There is a link between obesity
in pregnant mothers and high blood pressure and chronic kidney disease
in their children, suggested previous studies. This leads to a greater risk of cardiovascular disease,
such as heart attacks, later in life.
Exposure of babies to high levels of the 'fullness' hormone, leptin,
in the womb irreversibly activates receptors in the brain that regulate
blood pressure, revealed a new study by researchers from King's
College London, part-funded by the British Heart Foundation. This
activation may lead to a lifelong increased risk of high blood pressure
and kidney disease.
‘Exposure of babies to high levels of the 'fullness' hormone, leptin, in the womb irreversibly activates receptors in the brain that regulate blood pressure.’
The new research, published in the journal Proceedings of the National Academic of Sciences
used a mouse model to investigate the role of the hormone leptin, as
children of obese mothers are exposed to high levels of leptin during
development in the womb. Leptin is a signal produced by cells in the
body, especially fat cells, after eating to indicate satiety - fullness -
and is important in suppressing appetite, but it is also thought to
play an important role in the control of blood pressure.
Exposure of newborn immature mice to high levels of leptin activated
neurons with a melanocortin-4 receptor (Mc4r) in the brains of infant
mice. The Mc4r is found on neurons in a region of the hypothalamus in
the brain, which controls hunger and blood pressure.
Mice that experienced activation of Mc4r neurons by elevated leptin
had high blood pressure and kidney damage later in life. The exposure to
leptin reset the brain's response to leptin, so that in adulthood their
brains produced a bigger increase in blood pressure in response to
Professor Lucilla Poston, senior author on the paper, Head of the
Division of Women's Health at King's College London and co-leader of the
Women's Health Clinical Academic Group at King's Health Partners said, "We are increasingly aware of the important role played by maternal
metabolic and nutritional status in the risk of adulthood disease in the
offspring. Maternal obesity has been linked to later obesity, diabetes
and hypertension in the child, but the mechanisms have proved elusive.
This study identifies an exquisite vulnerability of certain cells in the
developing brain to metabolic disturbance associated with maternal
obesity, and shows how this may contribute to development of high blood
pressure in later life."
Dr. Anne-Maj Samuelsson, lead author on the paper from the Division
of Women's Health at King's College London, said, "Several recent
mother-child cohorts demonstrate higher blood pressure in children born
to obese mothers. High blood pressure in children is an important risk
factor for cardiovascular disorders in adulthood. This study identified a
mechanistic link between maternal obesity and childhood hypertension.
The absence of one specific gene, called Mc4r, in the brain, protected
the offspring of obese mice from hypertension. By adding the Mc4r back
to the mouse brain, we were able to reinstate the hypertension in
offspring born to obese mice. Our findings need to be verified in human
studies to determine if Mc4r is a therapeutic target for hypertension."