Postnatal growth restriction alters myocardial mitochondrial energetics in mice

Author:

Visker Joseph R.12ORCID,Leszczynski Eric C.2,Wellette‐Hunsucker Austin G.23,McPeek Ashley C.2,Quinn Melissa A.2,Kim Seong Hyun2,Bazil Jason N.4,Ferguson David P.2ORCID

Affiliation:

1. The Nora Eccles Harrison Cardiovascular Research and Training Institute University of Utah Salt Lake City Utah USA

2. Department of Kinesiology Michigan State University East Lansing Michigan USA

3. Department of Physiology University of Kentucky Lexington Kentucky USA

4. Department of Physiology Michigan State University East Lansing Michigan USA

Abstract

AbstractPostnatal 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 ∼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, ) and fluorimetry (reactive oxygen species emission, ) 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 α‐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.

Funder

National Heart, Lung, and Blood Institute

Publisher

Wiley

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