Diet-induced loss of cyclic ovarian function at normal body weight in a rodent model for bulimia nervosa.
A bulimic rat model was used to test whether type and frequency of food intake mimicking that in human bulimia nervosa could disrupt oestrous cyclicity, induce an effect on glycoprotein (LH) structure, or affect 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 palatable choice of human food items--the 'cafeteria diet'. There were four groups: control (normal chow), obese (continuous cafeteria diet), post-obese (cafeteria diet, then fasted to reduce weight to that of controls) and binge (cafeteria alternated with normal diet every few days). Animals 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. Twenty-four hours later, half of the animals in each group were killed for assessment of effects on their reproductive organs. The remaining animals 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 later (phase II). All animals on the cafeteria diet in phase I exhibited significant disruption of oestrous cyclicity irrespective of body weight. LH released in response to the first GnRH challenge showed a prolonged half-life, and/or increased rate of secretion in the obese and post-obese groups but in the binge group the secretory/clearance properties resembled those of control animals. After the second GnRH challenge at the end of phase II, however, the LH of the binge group appeared to have different secretory or clearance characteristics, whereas that of the previously obese animals had returned to normal. These data show ovarian cyclicity was disrupted by hyperphagia and irregular eating, even at normal body weight. Relating ovarian function to pituitary output in terms of LH, the effects of the continuous cafeteria diet did not appear to persist in the animals that returned to normal diets, but in the binge group the effect, presumably of the diet manipulation, was manifested after return to a normal eating pattern. This finding suggests that irregular eating habits may exert a direct (and acute) effect on the ovary, but that effects on the pituitary (and LH glycoforms) take longer to be expressed, explaining many features of bulimia nervosa.
Leigh
A J
AJ
Department of Obstetrics and Gynaecology, St George's Hospital Medical School, London, UK.
Stock
M J
MJ
Lacey
J H
JH
Wilson
C A
CA
D000704:Analysis of Variance; D000818:Animals; D001835:Body Weight; D002032:Bulimia / Q000503:physiopathology*; D004195:Disease Models, Animal; D004435:Eating; D004971:Estrus / Q000502:physiology*; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology; D006207:Half-Life; D007986:Luteinizing Hormone / Q000097:blood; D009765:Obesity / Q000097:blood / Q000503:physiopathology; D009929:Organ Size; D010053:Ovary / Q000033:anatomy & histology / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014599:Uterus / Q000033:anatomy & histology
D007987:Gonadotropin-Releasing Hormone; D007986:Luteinizing Hormone