but not when they were repleted beginning at 120 d (after the peak incidence of diabetes). EFA deficiency did lead to growth retardation, but calorically restricted control rats demonstrated that the protective effect of the deficiency state was not a function of decreased weight. To examine the relationship between the biochemical changes of EFA deficiency and its physiological effects in this system, we compared the fatty acid changes that occurred in EFA-deficient animals that did and did not develop diabetes. Nondiabetic animals had significantly lower levels of (n-6) fatty acids (i.e., linoleate and arachidonate) and higher levels of oleate, an (n-9) fatty acid, than did diabetic animals. Levels of 20:3(n-9), the fatty acid that uniquely characterizes EFA deficiency, were similar in both groups, however. Among diabetic EFA-deficient rats, the age at onset of diabetes was found to correlate inversely with the level of (n-6) fatty acids, the least depleted animals becoming diabetic earliest, whereas there was no correlation with levels of 20:3(n-9). Among animals repleted with linoleate beginning at 70 d, restoration of susceptibility to diabetes correlated with normalization of the level of arachidonate. In summary, EFA deprivation reduced the frequency of diabetes in both DP and RT6-depleted DR-BB rats. This protective effect was strongly associated with depletion of (n-6) fatty acids, particularly arachidonate, but not with accumulation of the abnormal 20:3(n-9). Conjecturally, arachidonate and/or a metabolite may play a key role in mediating inflammatory injury in this animal model of autoimmune diabetes.

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