DIET-INDUCED LOSS OF CYCLIC OVARIAN-FUNCTION AT NORMAL BODY-WEIGHT INA RODENT MODEL FOR BULIMIA-NERVOSA

A bulimic rat model was used to test whether type and frequency of foo d intake mimicking that in human bulimia nervosa could disrupt oestrou s cyclicity, induce an effect on glycoprotein (LH) structure, or affec t both processes and if so, to determine whether any such effects were acute, or persisted after return to normal eating patterns. Voluntary hyperphagia was induced by offering female rats a varied and palatabl e choice of human food items - the 'cafeteria diet'. There were four g roups: control (normal chow), obese (continuous cafeteria diet), post- obese (cafeteria diet, then fasted to reduce weight to that of control s) and binge (cafeteria alternated with normal diet every few days). A nimals were maintained on these diets for 60 days (phase I). They were then given a GnRH challenge on day 2 of dioestrus of the cycle. Twent y-four hours later, half of the animals in each group were killed for assessment of effects on their reproductive organs. The remaining anim als were returned to normal diets and kept for a further 40 days, when the GnRH challenge was repeated and the animals were killed 24 h late r (phase II). All animals on the cafeteria diet in phase I exhibited s ignificant disruption of oestrous cyclicity irrespective of body weigh t. LH released in response to the first GnRH challenge showed a prolon ged half-life, and/or increased rate of secretion in the obese and pos t-obese groups but in the binge group the secretory/clearance properti es resembled those of control animals. After the second GnRH challenge at the end of phase II, however, the LH of the binge group appeared t o have different secretory or clearance characteristics, whereas that of the previously obese animals had returned to normal. These data sho w ovarian cyclicity was disrupted by hyperphagia and irregular eating, even at normal body weight. Relating ovarian function to pituitary ou tput in terms of LH, the effects of the continuous cafeteria diet did not appear to persist in the animals that returned to normal diets, bu t in the binge group the effect, presumably of the diet manipulation, was manifested after return to a normal eating pattern. This finding s uggests that irregular eating habits may exert a direct (and acute) ef fect on the ovary, but that effects on the pituitary (and LH glycoform s) take longer to be expressed, explaining many features of bulimia ne rvosa.