Postpartum hypophagia in primiparous sows: II. 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.

W. C. Weldon, A. J. Lewis, G. F. Louis, J. L. Kovar, P. S. Miller

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Abstract

The objectives of this experiment were 1) to determine whether allowing sows ad libitum access to feed from d 60 of gestation affects glucose tolerance and 2) to determine whether exogenous insulin increases feed intake by preventing mobilization of nonesterified fatty acids (NEFA). 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 allowed 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 insulin 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 affected by feeding level during gestation (P = .4). Baseline and peak concentrations of NEFA were greater in AL sows than in SL sows (P < .001) and were not affected by insulin treatment (P = .39). Release of NEFA after epinephrine stimulation was greater in AL sows than in SL sows (P < .05). The data indicate that the reduced feed 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 affecting plasma NEFA.

Original languageEnglish (US)
Pages (from-to)395-403
Number of pages9
JournalJournal of animal science
Volume72
Issue number2
DOIs
StatePublished - Feb 1994

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undereating
epinephrine
feeding level
glucose tolerance
Lactation
Nonesterified Fatty Acids
Postpartum Period
Epinephrine
sows
free fatty acids
insulin
lactation
feed intake
pregnancy
Insulin
Glucose
Pregnancy
glucose
Insulin Resistance
insulin resistance

ASJC Scopus subject areas

  • Food Science
  • Animal Science and Zoology
  • Genetics

Cite this

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title = "Postpartum hypophagia in primiparous sows: II. 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.",
abstract = "The objectives of this experiment were 1) to determine whether allowing sows ad libitum access to feed from d 60 of gestation affects glucose tolerance and 2) to determine whether exogenous insulin increases feed intake by preventing mobilization of nonesterified fatty acids (NEFA). 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 allowed 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 insulin 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 affected by feeding level during gestation (P = .4). Baseline and peak concentrations of NEFA were greater in AL sows than in SL sows (P < .001) and were not affected by insulin treatment (P = .39). Release of NEFA after epinephrine stimulation was greater in AL sows than in SL sows (P < .05). The data indicate that the reduced feed 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 affecting plasma NEFA.",
author = "Weldon, {W. C.} and Lewis, {A. J.} and Louis, {G. F.} and Kovar, {J. L.} and Miller, {P. S.}",
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T2 - II. 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.

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AU - Lewis, A. J.

AU - Louis, G. F.

AU - Kovar, J. L.

AU - Miller, P. S.

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N2 - The objectives of this experiment were 1) to determine whether allowing sows ad libitum access to feed from d 60 of gestation affects glucose tolerance and 2) to determine whether exogenous insulin increases feed intake by preventing mobilization of nonesterified fatty acids (NEFA). 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 allowed 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 insulin 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 affected by feeding level during gestation (P = .4). Baseline and peak concentrations of NEFA were greater in AL sows than in SL sows (P < .001) and were not affected by insulin treatment (P = .39). Release of NEFA after epinephrine stimulation was greater in AL sows than in SL sows (P < .05). The data indicate that the reduced feed 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 affecting plasma NEFA.

AB - The objectives of this experiment were 1) to determine whether allowing sows ad libitum access to feed from d 60 of gestation affects glucose tolerance and 2) to determine whether exogenous insulin increases feed intake by preventing mobilization of nonesterified fatty acids (NEFA). 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 allowed 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 insulin 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 affected by feeding level during gestation (P = .4). Baseline and peak concentrations of NEFA were greater in AL sows than in SL sows (P < .001) and were not affected by insulin treatment (P = .39). Release of NEFA after epinephrine stimulation was greater in AL sows than in SL sows (P < .05). The data indicate that the reduced feed 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 affecting plasma NEFA.

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