[Spontaneous model] Lean diabetes mice, originated from ICR mice. There is a significant difference in the time when diabetes occurs between male and female mice. The incidence of disease in female rats was more than 90 days old, and the incidence of incidence rate in female rats of 200 days old reached 80%. The onset time of male rats was about 150 days old, and the cumulative incidence rate was less than 20%. There was no prodromal symptoms and diabetes suddenly appeared.
[Result analysis] The indexes of lean diabetes mice before onset were within the normal range, and it was not possible to predict whether diabetes would occur in the future from these indexes. After the onset of the disease, animals exhibit obvious symptoms such as excessive drinking, polyuria, hyperglycemia, and urinary sugar. As clinical symptoms worsen, weight begins to decrease and there is a phenomenon of overeating; Some mice developed ketonuria, and there was no difference in their glucose tolerance test before the onset of the disease compared to normal mice. However, the glucose tolerance of the mice significantly decreased after the onset of the disease. Once female mice exhibit dominant urine sugar, it is difficult to turn negative again. About one month, one will die due to weakness, and at the time of death, their weight will drop below 20g. After the appearance of dominant diabetes in male mice, urine sugar often turns negative again. Most male mice do not experience rapid decline like female mice. Sick mice have a good response to exogenous insulin. Injecting insulin at a dose of 40U/kg body weight can greatly prolong the animal's lifespan. The pathological feature of the pancreas is insulitis. Mice cannot see this pathological change before 3 weeks of age, and mice after 5 weeks of age show 70% to 90% of this pathological change. There is almost no difference between male and female, but there is varying degrees of lymphocyte infiltration. After the onset of the disease, this infiltration phenomenon gradually decreases. The pancreatic islets of diseased animals showed significant atrophy and a sharp decrease in number. In the remaining cells of the pancreatic islets, almost no B cells with aldehyde fuchsin positive particles were found. There were no significant changes in organs other than the pancreas, such as the heart, brain, spleen, kidney, adrenal gland, pituitary gland, testicles, ovaries, etc. of the diseased animals.
The clinical manifestations and pathological changes of islets in lean diabetes mice are very similar to human insulin dependent diabetes. The diabetes mouse had islet inflammation before the onset of dominant diabetes, so it can be used as a model animal to study the causes of human lean diabetes.