The University of Southampton
University of Southampton Institutional Repository

11beta-hydroxysteroid dehydrogenase type 1 activity in lean and obese males with type 2 diabetes mellitus

11beta-hydroxysteroid dehydrogenase type 1 activity in lean and obese males with type 2 diabetes mellitus
11beta-hydroxysteroid dehydrogenase type 1 activity in lean and obese males with type 2 diabetes mellitus
Glucocorticoids play an important role in the pathogenesis of obesity and insulin resistance. Impaired conversion of cortisone (E) to cortisol (F) by the type 1 isoenzyme of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) in obesity may represent a protective mechanism preventing ongoing weight gain and glucose intolerance. We have studied glucocorticoid metabolism in 33 male subjects with type 2 diabetes mellitus [age, 44.2 +/- 13 yr; body mass index (BMI), 31.1 +/- 7.5 kg/m(2) (mean +/- sd)] and 38 normal controls (age, 41.4 +/- 14 yr; BMI, 38.2 +/- 12.8 kg/m(2)).Circulating F:E ratios were elevated in the diabetic group and correlated with serum cholesterol and homeostasis model assessment-S. There was no difference in 11beta-HSD1 activity between diabetic subjects and controls. In addition, 11beta-HSD1 activity was unaffected by BMI in diabetic subjects. However, in control subjects, increasing BMI was associated with a reduction in the urinary tetrahydrocortisol+5alpha-tetrahydrocortisol:tetrahydrocortisone ratio (P < 0.05) indicative of impaired 11beta-HSD1 activity. The degree of inhibition correlated tightly with visceral fat mass. Changes in 11beta-HSD1 activity could not be explained by circulating levels of adipocytokines.Impaired E to F metabolism in obesity may help preserve insulin sensitivity and prevent diabetes mellitus. Failure to down-regulate 11beta-HSD1 activity in patients with diabetes may potentiate dyslipidemia, insulin resistance, and obesity. Inhibition of 11beta-HSD1 may therefore represent a therapeutic strategy in patients with type 2 diabetes mellitus and obesity.
age factors, weight, glucose intolerance, obesity, role, 11-beta-hydroxysteroid dehydrogenase type 1, insulin, cortisone, cortisol, hydrocortisone, middle aged, glucocorticoids, body mass index, patients, glucose, cholesterol, aged, european continental ancestry group, enzymology, diabetes mellitus, asian continental ancestry group, adult, activity, homeostasis, weight gain, type 2, humans, diabetes, metabolism, male, insulin resistance, thinness
0021-972X
4755-4761
Valsamakis, G.
d5b12649-9df1-4f9b-92d6-c8384ada3657
Anwar, A.
b9987a1b-f317-46cb-9106-1d5cb2b380ec
Tomlinson, J.W.
3943cfdd-1d4b-423d-8314-b107b2f40381
Shackleton, C.H.
45a30d0b-6913-42cd-bf17-692a8296cc6e
McTernan, P.G.
0e3835cf-27a9-4a61-926c-3421f1dce3c0
Chetty, R.
e4298172-0633-4899-910d-6cedce416e89
Wood, P.J.
f0dfe718-fa0f-43b1-9b2d-4bdc9c41320a
Banerjee, A.K.
eefa86ce-771e-46e0-83df-49394d3a2ba4
Holder, G.
1c33558a-f13b-4adc-b9c5-12dcd0562954
Barnett, A.H.
88f0298d-bb5e-452d-93c2-1517dcf312a6
Stewart, P.M.
5ba66e34-c467-4089-956f-cf3103b277b9
Kumar, S.
695e30ec-08ac-4ad7-9f6b-b18dc52bcd0b
Valsamakis, G.
d5b12649-9df1-4f9b-92d6-c8384ada3657
Anwar, A.
b9987a1b-f317-46cb-9106-1d5cb2b380ec
Tomlinson, J.W.
3943cfdd-1d4b-423d-8314-b107b2f40381
Shackleton, C.H.
45a30d0b-6913-42cd-bf17-692a8296cc6e
McTernan, P.G.
0e3835cf-27a9-4a61-926c-3421f1dce3c0
Chetty, R.
e4298172-0633-4899-910d-6cedce416e89
Wood, P.J.
f0dfe718-fa0f-43b1-9b2d-4bdc9c41320a
Banerjee, A.K.
eefa86ce-771e-46e0-83df-49394d3a2ba4
Holder, G.
1c33558a-f13b-4adc-b9c5-12dcd0562954
Barnett, A.H.
88f0298d-bb5e-452d-93c2-1517dcf312a6
Stewart, P.M.
5ba66e34-c467-4089-956f-cf3103b277b9
Kumar, S.
695e30ec-08ac-4ad7-9f6b-b18dc52bcd0b

