Effects of lack of pubertal, ovary-dependent programming on fructose induced dysmetabolism

VILLAGARCIA H; CASTRO MC; MASSA ML; SPINEDI E; FRANCINI F

Punta Cana

Congreso; XXV Annual Meeting of the ALEH; 2018

ALEH

Background: Bilateral ovariectomy (OVX)-inducedMetabolic Syndrome in rats is characterized by increased body weight (BW)/fatand endocrine-metabolic dysfunctions. We currently evaluated the effect oflacking pubertal programming by endogenous peak of ovary-derived estradiol(E2), on endocrine-metabolic and liver functions when adulthood (90 days old)was reached. Methods: Sprague-Dawley rats were either OVX on day 23/25of life (pre-pubertal OVX; OP), day 60 of life (adult OVX; OA) or sham (S)operated. Recovered rats were allocated with free access to rat chow and waterup to 69 days of age; then divided in groups either receiving drinking water(C) or fructose rich diet (F; 10% F in drinking water). Groups: CS, COP, COA,FS, FOP and FOA. Subsets of groups were sacrificed in non-fasting (basal)condition, and overnight-fasting rats were submitted to ip glucose tolerancetest (GTT; 2 g/kg BW). BWs, food-intake and drank solution were recorded daily.Pasma glucose (GLU) and triglyceride (TG) levels were quantified. Glycemias weremonitored throughout the GTT, individual area under the curve (AUC) of GLUlevels was calculated. Finally, liver expression mRNA levels of FAS and GPATwere quantified. Results: Non-fasting COP and COA rats showed increasedfood intake, BW gain and decreased triglyceridemia, although similar glycemias.All F groups developed increased BW gain, increased TG levels (attenuated inOVX rats) however glycemia increased only in FS rats. Finally, while FS ratswere intolerant to glucose overload, this effect was absent in FOP and FOArats. A diminished gene expression of FAS was noticed in both COP and COA rats.Conclusions: Increased OVX-dependent BW gain seems to be related to thelack of E2 anorectic activity. This programming in lipid metabolism exerted by thelack of hormones/ovarian factors appears to protect the individual fromdeveloping dyslipidemia and pre-diabetes.