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Home > Health Conditions > 11beta-HSD1.
11beta-HSD1
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News & Research:
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Rosiglitazone decreases 11beta-hydroxysteroid dehydrogenase type 1 in
subcutaneous adipose tissue - Clin Endocrinol (Oxf). 2007 Jun 6 -
"Part of the beneficial effects of
rosiglitazone may be mediated by a reduction in the 11beta-HSD1 mRNA
expression and activity in subcutaneous abdominal fat"
-
Cortisol-cause and cure for metabolic syndrome? - Diabet Med. 2006
Dec;23(12):1281-8 - "reducing
cortisol action may provide a novel therapeutic approach in the metabolic
syndrome. There is substantial evidence that circulating cortisol
concentrations are higher in people with hypertension and glucose
intolerance ... Promising preclinical data suggest that novel 11beta-HSD1
inhibitors will have a role in lowering intracellular cortisol levels as a
treatment for the metabolic syndrome"
-
GH effect
on enzyme activity of 11{beta}HSD in abdominal obesity is dependent on
treatment duration - European Journal of Endocrinology, Vol 154, Issue
1, 69-74
-
Obesity and cortisol status - Horm
Metab Res. 2005 Apr;37(4):193-7 - "Tissue
hypercortisolism, due to increased intracellular activity of 11beta-HSD-1,
which catalyzes reduction of cortisone to cortisol, has been reported in
obese mice and humans"
-
Low-Dose Growth Hormone Inhibits 11beta-Hydroxysteroid Dehydrogenase Type 1 but Has No Effect upon Fat Mass in Patients with Simple Obesity -J Clin Endocrinol
Metab 2003 May;88(5):2113-8 - "Although GH treatment significantly raised IGF-I, we were unable to demonstrate significant differences in body
composition or metabolic profiles between GH- and placebo-treated groups. In addition, there was no alteration in total fat mass over time in the GH-treated group ... However, in comparison with baseline values, systolic blood pressure increased (119 +/- 3 vs. 130 +/- 4 mm Hg, P < 0.05 vs. baseline) and serum F/E
ratio decreased (6.1 +/- 0.5 vs. 3.9 +/- 0.5, P < 0.05 vs. baseline) in the GH-treated group only ... Treatment with low-dose GH in obesity fails to alter fat mass despite a significant elevation in IGF-I and a shift in the
global set point of E to F conversion consistent with inhibition of 11beta-HSD1" - I think it's saying that it reduced the active form of cortisol by a third. That sounds like a big plus in itself.
- Arylsulfonamidothiazoles as a new class of potential antidiabetic drugs. Discovery of potent and selective inhibitors of the 11beta-hydroxysteroid dehydrogenase type 1
- J Med Chem 2002 Aug 29;45(18):3813-5
- Is the "Metabolic Syndrome" a Mild Form of Cushing's Syndrome? The Curious Story of 11beta-Hydroxysteroid Dehydrogenase - Medscape, 6/02 -
"Recent investigations, both in humans
and in mice, have returned it and its twin, 11beta-HSD1, to the limelight as possible players in the complex pathophysiology of the metabolic syndrome ... The 11beta-HSD1 knockout animal has a different phenotype,
reflecting the fact that this enzyme normally functions as the reverse of 11beta-HSD2, converting inactive cortisone to active cortisol within cells in the liver, adipose tissue, and brain. Lacking the ability to perform this localized glucocorticoid
"re-activating" biochemical conversion, the 11beta-HSD1 knockout mouse is resistant to glucose intolerance when fed a high-fat diet. It also weighs less than its wild-type littermate despite eating more, and has a higher resting metabolic rate. Interestingly, wild-type mice downregulate 11beta-HSD1 expression in adipose tissues in response to high-fat feeding, indicating that this enzyme is subject to regulatory feedback by alterations in energy balance. Together, these findings
suggest that an improperly regulated increase in 11beta-HSD activity or expression in liver, fat cells, or brain might contribute to the tendency to develop several features of the metabolic syndrome, such as visceral adiposity, hypertension, and insulin resistance"
- 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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Association studies between microsatellite markers within the gene encoding human 11beta-hydroxysteroid dehydrogenase type 1 and body mass index, waist to hip ratio, and glucocorticoid metabolism - J Clin Endocrinol
Metab 2002 Nov;87(11):4984-90 - "Two isozymes of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) interconvert active cortisol (F) and inactive cortisone (E)"
-
Peroxisome proliferator-activated receptor-gamma ligands inhibit adipocyte
11beta -hydroxysteroid dehydrogenase type 1 expression and activity - J
Biol Chem. 2001 Apr 20;276(16):12629-35. Epub 2001 Jan 22 -
"treatment of diabetic db/db mice
with rosiglitazone inhibited expression of
11beta-HSD-1 in adipose tissue. This decrease in enzyme expression
correlated with a significant decline in plasma corticosterone levels. In
sum, these data indicate that some of the beneficial effects of PPARgamma
antidiabetic agents may result, at least in part, from the down-regulation
of 11beta-HSD-1 expression in adipose tissue"
- 11beta-hydroxysteroid dehydrogenase type 1 (11beta HSD1) is expressed in human brain: inhibition with carbenoxolone improves cognitive function in healthy elderly men -
"Inhibition of 11beta-HSD1 therefore provides an exciting new therapeutic target to prevent/ameliorate age-associated cognitive dysfunction in humans"
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