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       Gut bacteria metabolism may factor into hypertension
   DIR By: Admin
       Date: May 3, 2019, 11:30 am
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       Gut bacteria metabolism may factor into hypertension
       Date:
       October 3, 2017
       Source:
       University of Illinois College of Agricultural, Consumer and
       Environmental Sciences
       Summary:
       One in three American adults suffers from high blood
       pressure, or hypertension. The disease can be passed down in
       families, and certain lifestyle factors such as smoking,
       high-sodium diets, and stress can increase the risk. In recent
       years, scientists have discovered that certain gut bacteria may
       contribute to hypertension, as well.
       One in three American adults suffers from high blood pressure,
       or hypertension. The disease can be passed down in families, and
       certain lifestyle factors such as smoking, high-sodium diets,
       and stress can increase the risk. In recent years, scientists
       have discovered that certain gut bacteria may contribute to
       hypertension, as well.
       In a few studies, when gut bacteria were killed off with
       antibiotics, patients with hypertension saw a drop in blood
       pressure. And when gut bacteria were transplanted from
       hypertensive people into normal mice, they developed high blood
       pressure. The evidence is compelling, but until now, scientists
       have not identified a mechanism to explain how bacteria increase
       blood pressure.
       Researchers from the University of Illinois and Brown University
       are pursuing a promising lead. Jason Ridlon, an assistant
       professor in the Department of Animal Sciences at U of I, first
       discovered the gene for an enzyme in certain bacteria that
       changes cortisol, a steroid hormone, into another steroid known
       as an androgen.
       Ridlon worked with endocrinologist David Morris at Brown and
       found that when bacteria break that androgen down further, the
       end product, a molecule called a GALF, disrupts a process that
       regulates sodium transport out of human kidney cells. When that
       happens, sodium builds up in cells, and blood pressure rises.
       To maintain normal blood pressure, a particular receptor has to
       bind with a molecule called aldosterone and then move into the
       cell nucleus. That sparks a cascade of reactions whose
       end-product is a protein that manages normal sodium and
       potassium transport into and out of the cell. But the receptor
       can be fooled, binding to cortisol instead of aldosterone. If
       that happens, as it does in rare individuals with a disease
       called apparent mineralocorticoid excess (AME), the cascade of
       reactions goes into hyperdrive. Sodium is imported faster than
       it can be exported, and the cell begins to swell into a
       dangerous hypertensive state.
       In normal individuals, an enzyme called 11βHSD2 acts as the
       guardian of that receptor, keeping cortisol from binding by
       changing it to cortisone. GALFs -- and there are a number of
       them -- stop 11βHSD2 from working. Cortisol floods the
       receptor binding sites, and hypertension ensues as previously
       described.
       "There are probably multiple mechanisms through which gut
       bacteria can affect hypertension, but this is one that needs to
       be pursued," Ridlon says. He and Morris explore the idea in
       depth in a new article published in the journal Steroids.
       From a different research effort, Ridlon has found that not all
       gut bacteria metabolize cortisol in the same way, or generate
       GALFs.
       "Two people might have same amount of the bacterium Clostridium
       scindens, for example, but one person might have the type that
       has the pathway for generating these steroids. You can only tell
       by quantifying the genes, but we have to find them first,"
       Ridlon says.
       In a recent article, published in the Journal of Lipid Research,
       he does just that, reporting the genes involved in GALF
       formation in Butyricicoccus desmolans.
       "The next step is trying to see if these pathways correlate in
       patients that have certain forms of hypertension," Ridlon says.
       "Are there higher abundances of these genes?"
       The hope is that one day the research will lead to a drug
       therapy to combat hypertension. Ridlon says if they are better
       able to understand what the bacteria are doing, it would be
       possible to develop inhibitors of the enzymes that produce GALFs
       in these bacteria. "It would be great if we could find a
       targeted solution instead of wiping out everything with
       antibiotics," he says.
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