Impaired endocrine-metabolic homeostasis: Underlying mechanism of its induction by unbalanced diet

To characterize the intrinsic mechanism by which sucrose induces β-cell dysfunction. Normal rats received for 3 weeks a standard diet supplemented with 10% sucrose in the drinking water (high sucrose (HS)) with/out an antioxidant agent (R/S α-lipoic acid). We measured plasma glucose, insulin, trigly...

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Autores principales: Maiztegui, Bárbara, Roman, Carolina Lisi, Gagliardino, Juan José, Flores, Luis Emilio
Formato: Articulo Preprint
Lenguaje:Inglés
Publicado: 2018
Materias:
Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/104503
http://hdl.handle.net/11336/93125
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id I19-R120-10915-104503
record_format dspace
institution Universidad Nacional de La Plata
institution_str I-19
repository_str R-120
collection SEDICI (UNLP)
language Inglés
topic Bioquímica
Ciencias Médicas
Leptin stress
Oxidative stress
Unbalanced diets
spellingShingle Bioquímica
Ciencias Médicas
Leptin stress
Oxidative stress
Unbalanced diets
Maiztegui, Bárbara
Roman, Carolina Lisi
Gagliardino, Juan José
Flores, Luis Emilio
Impaired endocrine-metabolic homeostasis: Underlying mechanism of its induction by unbalanced diet
topic_facet Bioquímica
Ciencias Médicas
Leptin stress
Oxidative stress
Unbalanced diets
description To characterize the intrinsic mechanism by which sucrose induces β-cell dysfunction. Normal rats received for 3 weeks a standard diet supplemented with 10% sucrose in the drinking water (high sucrose (HS)) with/out an antioxidant agent (R/S α-lipoic acid). We measured plasma glucose, insulin, triglyceride, leptin, and lipid peroxidation levels; homeostasis model assessment (HOMA)-insulin resistance (HOMA-IR) and HOMA for β-cell function (HOMA-β) indexes were also determined. Insulin secretion, β-cell apoptosis, intracellular insulin and leptin mediators, and oxidative stress (OS) markers were also measured in islets isolated from each experimental group. HS rats had increased plasma triglyceride, insulin, leptin, and lipid peroxidation (OS marker) levels associated with an insulin-resistant state. Their islets developed an initial compensatory increase in glucose-induced insulin secretion and mRNA and protein levels of β-cell apoptotic markers. They also showed a significant decrease in mRNA and protein levels of insulin and leptin signaling pathway mediators. Uncoupling protein 2 (UCP2), peroxisome proliferator-activated receptor (PPAR)-α and -δ mRNA and protein levels were increased whereas mRNA levels of Sirtuin-1 (Sirt-1), glutathione peroxidase, and catalase were significantly lower in these animals. Development of all these endocrine-metabolic abnormalities was prevented by co-administration of R/S a-lipoic acid together with sucrose. OS may be actively involved in the mechanism by which unbalanced/unhealthy diet induces β-cell dysfunction. Since metabolic-endocrine dysfunctions recorded in HS rats resembled those measured in human pre-diabetes, knowledge of its molecular mechanism could help to develop appropriate strategies to prevent the progression of this metabolic state toward type 2 diabetes (T2D).
format Articulo
Preprint
author Maiztegui, Bárbara
Roman, Carolina Lisi
Gagliardino, Juan José
Flores, Luis Emilio
author_facet Maiztegui, Bárbara
Roman, Carolina Lisi
Gagliardino, Juan José
Flores, Luis Emilio
author_sort Maiztegui, Bárbara
title Impaired endocrine-metabolic homeostasis: Underlying mechanism of its induction by unbalanced diet
title_short Impaired endocrine-metabolic homeostasis: Underlying mechanism of its induction by unbalanced diet
title_full Impaired endocrine-metabolic homeostasis: Underlying mechanism of its induction by unbalanced diet
title_fullStr Impaired endocrine-metabolic homeostasis: Underlying mechanism of its induction by unbalanced diet
title_full_unstemmed Impaired endocrine-metabolic homeostasis: Underlying mechanism of its induction by unbalanced diet
title_sort impaired endocrine-metabolic homeostasis: underlying mechanism of its induction by unbalanced diet
publishDate 2018
url http://sedici.unlp.edu.ar/handle/10915/104503
http://hdl.handle.net/11336/93125
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AT gagliardinojuanjose impairedendocrinemetabolichomeostasisunderlyingmechanismofitsinductionbyunbalanceddiet
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