Aquaporin 7: Modulator of cardiac energy metabolism in the metabolic syndrome during age progression

LISTA F; CERNADAS G; BALASZCZUK AM; HID EJ; GALLEANO M; ARRECHE N; FELLET A

Mar del Plata

Congreso; LXIV Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC) ? Reunión conjunta SAFE ? SAB ? SAP 2019; 2019

SAIC

It has been shown that dysfunction of some type of aquaporin (AQP) can be related with metabolic diseases. In addition, advancing on age could be associated with the change in density or functions of different isoforms of AQPs. AQP7 is a glycerol transporter through the plasma membrane, mainly in adipocytes and cardiac tissue. However, in the heart, the role of this channel in metabolic syndrome (MS) is little known. The objective of this study was to investigate changes in cardiac AQP7 in the experimental model of fructose-induced MS during age progression. Male Sprague Dawley rats were used according to the following groups: C1: 1-month old rats, F1: 1-month old rats + fructose treatment for 8 weeks; C6: 6-month old rats, F6: 1-month old rats + fructose; C12: 12-months old rats, F12: 12-month old rats + fructose. The weight gain of the animals of group F1 and F6 was greater than that of group C1 and C6 from the sixth and fifth week of treatment respectively. There was no difference in this parameter in the 12-month animals. SBP and plasma triglycerides increased in F1, F6 and F12 and a Triglyceride/C-HDL ratio greater than 3 was obtained in these groups. Basal glycemia only increased in F12 compared to C12. It was observed that the advancing age induced an increase in the expression of AQP7 in heart. The SM induced by fructose overload decreased AQP7 levels in 12-month-old animals. Our findings propose that changes in cardiac protein levels of AQP7 could be involved in metabolic and hemodynamic alterations associated to fructose treatment along age progression.