Abstract
Poor prenatal development, followed by rapid childhood growth, conveys greater cardiometabolic risk in later life. Microswine offspring exposed to perinatal maternal protein restriction [MPR; “low protein offspring” (LPO)] grow poorly in late-fetal/neonatal stages. After weaning to an ad libitum (AL) diet, LPO-AL exhibit accelerated growth and fat deposition rates with low adiponectin mRNA, despite low-normal body fat and small intra-abdominal adipocytes. We examined effects of caloric restriction (CR) on growth and metabolic status in LPO and normal protein offspring (NPO) randomized to AL or CR diets from weaning. CR transiently reduced growth in both LPO and NPO, delaying recovery in female LPO-CR. Over 7.5–12.5 weeks, linear growth rates in LPO-CR were slower than LPO-AL (P < 0.001) but exceeded NPO-AL; body weight growth rates fell but were lower in LPO-CR versus NPO-CR. Linear acceleration ceased after 12 weeks. At 16 weeks, percent catch-up in LPO-CR was reduced versus LPO-AL (P < 0.001). Plasma growth hormone was low in LPO (P < 0.02). CR normalized fat deposition rate, yet adiponectin mRNA remained low in LPO-CR (P < 0.001); plasma adiponectin was low in all LPO-AL and in female LPO-CR. Insulin sensitivity improved during CR. We conclude that in LPO: 1) CR delays onset of, but does not abolish, accelerated linear growth, despite low growth hormone; 2) CR yields stunting via delayed onset, plus a finite window for linear growth acceleration; 3) MPR lowers adiponectin mRNA independently of growth, adiposity, or adipocyte size; and 4) MPR reduces circulating adiponectin in LPO-AL and female LPO-CR, potentially enhancing cardiometabolic risk.
| Original language | English (US) |
|---|---|
| Pages (from-to) | R354-R368 |
| Journal | American Journal of Physiology - Regulatory Integrative and Comparative Physiology |
| Volume | 315 |
| Issue number | 2 |
| DOIs | |
| State | Published - Aug 20 2018 |
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Keywords
- Adiponectin
- Adipose tissue
- Catch-up growth
- Fetal programming
- Growth hormone
ASJC Scopus subject areas
- Physiology
- Physiology (medical)
Cite this
Effects of postweaning calorie restriction on accelerated growth and adiponectin in nutritionally programmed microswine offspring. / Dupriest, Elizabeth A.; Lin, Baoyu; Kupfer, Philipp; Sekiguchi, Kaiu; Bhusari, Amruta; Quackenbush, Alexandra; Celebic, Almir; Morgan, Terry; Purnell, Jonathan; Bagby, Susan.
In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 315, No. 2, 20.08.2018, p. R354-R368.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of postweaning calorie restriction on accelerated growth and adiponectin in nutritionally programmed microswine offspring
AU - Dupriest, Elizabeth A.
AU - Lin, Baoyu
AU - Kupfer, Philipp
AU - Sekiguchi, Kaiu
AU - Bhusari, Amruta
AU - Quackenbush, Alexandra
AU - Celebic, Almir
AU - Morgan, Terry
AU - Purnell, Jonathan
AU - Bagby, Susan
PY - 2018/8/20
Y1 - 2018/8/20
N2 - Poor prenatal development, followed by rapid childhood growth, conveys greater cardiometabolic risk in later life. Microswine offspring exposed to perinatal maternal protein restriction [MPR; “low protein offspring” (LPO)] grow poorly in late-fetal/neonatal stages. After weaning to an ad libitum (AL) diet, LPO-AL exhibit accelerated growth and fat deposition rates with low adiponectin mRNA, despite low-normal body fat and small intra-abdominal adipocytes. We examined effects of caloric restriction (CR) on growth and metabolic status in LPO and normal protein offspring (NPO) randomized to AL or CR diets from weaning. CR transiently reduced growth in both LPO and NPO, delaying recovery in female LPO-CR. Over 7.5–12.5 weeks, linear growth rates in LPO-CR were slower than LPO-AL (P < 0.001) but exceeded NPO-AL; body weight growth rates fell but were lower in LPO-CR versus NPO-CR. Linear acceleration ceased after 12 weeks. At 16 weeks, percent catch-up in LPO-CR was reduced versus LPO-AL (P < 0.001). Plasma growth hormone was low in LPO (P < 0.02). CR normalized fat deposition rate, yet adiponectin mRNA remained low in LPO-CR (P < 0.001); plasma adiponectin was low in all LPO-AL and in female LPO-CR. Insulin sensitivity improved during CR. We conclude that in LPO: 1) CR delays onset of, but does not abolish, accelerated linear growth, despite low growth hormone; 2) CR yields stunting via delayed onset, plus a finite window for linear growth acceleration; 3) MPR lowers adiponectin mRNA independently of growth, adiposity, or adipocyte size; and 4) MPR reduces circulating adiponectin in LPO-AL and female LPO-CR, potentially enhancing cardiometabolic risk.
AB - Poor prenatal development, followed by rapid childhood growth, conveys greater cardiometabolic risk in later life. Microswine offspring exposed to perinatal maternal protein restriction [MPR; “low protein offspring” (LPO)] grow poorly in late-fetal/neonatal stages. After weaning to an ad libitum (AL) diet, LPO-AL exhibit accelerated growth and fat deposition rates with low adiponectin mRNA, despite low-normal body fat and small intra-abdominal adipocytes. We examined effects of caloric restriction (CR) on growth and metabolic status in LPO and normal protein offspring (NPO) randomized to AL or CR diets from weaning. CR transiently reduced growth in both LPO and NPO, delaying recovery in female LPO-CR. Over 7.5–12.5 weeks, linear growth rates in LPO-CR were slower than LPO-AL (P < 0.001) but exceeded NPO-AL; body weight growth rates fell but were lower in LPO-CR versus NPO-CR. Linear acceleration ceased after 12 weeks. At 16 weeks, percent catch-up in LPO-CR was reduced versus LPO-AL (P < 0.001). Plasma growth hormone was low in LPO (P < 0.02). CR normalized fat deposition rate, yet adiponectin mRNA remained low in LPO-CR (P < 0.001); plasma adiponectin was low in all LPO-AL and in female LPO-CR. Insulin sensitivity improved during CR. We conclude that in LPO: 1) CR delays onset of, but does not abolish, accelerated linear growth, despite low growth hormone; 2) CR yields stunting via delayed onset, plus a finite window for linear growth acceleration; 3) MPR lowers adiponectin mRNA independently of growth, adiposity, or adipocyte size; and 4) MPR reduces circulating adiponectin in LPO-AL and female LPO-CR, potentially enhancing cardiometabolic risk.
KW - Adiponectin
KW - Adipose tissue
KW - Catch-up growth
KW - Fetal programming
KW - Growth hormone
UR - http://www.scopus.com/inward/record.url?scp=85052199898&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85052199898&partnerID=8YFLogxK
U2 - 10.1152/ajpregu.00162.2017
DO - 10.1152/ajpregu.00162.2017
M3 - Article
C2 - 29924631
AN - SCOPUS:85052199898
VL - 315
SP - R354-R368
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 2
ER -