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Home > Health Conditions > 11beta-HSD1.

11beta-HSD1

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News & Research:

  • Vitamin D pill a day may improve exercise performance and lower risk of heart disease - Science Daily, 11/1/15 - "Previous studies suggest that vitamin D can block the action of enzyme 11-βHSD1, which is needed to make the "stress hormone" cortisol. High levels of cortisol may raise blood pressure by restricting arteries, narrowing blood vessels and stimulating the kidneys to retain water. As Vitamin D may reduce circulating levels of cortisol, it could theoretically improve exercise performance and lower cardiovascular risk factors ... gave 13 healthy adults matched by age and weight 50μg of vitamin D per day or a placebo over a period of two weeks ... Adults supplementing with vitamin D had lower blood pressure compared to those given a placebo, as well as having lower levels of the stress hormone cortisol in their urine. A fitness test found that the group taking vitamin D could cycle 6.5km in 20 minutes, compared to just 5km at the start of the experiment. Despite cycling 30% further in the same time, the group taking vitamin D supplements also showed lower signs of physical exertion" - See vitamin D at Amazon.com.
  • Overexpression of hepatic 5α-reductase and 11β-hydroxysteroid dehydrogenase type 1 in visceral adipose tissue is associated with hyperinsulinemia in morbidly obese patients - Metabolism. 2011 Jun 23 - "11-β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts cortisone to cortisol, mainly in the liver and visceral adipose tissue (VAT), and has been implicated in several metabolic disorders. The absence of systemic hypercortisolism in central obesity could be due to increased inactivation of cortisol to its tetrahydrometabolites by the hepatic enzymes 5α- and 5β-reductases ... Forty-one patients were recruited (age, 41.8 +/- 10.6 years; body mass index, 42.1 +/- 6.6 kg/m(2); 71% women). The expression of hepatic 5α- and 5β-reductases was positively correlated (r = +0.53, P = .004), and their expression levels were correlated with hepatic 11β-HSD1 expression (r = +0.61, P < .001 for 5α-reductase and r = +0.50, P < .001 for 5β-reductase). Hepatic 5α-reductase was associated with insulin (r = +0.34, P = .015). Visceral adipose tissue 11β-HSD1 expression was associated with glucose (r = +0.37, P = .025) and insulin (r = +0.54, P = .002). Our results showed that 5α-reductase and VAT 11β-HSD1 expressions were associated with insulinemia. These findings suggest that overexpression of 5α-reductase, through a higher inactivation of cortisol in the liver, could have a protective role in preserving hepatic sensitivity to insulin. The overexpression of liver reductases in obesity could be an adaptive response to an increase in cortisol production by the liver and visceral 11β-HSD1 to avoid systemic hypercortisolism"
  • Older age memory loss tied to stress hormone receptor in brain - Science Daily, 4/6/11 - "one receptor was activated by low levels of cortisol, which helped memory. However, once levels of this stress hormone were too high they spilled over onto a second receptor. This activates brain processes that contribute to memory impairment ... high levels of the stress hormone in aged mice made them less able to remember how to navigate a maze. The memory recall problem was reversed when the receptor linked to poor memory was blocked ... lowering the levels of these stress hormones will prevent them from activating a receptor in the brain that is bad for memory ... The researchers are currently investigating a new chemical compound which blocks an enzyme -- 11beta-HSD1 -- that is involved in producing stress hormones within cells"
  • Errant Enzyme Causes Big Bellies - WebMD, 12/11/01 - "They looked at an enzyme called 11-beta hydroxysteroid dehydrogenase type 1. This enzyme is able to increase the level of cortisol in fat cells without raising the level of cortisol in the blood ... The researchers genetically engineered mice that overproduce this enzyme. They made sure that the level of the enzyme was equivalent to the level previously found in the fatty tissue of overweight humans. As expected, the mice produced extra amounts of cortisol in their fat cells, but not in their blood ... The next step was to compare these mice to mice that produced normal amounts of the enzyme. Even when fed a low-fat diet, the genetically-altered mice developed a pot belly while the normal mice did not. The problem was even worse when the altered mice were fed a high-fat diet ... We were surprised to find that it took only a modest increase in this enzyme to cause the mice to become ... obese"
  • Single enzyme to blame for potbellies: study - MSNBC, 12/6/01 - "What they found was that a single enzyme in fat cells that raises levels of cortisol — the “fight or flight” stress hormone — triggers fat accumulation around the belly and its associated ill effects ... The researchers were drawn to the role of cortisol because patients with a rare illness known as Cushing syndrome — who have too much of the steroid hormone in their blood — develop severe obesity concentrated around their middles and become diabetic ... Since overweight people without Cushing syndrome typically don’t have too much cortisol in their bloodstreams, Flier hypothesized that they may be producing high cortisol levels solely in their fat cells — possibly because the enzyme HSD-1, which makes cortisol from an inactive molecule, is overactive ... The level of cortisol in their stomach fat tissue was 15 percent to 30 percent higher than in their non-engineered counterparts"

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