Yes. Some animals do get diabetes naturally, including apes, pigs, sheep, horses, cats, and dogs. All mammals produce insulin, and will develop diabetes (defined as high blood glucose levels) if their pancreatic beta cells are removed. Vets classify canine diabetes into "insulin deficiency diabetes" and "insulin resistance" diabetes (perhaps somewhat analogous to type 1 and type 2 in humans). Female dogs may also develop a canine form of gestational diabetes. There is some evidence that dogs do actually develop a form of autoimmune diabetes, that is more similar to Latent Autoimmune Diabetes in Adults (LADA) than to childhood type 1 diabetes (Gale 2005c). Interestingly, some of the same autoantibodies found in humans with type 1 diabetes have also been found in some dogs with diabetes (Davison et al. 2008). (See the types of diabetes page for more on LADA and gestational diabetes, and the autoimmunity page for more on autoantibodies). Technically, only humans get type 1 diabetes (Gale 2008), although some authors do use the term type 1 to describe autoimmune diabetes in animals.

 

Scientists generally use rodents as animal models of type 1 diabetes in the laboratory. The two main rodent strains used are non-obese diabetic (NOD) mice and Biobreeding (BB) rats. These rodents have been bred to spontaneously develop diabetes. Both animals develop a form of autoimmune diabetes that includes the presence of some autoantibodies, although there are also differences between the autoimmune diabetes in these animals and type 1 diabetes in humans. While these animals may be useful for some purposes (such as developing a cure for type 1 diabetes once it develops, or identifying biological mechanisms), their usefulness is also in question.

How useful are NOD mice for predicting the effects of various environmental factors to either cause or prevent type 1 diabetes in humans? Perhaps not very. Most interventions-- at last count, 195 of them-- delay or prevent diabetes in NOD mice (Roep and Atkinson 2004). Some of these interventions have been tried in people and have not successfully prevented or delayed type 1 diabetes. For example:

Some researchers have used NOD mice to investigate the potential role of environmental contaminants in the development of autoimmune diabetes. I have found three studies on contaminants and NOD mice. These studies found that some contaminants do not accelerate or can even delay diabetes in NOD mice: mercury (Brenden et al. 2001), trichloroethylene (Ravel et al. 2005), and dioxin (Kerkvliet et al. 2009). Yet these contaminants have all been found to accelerate autoimmunity in other strains of mice. What these findings mean for humans is not clear.

 

Van der Werf et al. (2007) suggests that NOD mice are probably not appropriate to use for studying the role of viruses in the development of type 1 diabetes in humans; likewise, NOD mice are probably not appropriate to use to examine the effects of environmental contaminants on type 1 diabetes in humans. Researchers have in fact joked, "If you look cross-eyed at NOD mice, you prevent diabetes" (Roep and Atkinson 2004), although others point out that not quite everything prevents diabetes in NOD mice, and that the effects of various interventions may depend on timing and dosage (Shoda et al. 2005). Personally, I would not suggest giving children mercury, trichloroethylene, or dioxin with the hope that they might prevent type 1 diabetes, despite their effects on NOD mice.

Can other animals be used to study the potential effects of contaminants or other environmental factors on the development of type 1 diabetes? Perhaps. I have not found any studies on contaminants and BB rats, and I do not know if these animals could be a useful model or not. Perhaps dogs can, but I am not going to advocate any research on dogs.

 

Most convincing might be the ability of contaminants to induce diabetes in animals that are not prone to develop the disease. Helgason et al. (1982), for example, found that if mice consumed meat cured with nitrite before mating and during pregnancy, and their offspring consumed it for a time, then some of the offspring developed glucose abnormalities and diabetes. This strain of mice does not normally develop diabetes. This study supports previous findings in humans suggesting that parental consumption of this meat around the time of conception can lead to the development of type 1 diabetes in their children (see the nitrate and nitrite page for information).

A number of pages on this website discuss the ability of contaminants to induce or exacerbate autoimmunity in various strains of rodents (see, for example, the pages on bisphenol A, dioxin, heavy metals, phthalates, and trichloroethylene). What rodents were used in these studies? Many of them used rodents that are genetically susceptible to the autoimmune disease systemic lupus erythematosus (SLE, also known as lupus). Whether these findings would have any relevance for type 1 diabetes is not known. Some researchers are also beginning to investigate the effects of contaminants on animals not prone to autoimmunity or autoimmune diseases.

 

Phthalates have been shown to induce autoimmunity in various strains of mice, including some that are not prone to autoimmunity. Different strains show differing effects, however, in that the susceptible strains show signs of disease (in this case, SLE), while the others do not  (Lim and Ghosh 2005).

 

When mice not genetically prone to autoimmune disease were treated prenatally with dioxin (TCDD) during immune system development, they had immune dysregulation that included autoantibody production, and suggested an increased risk for later autoimmune disease. These findings suggest that developmental exposure to TCDD may increase the risk of autoimmune disease. These mice, however, are more sensitive than other strains of mice to the effects of dioxin (Mustafa et al. 2008).

 

While exposure to mercury can induce or exacerbate autoimmunity in genetically susceptible rodents (Hemdan et al. 2007), mercury has also been shown to induce autoimmunity even in mice that are not genetically susceptible to autoimmunity (Abedi-Valugerdi 2009). Exposure to mercury in combination with a bacterial infection aggravated autoimmune disease in genetically susceptible mice. And, mice that were not genetically susceptible to autoimmunity were made susceptible (Abedi-Valugerdi et al. 2005).

 

These examples show cases where contaminants could induce or affect autoimmunity even in animals not prone to autoimmunity. The health effects of the exposures varied by strain of animal. Perhaps the potential effects of environmental contaminants on the development of type 1 diabetes would likewise vary based on the genetic background of the individual.

NOD mice may not be appropriate for examining the effects of environmental contaminants or other environmental factors on the development of type 1 diabetes in humans. The ability of contaminants to influence the development of diabetes or autoimmunity in animals that are not bred to spontaneously develop these conditions might be more revealing. Animal research might be able to identify situations where timing is important (e.g., in the case of meat containing nitrites), or the mechanisms involved in disease development.