POSTPARTUM HYPOPHAGIA IN PRIMIPAROUS SOWS .2. EFFECTS OF FEEDING LEVEL DURING GESTATION AND EXOGENOUS INSULIN ON LACTATION FEED-INTAKE, GLUCOSE-TOLERANCE, AND EPINEPHRINE-STIMULATED RELEASE OF NONESTERIFIED FATTY-ACIDS AND GLUCOSE
Wc. Weldon et al., POSTPARTUM HYPOPHAGIA IN PRIMIPAROUS SOWS .2. EFFECTS OF FEEDING LEVEL DURING GESTATION AND EXOGENOUS INSULIN ON LACTATION FEED-INTAKE, GLUCOSE-TOLERANCE, AND EPINEPHRINE-STIMULATED RELEASE OF NONESTERIFIED FATTY-ACIDS AND GLUCOSE, Journal of animal science, 72(2), 1994, pp. 395-403
The objectives of this experiment were 1) to determine whether allowin
g sows ad libitum access to feed from d 60 of gestation affects glucos
e tolerance and 2) to determine whether exogenous insulin increases fe
ed intake by preventing mobilization of nonesterified fatty acids (NEF
A). Sixty crossbred sows were assigned to one of two feeding regimens
during gestation, either a standard level of feed (SL; 1.85 kg/d) or a
llowed ad libitum access to feed (AL). Sows also received an injection
of either .75 IU of insulin/kg BW or saline daily during the first 7
d of lactation. Exogenous insulin increased ADFI at d 7 of lactation (
p = .07) and increased total feed intake at d 7 and 14 of lactation (p
= .09). Total feed intake during d 0 to 21 was not affected by insuli
n treatment. Compared with the SL sows, the AL sows were less tolerant
of glucose infusion (1 g of glucose/kg BW, i.v.) on d 1 of lactation
(P < .01). Baseline and peak concentrations of insulin were not affect
ed by feeding level during gestation (P = .4). Baseline and peak conce
ntrations of NEFA were greater in AL sows than in SL sows (P < .001) a
nd were not affected by insulin treatment (P = .39). Release of NEFA a
fter epinephrine stimulation was greater in AL sows than the reduced f
eed intake during lactation exhibited by sows that are overfed during
gestation may be caused by insulin resistance. Exogenous insulin seems
to increase feed intake by reducing plasma glucose rather than be aff
ecting plasma NEFA.