Beta cells reside in the pancreas, where they do the important job of producing insulin for the body. Beta cells secrete, or release insulin when they are signaled to do so by an increase in glucose levels in the blood (Alberts et al. 1998). Without adequate insulin, blood glucose levels rise too high, a defining characteristic of diabetes. By the time someone is diagnosed with type 1 diabetes, they have lost 70-80% of their beta cell mass (it is thought, although more recent studies are testing this number). Beta cell loss occurs gradually over time, beginning before diagnosis, and continuing afterwards, until most beta cells are lost (Cnop et al. 2005).

 

Type 1 diabetes is an autoimmune disease, and beta cell death in type 1 is thought to be largely due to an autoimmune attack on the beta cells (Narendran et al. 2005). The attack on the beta cells is a type of inflammatory reaction called "insulitis." Beta cell apoptosis, or programmed cell death, is the main cause of beta cell death at the onset of type 1 diabetes (Cnop et al. 2005). The immune system cells involved in apoptosis are described further on the inflammation page. See the types of diabetes page for a discussion of beta cell loss in type 2 diabetes.

A number of researchers have proposed that environmental factors that can stress (some use the term "overload") beta cells may be critical to explain the increasing incidence of type 1 diabetes in children. For example, Dahlquist (2006) argues that overloading beta cells may make them more susceptible to the autoimmune attack in type 1 diabetes, thus accelerating their destruction. Ludvigsson (2006) argues that when the demand for insulin is great, beta cells may have to work harder to produce adequate insulin. If the immune system is prone to react against insulin overload (perhaps due to the bovine insulin in cow's milk), increased insulin production could stimulate the autoimmune process. Increased insulin resistance will also increase beta cell stress. Animal and human studies have found certain metabolic changes that increase the demands in the period leading up to type 1 diabetes, including an increase in insulin secretion (Sysi-Aho et al. 2011). 

Wilkin (2001) argues that a beta cell insufficiency leads to autoimmunity in those genetically prone to it-- a controversial view, but one that has some evidence behind it. In his view, weight gain and insulin resistance stress the beta cells, originally by high glucose levels, and then in some people the immune system targets the beta cells for removal, accelerating the disease process. The debate is rather like the chicken or the egg-- which came first, beta cell stress, or autoimmunity? The answer remains to be seen.

 

A number of environmental factors may be able to stress or overload beta cells, including increased growth rates (in height and weight), viruses, stress, puberty, and some nutritional factors. Vitamin D can protect beta cells from inflammation, while vitamin D deficiency can impair insulin secretion. 

A number of environmental contaminants have also been found to affect beta cells and/or processes of insulin secretion in animals or laboratory experiments. Some (e.g., bisphenol A, PCBs) have been found to increase insulin secretion. Some (e.g., arsenic, mercury) impair insulin secretion, or have been associated with impaired insulin secretion in humans (e.g., persistent organic pollutants). Some (e.g., dioxin) can impair or increase insulin secretion. And some (e.g., PCBs, cadmium, mercury) have been found to damage the beta cells themselves. Developmental exposure to phthalates has multiple effects on beta cells and the pancreas in animals. 

Hectors et al. (2011) review the effects of various chemicals on beta cells, including persistent organic pollutants, estrogenic compounds like bisphenol A, and organophosphorous pesticides. I asked these authors how chemicals could both increase and decrease insulin secretion? There may be a few reasons. One, some endocrine disruptors can have opposite effects at high or low doses (because of how hormones act). Two, the effect might vary depending on whether the experiment was done in animals or in cells, or which species of animal was used. Importantly, either increasing or decreasing insulin secretion could be significant for diabetes development. If secretion is decreased, it is easy to see how high glucose and then diabetes could result. If insulin secretion is increased, that could lead to increased levels of insulin in the body (increasing insulin resistance), and eventual beta cell exhaustion (Hectors, T., pers. commun., 2011). "It is clear that some environmental pollutants affect pancreatic beta cell function" and these mechanisms may play a role in diabetes development (Hectors et al. 2011).

See the linked pages for more information and for references.

Environmental factors that can affect beta cells may be involved in accelerating the progression of type 1 diabetes. As such, they may contribute to the increasing incidence of this disease in children and its appearance at younger ages.