- Obesity can cause high blood pressure (hypertension), which increases the risk of disability and death.
- Fat tissue releases a hormone called leptin into the bloodstream that sends signals to a part of the brain called the hypothalamus.
- When fat stores increase, a corresponding increase in leptin signals that the body has sufficient energy reserves.
- A new study in mice suggests that raised leptin levels as a result of obesity also triggers the growth of blood vessels in the hypothalamus, which in turn causes hypertension.
Scientists and other healthcare professionals know that obesity is a risk factor for atherosclerosis, which involves narrowing and stiffening of arteries and often leads to hypertension.
However, they know less about the effects of obesity on the small blood vessels around the body, including the brain.
According to a new study, the abnormal growth of small blood vessels in a particular part of the brain may be partly responsible for causing hypertension in people with obesity.
Both kinds of damage — to the large and the small vessels — are recognized factors in the increased risks of disability and mortality associated with obesity.
Older research in mice and humans revealed that eating a high-calorie diet triggers the growth of small blood vessels in the hypothalamus, which is a part of the brain that regulates appetite and blood pressure.
Prof. Cristina García-Cáceres and her colleagues at Helmholtz Zentrum München in Germany set out to discover whether blood vessel growth in the hypothalamus contributes to hypertension.
When the researchers fed mice a high-fat, high-sugar diet, they found increased growth of blood vessels in the animals’ hypothalamus just 2 weeks later.
This blood vessel growth coincided with weight gain and raised blood levels of leptin, a hormone produced by fat tissue to help regulate long-term food intake.
In further experiments, the researchers used mice that they genetically engineered to have obesity but no leptin. Despite having obesity, these mice did not show any vascular changes in the hypothalamus. Therefore, the researchers suggest that leptin is the key player in mediating vascular changes.
However, when the scientists injected the mice with leptin, the animals lost weight and sprouted more hypothalamic blood vessels.
In further experiments, the researchers showed that star-shaped cells in the hypothalamus called astrocytes mediated this effect.
Leptin induced the cells to produce “vascular endothelial growth factor” (VEGF) and stimulate blood vessel growth.
Crucially, VEGF and the overgrowth of blood vessels in this part of the brain appeared to trigger increased blood pressure in obese mice.
The study appears in the journal
Previously, researchers have focused on the effect of leptin on nerves in the hypothalamus to explain how obesity causes hypertension.
“We provide a paradigm shift in our understanding of how the hypothalamus controls blood pressure in obesity,” says first author Dr. Tim Gruber.
“While previous research has focused primarily on neurons, our research highlights the new role of astrocytes, historically assumed less relevant than neurons, in controlling blood pressure,” he adds.
The scientists note that the principal limitation of their study was that it did not explain how VEGF expression and blood vessel growth in the hypothalamus raises blood pressure.
In addition, as with any animal model of disease, the findings may not translate well to humans with obesity.