Food additive fuels weight gain, diabetes

New research shows that additives, which are a mainstay of many Western diets, may not be as benign as previously understood. A common anti- mold agent used as an additive in many foods has now been implicated in altering sugar metabolism and driving insulin resistance in mice and men.

Eating a Western diet, high in processed foods, sugar, and fat, is a known risk factor for obesity and type 2 diabetes. Processed foods filled with preservatives meant to keep the product fresh for longer are present in many places.

The anti-mold agent propionate, a short-chain fatty acid that the bacteria in our gut produce naturally, is used as an additive in many common foods such as breads and other baked products.

According to the international food standards guide by the World Health Organization (WHO) and the Food and Agriculture Organization of the United Nations, propionate, often abbreviated as E282, may be added to a host of foods, including breakfast cereals, dairy- and egg-based deserts, sausage casings, processed cheese, and sports drinks.

Researchers from Harvard School of Public Health in Boston, USA and the Sheba Medical Center, in Israel, have now found that propionate leads to high blood sugar in mice. The team gave healthy, non-obese mice a dose of the preservative and found that blood sugar levels rose significantly.

The researchers found that propionate activated the sympathetic nervous system, and increased the levels of the hormones glucagon and FABP4. This caused the liver to produce high levels of glucose, which in turn led to high levels of insulin in the blood.

Normally, these hormones act during fasting to protect against a dangerous drop in blood glucose. In this case, they were found to be engaging without such a threat and increasing blood glucose.

The mice were then fed a low dose of between 0.15 and 0.3 percent propionate in their diet over several weeks. This is equivalent to how much a person eating a Western diet would consume.

As a result, the mice developed higher levels of glucagon and FABP4, high levels of blood insulin, and insulin resistance — a hallmark of type 2 diabetes. They also put on more weight, with a significant increase in fat mass, compared with the mice receiving a standard diet.

Next, the research team recruited 14 healthy, non-obese volunteers. The study participants ate a meal supplemented with propionate in the form of 1 gram (g) of calcium propionate or placebo. The 1g is equivalent to the most commonly used amount of 0.3 percent to which humans are exposed when consuming a single processed food–based meal.

After 2 weeks, the same participants returned, and the groups were switched, meaning that the volunteers who were in the placebo group during the first visit ate the propionate-containing meal during the second visit. As with the mice, the study participants experienced spikes of norepinephrine, glucagon, and FABP4, increased blood insulin levels, and reduced insulin sensitivity.

The researchers acknowledge that the study’s limitations include that fact that they were unable to show cause and effect of propionate consumption on global obesity and type 2 diabetes. The team also did not study the long-term effects of chronic, low-level propionate exposure in humans. The research should serve as a proof-of-principle for the potential interference of propionate in normal metabolism, the team stated.

Meanwhile, the team’s research efforts continue, with a focus on how preservatives, artificial sweeteners, and other natural ingredients might affect our metabolism. Given the epidemic proportion of obesity and diabetes, there is a need, in our view, to extensively assess the potential long-term metabolic effects of many environmental factors that have changed over the past few decades, both for their potential harmful and useful effects, they added.