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Home > Health Conditions > 11beta-HSD1.
11beta-HSD1
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News & Research:
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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"
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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"
Abstracts:
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Vitamin
A Decreases Pre-receptor Amplification of Glucocorticoids in Obesity: Study
on the Effect of Vitamin A on 11beta-Hydroxysteroid Dehydrogenase Type 1
Activity in Liver and Visceral Fat of WNIN/Ob Obese Rats - Nutr J. 2011
Jun 23;10(1):70 - "11beta-hydroxysteroid
dehydrogenase type 1 (11beta-HSD1) catalyzes the conversion of inactive
glucocorticoids to active glucocorticoids and its inhibition ameliorates
obesity and metabolic syndrome. So far, no studies have reported the effect
of dietary vitamin A on 11beta-HSD1 activity in visceral fat and liver under
normal and obese conditions. Here, we studied the effect of chronic feeding
of vitamin A-enriched diet (129mg/kg diet) on 11beta-HSD1 activity in liver
and visceral fat of WNIN/Ob lean and obese rats ... Control groups received
stock diet containing 2.6mg vitamin A/kg diet, where as experimental groups
received diet containing 129mg vitamin A/Kg diet for 20 weeks ... Vitamin A
supplementation significantly decreased body weight, visceral fat mass and
11beta-HSD1 activity in visceral fat of WNIN/Ob obese rats. Hepatic
11beta-HSD1 activity and gene expression were significantly reduced by
vitamin A supplementation in both the phenotypes. CCAAT/enhancer binding
protein alpha(C/EBPalpha), the main transcription factor essential for the
expression of 11beta-HSD1, decreased in liver by vitamin A fed-obese rats,
but not in lean rats. Liver X receptor alpha (LXR alpha), a nuclear
transcription factor which is known to downregulate 11beta-HSD1 gene
expression was significantly increased by vitamin A supplementation in both
the phenotypes" - Note: 11beta-HSD1 goes hand in hand with
cortisol.
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Promising drug candidate reverses age-related memory loss in mice -
Science Daily, 10/12/10 - "Such memory loss has been
linked with high levels of 'stress' steroid hormones known as
glucocorticoids which have a deleterious effect on the part of the brain
that helps us to remember. An enzyme called 11beta-HSD1 is involved in
making these hormones and has been shown to be more active in the brain
during aging ... We found that life-long partial deficiency of 11beta-HSD1
prevented memory decline with aging. But we were very surprised to find that
the blocking compound works quickly over a few days to improve memory in old
mice suggesting it might be a good treatment for the already elderly ... We
previously showed that carbenoxolone, an old drug that blocks multiple
enzymes including 11beta-HSD1, improves memory in healthy elderly men and in
patients with type 2 diabetes after just a month of treatment, so we are
optimistic that our new compounds will be effective in humans. The next step
is to conduct further studies with our preclinical candidate to prove that
the compound is safe to take into clinical trials, hopefully within a year"
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Dietary
fatty acid composition alters 11beta-hydroxysteroid dehydrogenase type 1
gene expression in rat retroperitoneal white adipose tissue - Lipids
Health Dis. 2010 Oct 8;9(1):111 - "The enzyme
11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) amplifies
intracellular glucocorticoid action by converting inactive glucocorticoids
to their active forms in vivo. Adipose-specific overexpression of
11beta-HSD1 induces metabolic syndrome in mice, whereas 11beta-HSD1 null
mice are resistant to it. Dietary trans and saturated fatty acids (TFAs and
SFAs) are involved in the development of metabolic syndrome, whereas
polyunsaturated fatty acids (PUFA) offer protection against this. Here, we
report the effects of chronic feeding of different diets containing
vanaspati (TFA rich), palm oil (SFA rich) and sunflower oil (PUFA rich) at
10%level on 11beta-HSD1 gene expression in rat retroperitoneal adipose
tissue. 11beta-HSD1 gene expression was significantly higher in TFA rich
diet-fed rats compared to SFA rich diet-fed rats, which in turn was
significantly higher than PUFA rich diet-fed rats. Similar trend was
observed in the expression of CCAAT-enhancer binding protein-alpha
(C/EBP-alpha), the main transcription factor required for the expression of
11beta-HSD1. We propose that TFAs and SFAs increase local amplification of
glucocorticoid action in adipose tissue by upregulating 11beta-HSD1 by
altering C/EBP--gene expression. The increased levels of glucocorticoids in
adipose tissue may lead to development of obesity and insulin resistance,
thereby increasing the risk of developing metabolic syndrome" - Note:
11beta-HSD1 goes hand in hand with cortisol.
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Cerebrospinal Fluid Corticosteroid Levels and Cortisol Metabolism in
Patients with Idiopathic Intracranial Hypertension: A Link between
11{beta}-HSD1 and Intracranial Pressure Regulation? - J Clin Endocrinol
Metab. 2010 Sep 8
- Emodin,
a natural product, selectively inhibits 11beta-hydroxysteroid dehydrogenase
type 1 and ameliorates metabolic disorder in diet-induced obese mice -
Br J Pharmacol. 2010 Sep;161(1):113-26 -
"11beta-Hydroxysteroid dehydrogenase type 1 (11beta-HSD1) is an attractive
therapeutic target of type 2 diabetes and metabolic syndrome. Emodin, a
natural product and active ingredient of various Chinese herbs, has been
demonstrated to possess multiple biological activities ... Emodin is a
potent and selective 11beta-HSD1 inhibitor with the IC(50) of 186 and 86 nM
for human and mouse 11beta-HSD1, respectively. Single oral administration of
emodin inhibited 11beta-HSD1 activity of liver and fat significantly in
mice. Emodin reversed prednisone-induced insulin resistance in mice, whereas
it did not affect dexamethasone-induced insulin resistance, which confirmed
its inhibitory effect on 11beta-HSD1 in vivo. In DIO mice, oral
administration of emodin improved insulin sensitivity and lipid metabolism,
and lowered blood glucose and hepatic PEPCK, and glucose-6-phosphatase mRNA.
CONCLUSIONS AND IMPLICATIONS This study demonstrated a new role for emodin
as a potent and selective inhibitor of 11beta-HSD1 and its beneficial
effects on metabolic disorders in DIO mice. This highlights the potential
value of analogues of emodin as a new class of compounds for the treatment
of metabolic syndrome or type 2 diabetes" - Note: (11beta-HSD1)
goes hand in hand with cortisol. It seems like what came first, the
chicken or the egg. I googled emodin and didn't see any reliable
places that sold it.
One article said that it was in some resveratrol products and that the
emodin was what caused the stomach problems.
- Lack
of regulation of 11{beta}-hydroxysteroid dehydrogenase type 1 during short
term manipulation of growth hormone in patients with hypopituitarism -
Eur J Endocrinol. 2009 Jun 23
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Antidiabetic effects of 11beta-HSD1 inhibition in a mouse model of combined
diabetes, dyslipidaemia and atherosclerosis - Diabetes Obes Metab. 2009
Jul;11(7):688-99 - "Importantly, 11beta-HSD1
inhibition leads to improved glucose metabolism and does not result in a
worsening of atherosclerotic lesion area, yet retained antidiabetic
potential in the face of multiple severe metabolic aberrations. This study
reinforces the potential use of 11beta-HSD1 inhibitors in patients with the
metabolic syndrome without negatively impacting atherosclerosis"
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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"
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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
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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"
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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.
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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
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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)"
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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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