The University of Southampton
University of Southampton Institutional Repository

Glucose intolerance induced by glucocorticoid excess is further impaired by co-administration with β-hydroxy-β-methylbutyrate in rats

Glucose intolerance induced by glucocorticoid excess is further impaired by co-administration with β-hydroxy-β-methylbutyrate in rats
Glucose intolerance induced by glucocorticoid excess is further impaired by co-administration with β-hydroxy-β-methylbutyrate in rats
Glucocorticoid (GC) excess alters glucose homeostasis and promotes modifications in murinometric and anthropometric parameters in rodents and humans, respectively. β-hydroxy-β-methylbutyrate (HMB), a leucine metabolite, has been proposed as a nutritional strategy for preventing muscle wasting, but few data regarding its effects on glucose homeostasis are available. Here, we analyzed whether the effects of GC excess on glucose homeostasis may be attenuated or exacerbated by the concomitant ingestion of HMB. Adult Wistar rats (90-days-old) were assigned to four groups: (1) vehicle treated (Ctl), (2) dexamethasone (DEX) treated (Dex), (3) HMB treated (Hmb), and (4) DEX plus HMB treated (DexHmb). Dex groups received DEX (1 mg·kg body weight BW-1, intraperitoneal) for 5 consecutive days. HMB groups ingested HMB (320 mg·kg BW-1, oral gavage) for the same 5 days. HMB ingestion did not attenuate the effects of DEX on food intake and body weight loss, changes in masses of several organs, insulin resistance, and glucose intolerance (p > 0.05). In fact, in DexHmb rats, there was increased fasting glycemia and exacerbated glucose intolerance with the main effect attributed to DEX treatment (p < 0.05). HMB exerted no attenuating effect on plasma triacylglycerol levels from DexHmb rats, but it seems to attenuate the lipolysis induced by β-adrenergic stimulation (20 µmol·L-1 isoproterenol) in fragments of retroperitoneal adipose tissue from DexHmb rats. Therefore, HMB does not attenuate the diabetogenic characteristics of GC excess. In fact, the data suggest that HMB may exacerbate GC-induced glucose intolerance.
1715-5312
1137-1146
Nunes, E.
ca193ed2-d093-49a3-9deb-c67d3c2af29a
Gonçalves-Neto, L.
845996c4-4dea-4a18-9789-cd22c4e231a2
Ferreira, F.
316028c4-9ae3-41c8-b09a-f9a70020aae7
Dos Santos, C.
b89cca06-c4ca-4480-8985-db38c6a83b4d
Fernandes, L.
720f3244-8af4-4330-9e0d-a2aa42fb4743
Boschero, A.
1362ff4d-6d38-4765-9178-42d61344a68e
Calder, Philip C.
1797e54f-378e-4dcb-80a4-3e30018f07a6
Nunes, E.
ca193ed2-d093-49a3-9deb-c67d3c2af29a
Gonçalves-Neto, L.
845996c4-4dea-4a18-9789-cd22c4e231a2
Ferreira, F.
316028c4-9ae3-41c8-b09a-f9a70020aae7
Dos Santos, C.
b89cca06-c4ca-4480-8985-db38c6a83b4d
Fernandes, L.
720f3244-8af4-4330-9e0d-a2aa42fb4743
Boschero, A.
1362ff4d-6d38-4765-9178-42d61344a68e
Calder, Philip C.
1797e54f-378e-4dcb-80a4-3e30018f07a6

Nunes, E., Gonçalves-Neto, L., Ferreira, F., Dos Santos, C., Fernandes, L., Boschero, A. and Calder, Philip C. (2013) Glucose intolerance induced by glucocorticoid excess is further impaired by co-administration with β-hydroxy-β-methylbutyrate in rats. Applied Physiology, Nutrition and Metabolism, 38 (11), 1137-1146. (doi:10.1139/apnm-2012-0456). (PMID:24053521)

Record type: Article

Abstract

Glucocorticoid (GC) excess alters glucose homeostasis and promotes modifications in murinometric and anthropometric parameters in rodents and humans, respectively. β-hydroxy-β-methylbutyrate (HMB), a leucine metabolite, has been proposed as a nutritional strategy for preventing muscle wasting, but few data regarding its effects on glucose homeostasis are available. Here, we analyzed whether the effects of GC excess on glucose homeostasis may be attenuated or exacerbated by the concomitant ingestion of HMB. Adult Wistar rats (90-days-old) were assigned to four groups: (1) vehicle treated (Ctl), (2) dexamethasone (DEX) treated (Dex), (3) HMB treated (Hmb), and (4) DEX plus HMB treated (DexHmb). Dex groups received DEX (1 mg·kg body weight BW-1, intraperitoneal) for 5 consecutive days. HMB groups ingested HMB (320 mg·kg BW-1, oral gavage) for the same 5 days. HMB ingestion did not attenuate the effects of DEX on food intake and body weight loss, changes in masses of several organs, insulin resistance, and glucose intolerance (p > 0.05). In fact, in DexHmb rats, there was increased fasting glycemia and exacerbated glucose intolerance with the main effect attributed to DEX treatment (p < 0.05). HMB exerted no attenuating effect on plasma triacylglycerol levels from DexHmb rats, but it seems to attenuate the lipolysis induced by β-adrenergic stimulation (20 µmol·L-1 isoproterenol) in fragments of retroperitoneal adipose tissue from DexHmb rats. Therefore, HMB does not attenuate the diabetogenic characteristics of GC excess. In fact, the data suggest that HMB may exacerbate GC-induced glucose intolerance.

This record has no associated files available for download.

More information

Published date: 17 June 2013
Organisations: Human Development & Health

Identifiers

Local EPrints ID: 359028
URI: http://eprints.soton.ac.uk/id/eprint/359028
ISSN: 1715-5312
PURE UUID: 260c1cf0-cbb6-4ec0-b4d1-0405963887bf
ORCID for Philip C. Calder: ORCID iD orcid.org/0000-0002-6038-710X

Catalogue record

Date deposited: 18 Oct 2013 13:47
Last modified: 03 Oct 2023 01:33

Export record

Altmetrics

Contributors

Author: E. Nunes
Author: L. Gonçalves-Neto
Author: F. Ferreira
Author: C. Dos Santos
Author: L. Fernandes
Author: A. Boschero

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.

×