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

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

Congreso; XXV Congreso ALEH; 2018

Background: Bilateral ovariectomy (OVX)-induced Metabolic Syndrome in rats is characterized by increased body weight (BW)/fat and endocrine-metabolic dysfunctions. We currently evaluated the effect of lacking 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 23/25 of 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 water up 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 tolerance test (GTT; 2 g/kg BW). BWs, food-intake and drank solution were recorded daily. Pasma glucose (GLU) and triglyceride (TG) levels were quantified. Glycemias were monitored throughout the GTT, individual area under the curve (AUC) of GLU levels was calculated. Finally, liver expression mRNA levels of FAS and GPAT were quantified. Results: Non-fasting COP and COA rats showed increased food intake, BW gain and decreased triglyceridemia, although similar glycemias. All F groups developed increased BW gain, increased TG levels (attenuated in OVX rats) however glycemia increased only in FS rats. Finally, while FS rats were intolerant to glucose overload, this effect was absent in FOP and FOA rats. 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 the lack of E2 anorectic activity. This programming in lipid metabolism exerted by the lack of hormones/ovarian factors appears to protect the individual from developing dyslipidemia and pre-diabetes.