[Circadian variations in the content of plasma constituants in the brood mare].

Twenty-one circadian blood sample profiles were made in heavy brood mares during pregnancy, lactation or the dry, non-pregnant period. The mares were fed forage-rich diets containing different levels of energy and nitrogen (table 1). Each profile consisted of 7 samples taken at 8 a.m., 11 a.m., 3 p.m., 7 p.m., 11 p.m., 4 a.m. and 8 a.m. The animals were fed at 8:30 a.m. The eleven plasma components evaluated were glucose, non-esterified fatty acids, beta-hydroxybutyrate, acetate, alanine, insulin (energy metabolites), urea, total protein (nitrogen metabolites), calcium, inorganic phosphorus and magnesium (mineral metabolites). Profile results are shown in table 2 and figure 1. Glucose, insulin and alanine increased and non-esterified fatty acids, acetate and beta-hydroxybutyrate decreased during the prandial period (between 8 a.m. and 11 a.m.). The glucose and insulin peaks were short, while the other components returned slowly to preprandial values. Acetate and beta-hydroxybutyrate were maximal during the night, while urea increased moderately during the prandial period. Protein concentration did not vary. The effect of feeding on minerals was moderate: there was a slight increase in calcium and magnesium and a decrease in phosphorus. The following differences were related to diet or physiological state (figs. 2, 3, 4): --higher glucose and insulin peaks when concentrate intake was high; --lower circadian variation of non-esterified fatty acids, beta-hydroxybutyrate and acetate in dry, non-pregnant, well-fed mares; --higher acetate levels with a high-forage diet; --more rapid alanine decrease during late pregnancy than in early lactation; --higher circadian variations in minerals during lactation than during pregnancy. The prandial variations of the following factors were significantly correlated (table 3): --glucose and insulin, --acetate and beta-hydroxybutyrate, --beta-hydroxybutyrate and non-esterified fatty acids, --acetate and non-esterified fatty acids. The origin of these variations is discussed. Two factors intervened: 1) exogenous production Very rapid digestion of the concentrate induced an increase in glucose (and thus in insulin) and alanine. The volatile fatty acids produced in the hindgut caused nocturnal peaks of acetate and beta-hydroxybutyrate; 2) a lipogenic phase (which began after mean meal intake) alternating with a lipolytic phase, providing constant coverage of the energy needs. This explains the large post-prandial decreases in non-esterified fatty acids, acetate and beta-hydroxybutyrate.