Abstract: 90

DOES A REDUCTION IN FATTY ACID AVAILABILITY SUPPRESS ESTROUS CYCLES IN ADULT FEMALE RATS?

H I'Anson^{1 *}
Biology Department, Washington and Lee University, Lexington, VA ¹

Decreased glucose availability causes a brief suppression of reproductive function similar to food deprivation in adult, cycling female rats (Biol Reprod 58, suppl 1:136, 1998). This study determines if the reproductive axis of the female rat is also sensitive to lipoprivation induced by inhibition of fatty acid oxidation. Young adult female rats (~270 g BW) were fed ad libitum and vaginal cytology was performed daily to determine reproductive status. After 3 consecutive estrous cycles (4-5 days each), animals were treated with either methyl cellulose (vehicle) or methyl palmoxirate (MP, 30 mg/kg) by gavage every 6h for 72h, beginning the day after estrus. This dose of MP produces a 40-50% inhibition of whole body lipid oxidation and an 8- to 10-fold stimulation of carbohydrate oxidation in 24-h fasted rats (Am J Physiol 265:E592-600, 1993). All rats received a controlled ad libitum diet (16.2 g/day) to prevent increased food intake from negating the lipoprivic signal. Rats were returned to ad libitum feeding after treatment. Body weight was not significantly altered during the treatment period in either group. Although not quantified, MP-treated rats left more food each day than rats treated with vehicle. MP treatment did not cause an increase in cycle length when compared to pretreatment cycles, even though food intake was decreased (MP: 4.1±0.1 vs 4.2±0.1 days; Vehicle: 5.5±0.4 vs 4.3±0.2 days, respectively). In addition, MP-treated rats were inactive, moved slowly, and exhibited pilo-erection. These data suggest that a reduction in fatty acid availability does not disrupt reproductive function in the adult female rat. However, it appears to induce a redistribution of metabolic fuels such that feeding, thermoregulation and locomotor activity are suppressed while reproductive function is maintained. Supported by Washington and Lee Univ.

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