Air Pollution and Weight Gain, Insulin Resistance and Metabolic Syndrome: Recent Findings

written by Sarah Howard
Coordinator of the Diabetes-Obesity Spectrum Working Group

Sarah HowardTwo studies published this month provided strong support for the idea that air pollution may cause weight gain, insulin resistance, and metabolic syndrome.

In the first study, pregnant rats exposed to Beijing’s air gained significantly more weight during pregnancy than those breathing filtered air. Their offspring (exposed pre- and postnatally) were also significantly heavier at 8 weeks of age.

In the second study, Mexican Americans living in Southern California exposed to ambient air pollutants had lower glucose tolerance, higher insulin resistance, and adverse blood lipid concentrations.  According to the authors, “the magnitudes of effect from a 1-[standard deviation] difference of [fine particulate matter] on metabolic outcomes were similar compared with the impact of a 1-unit change in percent body fat or [body mass index] BMI on the same metabolic outcomes.”

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The Effect of Environmental Chemicals on Insulin Production: Implications for All Types of Diabetes

Sarah Howard
Coordinator of CHE’s Diabetes-Obesity Spectrum Working Group

In a recent review, published in the leading diabetes journal Diabetologia, Hectors et al. (2011) describe how numerous environmental chemicals affect the insulin-producing beta cells of the pancreas. These effects, the authors argue, may be significant in the development of type 2 diabetes. Chemicals like bisphenol A, PCBs, dioxin, organophosphorous pesticides, arsenic, heavy metals, and others, can all affect how the beta cells function, and can interfere with their capacity to secrete insulin.

In type 2 diabetes, both insulin resistance—the body’s inability to respond correctly to insulin—and beta cell malfunction contribute to the disease. The inability of the beta cells to produce enough insulin leads to high blood glucose levels, and eventually diabetes (in many people with type 2, insulin production is higher than normal, to compensate for the insulin resistance—but it is still inadequate to bring blood glucose under control).   

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