PMID- 38180279
OWN - NLM
STAT- MEDLINE
DCOM- 20240403
LR  - 20240410
IS  - 1469-445X (Electronic)
IS  - 0958-0670 (Print)
IS  - 0958-0670 (Linking)
VI  - 109
IP  - 4
DP  - 2024 Apr
TI  - Postnatal growth restriction alters myocardial mitochondrial energetics in mice.
PG  - 562-575
LID - 10.1113/EP091304 [doi]
AB  - Postnatal growth restriction (PGR) can increase the risk of cardiovascular 
      disease (CVD) potentially due to impairments in oxidative phosphorylation 
      (OxPhos) within cardiomyocyte mitochondria. The purpose of this investigation was 
      to determine if PGR impairs cardiac metabolism, specifically OxPhos. FVB (Friend 
      Virus B-type) mice were fed a normal-protein (NP: 20% protein), or low-protein 
      (LP: 8% protein) isocaloric diet 2 weeks before mating. LP dams produce  approximately 20% less 
      milk, and pups nursed by LP dams experience reduced growth into adulthood as 
      compared to pups nursed by NP dams. At birth (PN1), pups born to dams fed the NP 
      diet were transferred to LP dams (PGR group) or a different NP dam (control 
      group: CON). At weaning (PN21), all mice were fed the NP diet. At PN22 and PN80, 
      mitochondria were isolated for respirometry (oxygen consumption rate, JO2 ) and 
      fluorimetry (reactive oxygen species emission, JH2O2 ) analysis measured as 
      baseline respiration (LEAK) and with saturating ADP (OxPhos). Western blotting at 
      PN22 and PN80 determined protein abundance of uncoupling protein 3, 
      peroxiredoxin-6, voltage-dependent anion channel and adenine nucleotide 
      translocator 1 to provide further insight into mitochondrial function. ANOVAs 
      with the main effects of diet, sex and age with alpha-level of 0.05 was set a priori. 
      Overall, PGR (7.8 +/- 1.1) had significant (P = 0.01) reductions in respiratory 
      control in complex I when compared to CON (8.9 +/- 1.0). In general, our results 
      show that PGR led to higher electron leakage in the form of free radical 
      production and reactive oxygen species emission. No significant diet effects were 
      found in protein abundance. The observed reduced respiratory control and 
      increased ROS emission in PGR mice may increase risk for CVD in mice.
CI  - (c) 2024 The Authors. Experimental Physiology published by John Wiley & Sons Ltd on 
      behalf of The Physiological Society.
FAU - Visker, Joseph R
AU  - Visker JR
AUID- ORCID: 0000-0002-8490-6111
AD  - The Nora Eccles Harrison Cardiovascular Research and Training Institute, 
      University of Utah, Salt Lake City, Utah, USA.
AD  - Department of Kinesiology, Michigan State University, East Lansing, Michigan, 
      USA.
FAU - Leszczynski, Eric C
AU  - Leszczynski EC
AD  - Department of Kinesiology, Michigan State University, East Lansing, Michigan, 
      USA.
FAU - Wellette-Hunsucker, Austin G
AU  - Wellette-Hunsucker AG
AD  - Department of Kinesiology, Michigan State University, East Lansing, Michigan, 
      USA.
AD  - Department of Physiology, University of Kentucky, Lexington, Kentucky, USA.
FAU - McPeek, Ashley C
AU  - McPeek AC
AD  - Department of Kinesiology, Michigan State University, East Lansing, Michigan, 
      USA.
FAU - Quinn, Melissa A
AU  - Quinn MA
AD  - Department of Kinesiology, Michigan State University, East Lansing, Michigan, 
      USA.
FAU - Kim, Seong Hyun
AU  - Kim SH
AD  - Department of Kinesiology, Michigan State University, East Lansing, Michigan, 
      USA.
FAU - Bazil, Jason N
AU  - Bazil JN
AD  - Department of Physiology, Michigan State University, East Lansing, Michigan, USA.
FAU - Ferguson, David P
AU  - Ferguson DP
AUID- ORCID: 0000-0003-1203-0920
AD  - Department of Kinesiology, Michigan State University, East Lansing, Michigan, 
      USA.
LA  - eng
GR  - L30 HL165508/HL/NHLBI NIH HHS/United States
GR  - R03 HD101654/HD/NICHD NIH HHS/United States
GR  - T32 HL007576/HL/NHLBI NIH HHS/United States
GR  - T32HL007576/HL/NHLBI NIH HHS/United States
PT  - Journal Article
DEP - 20240105
PL  - England
TA  - Exp Physiol
JT  - Experimental physiology
JID - 9002940
RN  - 0 (Reactive Oxygen Species)
SB  - IM
MH  - Animals
MH  - Mice
MH  - Reactive Oxygen Species/metabolism
MH  - *Mitochondria, Heart/metabolism
MH  - Myocardium/metabolism
MH  - Diet, Protein-Restricted
MH  - *Cardiovascular Diseases
PMC - PMC10984791
MID - NIHMS1953878
OTO - NOTNLM
OT  - cardiovascular disease
OT  - development
OT  - growth restriction
OT  - mitochondrial function
OT  - oxidative stress
OT  - reactive oxygen species
COIS- The authors declare no conflicts of interest. The results of this study are 
      presented clearly, honestly and without fabrication, falsification or 
      inappropriate data manipulation, and results of the present study do not 
      constitute endorsement by the publisher.
EDAT- 2024/01/05 12:42
MHDA- 2024/04/03 06:44
PMCR- 2024/01/05
CRDT- 2024/01/05 09:55
PHST- 2023/05/17 00:00 [received]
PHST- 2023/12/14 00:00 [accepted]
PHST- 2024/04/03 06:44 [medline]
PHST- 2024/01/05 12:42 [pubmed]
PHST- 2024/01/05 09:55 [entrez]
PHST- 2024/01/05 00:00 [pmc-release]
AID - EPH13479 [pii]
AID - 10.1113/EP091304 [doi]
PST - ppublish
SO  - Exp Physiol. 2024 Apr;109(4):562-575. doi: 10.1113/EP091304. Epub 2024 Jan 5.