IMBICE   05372
INSTITUTO MULTIDISCIPLINARIO DE BIOLOGIA CELULAR
Unidad Ejecutora - UE
artículos
Título:
Fructose-rich diet-induced abdominal adipose tissue endocrine dysfunction in normal male rats
Autor/es:
ALZAMENDI, ANA; GIOVAMBATTISTA , ANDRÉS; RASCHIA, AGUSTINA; MADRID, VIVIANA; GAILLARD, ROLF; REBOLLEDO, OSCAR; GAGLIARDINO, JUAN J; SPINEDI, EDUARDO
Revista:
ENDOCRINE
Editorial:
HUMANA PRESS INC
Referencias:
Año: 2009 vol. 35 p. 227 - 232
ISSN:
0969-711X
Resumen:
We have currently studied the changes induced
by administration of a fructose-rich diet (FRD) to normal
rats in the mass and the endocrine function of abdominal
(omental) adipose tissue (AAT). Rats were fed ad libitum a
standard commercial chow and tap water, either alone
(control diet, CD) or containing fructose (10%, w/vol)
(FRD). Three weeks after treatment, circulating metabolic
markers and leptin release from adipocytes of AAT were
measured. Plasma free fatty acids (FFAs), leptin, adiponectin,
and plasminogen activator inhibitor-1 (PAI-1)
levels were significantly higher in FRD than in CD rats.
AAT mass was greater in FRD than in CD rats and their
adipocytes were larger, they secreted more leptin and
showed impaired insulin sensitivity. While leptin mRNA
expression increased in AAT from FRD rats, gene
expression of insulin receptor substrate, IRS1 and IRS2
was significantly reduced. Our study demonstrates that
administration of a FRD significantly affects insulin sensitivity
and several AAT endocrine/metabolic functions.
These alterations could be part of a network of interacting
abnormalities triggered by FRD-induced oxidative stress at
the AAT level. In view of the impaired glucose tolerance
observed in FRD rats, these alterations could play a key
role in both the development of metabolic syndrome (MS)
and b-cell failure.
role in both the development of metabolic syndrome (MS)
and b-cell failure.
role in both the development of metabolic syndrome (MS)
and b-cell failure.
role in both the development of metabolic syndrome (MS)
and b-cell failure.