Valsamakis, G., Anwar, A., Tomlinson, J.W., Shackleton, C.H., McTernan, P.G., Chetty, R., Wood, P.J., Banerjee, A.K., Holder, G., Barnett, A.H., Stewart, P.M. and Kumar, S. (2004) 11beta-hydroxysteroid dehydrogenase type 1 activity in lean and obese males with type 2 diabetes mellitus. Journal of Clinical Endocrinology & Metabolism, 89 (9), 4755-4761.

Record type: Article

Abstract

Glucocorticoids play an important role in the pathogenesis of obesity and insulin resistance. Impaired conversion of cortisone (E) to cortisol (F) by the type 1 isoenzyme of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) in obesity may represent a protective mechanism preventing ongoing weight gain and glucose intolerance. We have studied glucocorticoid metabolism in 33 male subjects with type 2 diabetes mellitus [age, 44.2 +/- 13 yr; body mass index (BMI), 31.1 +/- 7.5 kg/m(2) (mean +/- sd)] and 38 normal controls (age, 41.4 +/- 14 yr; BMI, 38.2 +/- 12.8 kg/m(2)).Circulating F:E ratios were elevated in the diabetic group and correlated with serum cholesterol and homeostasis model assessment-S. There was no difference in 11beta-HSD1 activity between diabetic subjects and controls. In addition, 11beta-HSD1 activity was unaffected by BMI in diabetic subjects. However, in control subjects, increasing BMI was associated with a reduction in the urinary tetrahydrocortisol+5alpha-tetrahydrocortisol:tetrahydrocortisone ratio (P < 0.05) indicative of impaired 11beta-HSD1 activity. The degree of inhibition correlated tightly with visceral fat mass. Changes in 11beta-HSD1 activity could not be explained by circulating levels of adipocytokines.Impaired E to F metabolism in obesity may help preserve insulin sensitivity and prevent diabetes mellitus. Failure to down-regulate 11beta-HSD1 activity in patients with diabetes may potentiate dyslipidemia, insulin resistance, and obesity. Inhibition of 11beta-HSD1 may therefore represent a therapeutic strategy in patients with type 2 diabetes mellitus and obesity.

This record has no associated files available for download.

More information

Published date: 2004
Keywords: age factors, weight, glucose intolerance, obesity, role, 11-beta-hydroxysteroid dehydrogenase type 1, insulin, cortisone, cortisol, hydrocortisone, middle aged, glucocorticoids, body mass index, patients, glucose, cholesterol, aged, european continental ancestry group, enzymology, diabetes mellitus, asian continental ancestry group, adult, activity, homeostasis, weight gain, type 2, humans, diabetes, metabolism, male, insulin resistance, thinness

Identifiers

Local EPrints ID: 60353
URI: http://eprints.soton.ac.uk/id/eprint/60353
ISSN: 0021-972X
PURE UUID: 17defd62-6419-4257-91b0-e03ac0625060

Catalogue record

Date deposited: 04 Sep 2008
Last modified: 22 Jul 2022 21:12

Export record

Contributors

Author: G. Valsamakis
Author: A. Anwar
Author: J.W. Tomlinson
Author: C.H. Shackleton
Author: P.G. McTernan
Author: R. Chetty
Author: P.J. Wood
Author: A.K. Banerjee
Author: G. Holder
Author: A.H. Barnett
Author: P.M. Stewart
Author: S. Kumar

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×