Chinas 2022 Metabolites

From Bioblast
Publications in the MiPMap
ChiΓ±as Merlin A, Gonzalez K, Mockler S, Perez Y, Jia UA, Chicco AJ, Ullevig SL, Chung E (2022) Switching to a standard chow diet at weaning improves the effects of maternal and postnatal high-fat and high-sucrose diet on cardiometabolic health in adult male mouse offspring.

Β» Metabolites 12:563. PMID: 35736495 Open Access

Chinas Merlin Andrea, Gonzalez Kassandra, Mockler Sarah, Perez Yessenia, Jia U-Ter Aondo, Chicco Adam J, Ullevig Sarah L, Chung Eunhee (2022) Metabolites

Abstract: Cardiac mitochondrial dysfunction contributes to obesity-associated heart disease. Maternal and postnatal diet plays an important role in cardiac function, yet the impacts of a mismatch between prenatal and postweaning diet on cardiometabolic function are not well understood. We tested the hypothesis that switching to a standard chow diet after weaning would attenuate systemic metabolic disorders and cardiac and mitochondrial dysfunction associated with maternal and postnatal high-fat/high-sucrose (HFHS) diet in mice. Six-month-old male CD1 offspring from dams fed a HFHS diet and weaned to the same HFHS diet (HH) or switched to a standard chow diet (HC) were compared to offspring from dams fed a low-fat/low-sucrose diet and maintained on the same diet (LL). HC did not decrease body weight (BW) but normalized glucose tolerance, plasma cholesterol, LDL, and insulin levels compared to the HH. Systolic function indicated by the percent fractional shortening was not altered by diet. In freshly isolated cardiac mitochondria, maximal oxidative phosphorylation-linked respiratory capacity and coupling efficiency were significantly higher in the HC in the presence of fatty acid substrate compared to LL and HH, with modification of genes associated with metabolism and mitochondrial function. Switching to a standard chow diet at weaning can attenuate the deleterious effects of long-term HFHS in adult male mouse offspring.
β€’ Keywords: Diabetes, Glucose and insulin tolerance tests, Male mouse offspring, Obesity, Systolic function β€’ Bioblast editor: Plangger M β€’ O2k-Network Lab: US CO Fort Collins Chicco AJ

Labels: MiParea: Respiration, Developmental biology, Exercise physiology;nutrition;life style  Pathology: Cardiovascular 

Organism: Mouse  Tissue;cell: Heart  Preparation: Isolated mitochondria 

Coupling state: LEAK, OXPHOS  Pathway: F, N, NS  HRR: Oxygraph-2k 

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