Unbalanced maternal diet during development alters miR27a expression in male adult mice.

AGUSTINA CASTRO; PATRICIA CASTRO; MARÍA AMANDA REY; ANDRÉS GIOVAMBATTISTA; ANA ALZAMENDI

Mar del Plata

Congreso; LXVIII Reunión Anual Sociedad Argentina de Investigación Clínica; 2023

Sociedad Argentina de Investigación Clínica

It is accepted that diet quality supply during gestation and lactation programs pup´s development. Our aim was to evaluate the impact of maternal fructose rich diet (FRD; during pregnancy and lactation) intake on adipose tissue (AT) development in adult male mice, with special focus on thermogenesis and miRNA27a and miRNA30b factors barely studied in this model. On pregnancy day 1, dams were provided either with tap water alone or containing fructose (20% w/v; FRD) and fed ad libitum up to delivery. Six pups were left per mom and same diet was provided until pups were 21 days old. Males were separated and maintained until 120-days old (experimental day) with normal diet ad libitum. From weaning until experimental day, body weight and food intake were registered. C and F indicate pups born to control and FRD dams, respectively. On experimental day, trunk blood was collected, AT depots were dissected and weighted. Epididymal AT (EAT) was used for H&E staining and mRNA expression levels quantification. Our results show that F pups gain more weight due to a higher food intake. Nevertheless, no differences in AT mass were observed, despite a tendency towards a higher EAT adipocyte area. No differences were found in functional AT gene expression markers such as leptin and adiponectin, but a lower expression of ucp-1 was found in F EAT, maybe due to a lower thermogenic capacity. Considering miRNA biosynthesis, F pups showed significant lower expression levels of exportin 5. Finally, miR27a expression was significantly increased in F pups, without changes in miR30b. It is known that miR27a is negatively regulated during adipogenesis, and concomitantly a lower PPARγ tissue expression was observed. In conclusion, these results suggest that unbalanced maternal diet provided during a key period of the individual’s development, can generate permanent alterations in miRNA27a levels, which condition AT expansion, causing alterations that persist into adulthood.