Bisphenol A Suppresses Release of Adipose Hormone
Exposure May Contribute to Metabolic Syndrome
Bisphenol A (BPA), a chemical used in the manufacture of numerous
consumer products, is ubiquitous throughout the environment, and its
widespread presence in human serum has been well documented. Although
animal research indicates that BPA can alter several metabolic
functions, interpretation of human data has been more controversial. A
new study now presents evidence confirming that exposure of human
adipose tissue and isolated fat cells to environmentally relevant
levels of BPA suppresses release of the hormone adiponectin
EHP 116:1642–1647; Hugo et al.].
A high-calorie diet and sedentary lifestyle have both
traditionally been linked to metabolic syndrome—the presence of a
constellation of metabolic risk factors including insulin resistance,
hypertension, and elevated blood sugar and lipid levels—but researchers
are now examining environmental factors as additional causes.
Adiponectin increases insulin sensitivity and reduces tissue
inflammation, so suppression of its release could lead to insulin
resistance and increased susceptibility to metabolic syndrome, the
The study examined three types of adipose tissue samples taken
during breast reduction, abdominoplasty, and gastric bypass surgery.
The research team incubated each type of tissue for 6 hours in BPA or
an endogenous human estrogen. They used enzyme-linked immunosorbent
assay to measure secreted adiponectin. They also used quantitative
real-time polymerase chain reaction to compare the expression of
estrogen receptors and estrogen-related receptors in these tissues.
In all three tissue types, exposure to low-nanomolar concentrations
of BPA suppressed adiponectin as effectively or more effectively
compared with equimolar concentrations of E2.
The authors also showed that the dose response to BPA was nonmonotonic,
meaning lower doses caused different effects than higher doses.
Finally, they report for the first time similar mRNA expression levels
for several estrogen receptors in visceral adipose tissue, although the
role of these receptors in the suppressive nature of BPA and E2 has yet to be determined.
The results of the data are limited by the relatively small sample
size in each tissue category, as well as the potential unknown effects
of age or obesity on tissue responsiveness. However, the authors write
that their data present clear evidence that BPA suppresses adiponectin,
potentially leading to a much higher risk of developing metabolic
syndrome and its resultant adverse health effects. They conclude that
with BPA's persistence in the environment, more research should be done
to determine the mechanism by which the chemical suppresses