Summary: Drinking water can suppress the vasopressin hormone receptor, mitigating obesity and metabolic syndrome in mice.
Source: University of Colorado
Researchers at the University of Colorado Anschutz Medical Campus have discovered that fructose stimulates the release of vasopressin, a hormone linked to obesity and diabetes. They also found that water can suppress the hormone and alleviate these conditions in mice.
“The clinical significance of this work is that it may encourage studies to evaluate whether simple increases in water intake may effectively mitigate obesity and metabolic syndrome,” said the study’s lead author Miguel A. Lanaspa, PhD, an associate professor at the University of Colorado School of Medicine specializing in renal disease and hypertension.
The study was published today in the journal JCI Insight.
Lanaspa and his colleague, Richard Johnson, MD, also a professor at the CU School of Medicine, wanted to understand why vasopressin, which maintains the body’s water levels, was elevated in those with obesity and diabetes.
They fed mice sugar water, specifically fructose, and found that it stimulated the brain to make vasopressin. The vasopressin in turn stored the water as fat causing dehydration which triggered obesity. Treating the mice with non-sugary water reduced the obesity.
According to Lanaspa, this is the first time scientists have shown how vasopressin acts on dietary sugar to cause obesity and diabetes.
“We found that it does this by working through a particular vasopressin receptor known as V1b,” he said. “This receptor has been known for a while but no one has really understood its function. We found that mice lacking V1b were completely protected from the effects of sugar. We also show that the administration of water can suppress vasopressin and both prevent and treat obesity.”
The researchers also discovered that dehydration can stimulate the formation of fat.
“This explains why vasopressin is so high in desert mammals as they do not have easy access to water,” Johnson said. “So vasopressin conserves water by storing it as fat.”
This data fits with observations showing that obese people often have signs of dehydration. It also explains why high salt diets may also cause obesity and diabetes.
The researchers found that water therapy in mice effectively protected against metabolic syndrome – a collection of conditions including high blood pressure, high blood sugar and high triglyceride levels that increase the risk of heart disease, stroke and type 2 diabetes.
“The best way to block vasopressin is to drink water,” Lanaspa said. “This is hopeful because it means we may have a cheap, easy way of improving our lives and treating metabolic syndrome.”
Johnson summed up the findings this way.
“Sugar drives metabolic syndrome in part by the activation of vasopressin. Vasopressin drives fat production likely as a mechanism for storing metabolic water,” he said. “The potential roles of hydration and salt reduction in the treatment of obesity and metabolic syndrome should be considered.”
About this metabolism research news
Source:University of Colorado Contact: David Kelly – University of Colorado Image: The image is in the public domain
Vasopressin mediates fructose-induced metabolic syndrome by activating the V1b receptor
Subjects with obesity frequently have elevated serum vasopressin levels, noted by the stable analog, copeptin. Vasopressin acts primarily to reabsorb water via urinary concentration. However, fat is also a source of metabolic water, raising the possibility that vasopressin might have a role in fat accumulation. Fructose has also been reported to stimulate vasopressin. Here we tested the hypothesis that fructose induced metabolic syndrome is mediated by vasopressin. Orally administered fructose, glucose or high fructose corn syrup increased vasopressin (copeptin) concentrations and was mediated by fructokinase, an enzyme specific for fructose metabolism. Suppressing vasopressin with hydration both prevented and ameliorated fructose-induced metabolic syndrome. The vasopressin effects were mediated by the Vasopressin 1b receptor, as Vasopressin 1b receptor knockout mice were completely protected while V1a knockout paradoxically showed worse metabolic syndrome. The mechanism is likely mediated in part by de novo expression of V1b in the liver that amplifies fructokinase expression in response to fructose. Thus, our studies document a new role for vasopressin in water conservation via the accumulation of fat as a source of metabolic water. Clinically, it also suggests that increased water intake may be a beneficial way to both prevent or treat metabolic syndrome.