Examinando por Autor "DeSolis, Alain J."

Mostrando 1 - 2 de 2

Development of Insulin Resistance During Aging: Involvement of Central Processes and Role of Adipokines
(Current Protein and Peptide Science, 2011-06-01) Carrascosa, Jose M.; Andres, Antonio; Ros, Manuel; Bogonez, Elena; Arribas, Carmen; Fernandez-Agullo, Teresa; DeSolis, Alain J.; Gallardo, Nilda; Martinez, Carmen
Aging in mammals associates with the development of peripheral insulin resistance. Additionally, adiposity usually increases with aging and this could play a relevant role in the gradual impairment of insulin action. In fact, fat accretion leads to changes in the expression and circulating concentrations of factors originated in adipose tissue like leptin, resistin and inflammatory cytokines which have been shown to modulate insulin signaling in insulin target tissues acting both, directly or through the central nervous system. Even insulin action on peripheral target tissues has been recently demonstrated to be partially mediated by its central action, suggesting that a decrease in central insulin action could be involved in the development of peripheral insulin resistance. In the present review we analyze the available research data on aging-associated insulin resistance making emphasis in the following aspects: 1) The time-course of development of overall insulin resistance and the evolution of changes in circulating adipokines; 2) The effect of caloric restriction and the decrease of adiposity in insulin action; 3) The influence of changes in the central action of factors like leptin or insulin in the development and maintenance of insulin resistance during aging.
Impairment of skeletal muscle insulin action with aging in Wistar rats: Role of leptin and caloric restriction
(Elsevier, 2012-05-01) DeSolis, Alain J.; Fernandez-Agullo, Teresa; Garcia-San Frutos, Miriam; Perez-Pardo, Paula; Bogonez, Elena; Andres, Antonio; Ros, Manuel; Carrascosa, Jose M.
Insulin resistance develops with aging in rats in parallel to fat mass accretion, central leptin resistance and hyperleptinemia. Previous studies demonstrated that insulin resistance appears earlier in adipose tissue than in muscle during aging and pointed to a role of hyperleptinemia in the impairment of insulin action. Here we explored the evolution along aging of insulin sensitivity in soleus and EDL muscles by analyzing insulin signaling in vivo and insulin-dependent glucose transport ex vivo. A decrease in insulin action was observed in both muscles. Caloric restriction improves insulin sensitivity at early aging but not in older animals. We also tested the role of leptin on insulin action in skeletal muscle. Short-term pretreatment with leptin inhibits in vivo muscle insulin signaling and insulin-dependent glucose transport in isolated muscle strips. This effect is mediated by its action on early insulin signaling as well as by the inhibition of p38. In contrast, chronic central administration of leptin elicits an insulin sensitizing effect on soleus. These data suggest that leptin can act as muscle insulin sensitizer, when acting at central level, and as insulin antagonistic when interacting directly with soleus muscle. This effect may be relevant in situations of hyperleptinemia such as aging.