PMID- 10352119
OWN - NLM
STAT- MEDLINE
DCOM- 19990608
LR  - 20200930
IS  - 0037-9727 (Print)
IS  - 0037-9727 (Linking)
VI  - 221
IP  - 2
DP  - 1999 Jun
TI  - Caloric restriction abolishes enhanced metabolic efficiency induced by ectopic 
      agouti protein in yellow mice.
PG  - 99-104
AB  - Caloric restriction (CR), from approximately 3 months of age, at 70% of the ad 
      libitum (AL) caloric intake prevented development of overt obesity in female 
      "viable yellow" Avy/A (BALB/cStCrlfC3Hf/Nctr x VY/WffC3Hf/Nctr-Avy) F1 hybrid 
      mice. In adult yellow Avy/A mice, caloric restriction eliminated the increased 
      metabolic efficiency associated with the presence of agouti protein in ectopic 
      sites. At 4 weeks of age, the yellow Avy/A mice were approximately 14% heavier 
      and by 12 weeks of age, when caloric restriction began, they were approximately 
      24% heavier than the congenic agouti A/a mice. Between 4 and 12 weeks, the yellow 
      mice gained approximately 63% in body weight, whereas the agouti mice gained only 
      approximately 44%. While the comparable AL Avy/A mice gained approximately 128% 
      and the AL A/a mice gained approximately 41% between 12 and 51 weeks of age, the 
      CR Avy/A and A/a mice gained only 16% and 15%, respectively. Mean brain weights 
      of CR mice of both genotypes were lower than those of the comparable ad 
      libitum-fed (AL) groups; however, CR Avy/A mice had slightly, but significantly 
      (P < 0.0001), higher brain weights than CR A/a mice. The larger mean brain weight 
      and retention, during caloric restriction, of the somewhat greater prerestriction 
      Avy/A mean body weight compared with prerestriction A/a mice were consonant with 
      the hypothesis that ectopic agouti protein affects somatic growth directly or 
      indirectly. This may be related to altered developmental/metabolic programming in 
      yellow mice, indicated by greater metabolic efficiency and by an early transient 
      increase in circulating IGF-1 levels. The specific cellular processes modulated 
      by the agouti protein in ectopic sites remain to be identified.
FAU - Wolff, G L
AU  - Wolff GL
AD  - Division of Biochemical Toxicology, National Center for Toxicological 
      Research/Food and Drug Administration, Jefferson, Arkansas 72079, USA. 
      GWOLFF@NCTR.FDA.GOV
FAU - Kodell, R L
AU  - Kodell RL
FAU - Kaput, J A
AU  - Kaput JA
FAU - Visek, W J
AU  - Visek WJ
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Proc Soc Exp Biol Med
JT  - Proceedings of the Society for Experimental Biology and Medicine. Society for 
      Experimental Biology and Medicine (New York, N.Y.)
JID - 7505892
RN  - 0 (Agouti Signaling Protein)
RN  - 0 (Blood Glucose)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Proteins)
RN  - 0 (a protein, mouse)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
SB  - IM
MH  - Age Factors
MH  - Agouti Signaling Protein
MH  - Animals
MH  - Blood Glucose/analysis
MH  - Body Weight
MH  - Brain/metabolism
MH  - *Energy Intake
MH  - Female
MH  - Hybridization, Genetic
MH  - Insulin-Like Growth Factor I/analysis
MH  - *Intercellular Signaling Peptides and Proteins
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Organ Size
MH  - Phenotype
MH  - Proteins/genetics/*metabolism
EDAT- 1999/06/03 00:00
MHDA- 1999/06/03 00:01
CRDT- 1999/06/03 00:00
PHST- 1999/06/03 00:00 [pubmed]
PHST- 1999/06/03 00:01 [medline]
PHST- 1999/06/03 00:00 [entrez]
AID - 10.1046/j.1525-1373.1999.d01-61.x [doi]
PST - ppublish
SO  - Proc Soc Exp Biol Med. 1999 Jun;221(2):99-104. doi: 
      10.1046/j.1525-1373.1999.d01-61.x.