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Tytuł pozycji:

Maternal high-fat high-sucrose diet and gestational exercise modulate hepatic fat accumulation and liver mitochondrial respiratory capacity in mothers and male offspring.

Tytuł:
Maternal high-fat high-sucrose diet and gestational exercise modulate hepatic fat accumulation and liver mitochondrial respiratory capacity in mothers and male offspring.
Autorzy:
Stevanović-Silva J; Laboratory of Metabolism and Exercise (LaMetEx), Research Centre in Physical Activity, Health and Leisure (CIAFEL), Faculty of Sport, University of Porto, 4200-450, Porto, Portugal. Electronic address: .
Beleza J; Department of Cell Biology, Physiology & Immunology, Faculty of Biology, University of Barcelona, Barcelona, Spain.
Coxito P; Laboratory of Metabolism and Exercise (LaMetEx), Research Centre in Physical Activity, Health and Leisure (CIAFEL), Faculty of Sport, University of Porto, 4200-450, Porto, Portugal.
Pereira S; Laboratory of Metabolism and Exercise (LaMetEx), Research Centre in Physical Activity, Health and Leisure (CIAFEL), Faculty of Sport, University of Porto, 4200-450, Porto, Portugal; CNC - Center for Neuroscience and Cell Biology, UC-Biotech, University of Coimbra, 3060-197 Cantanhede, Portugal.
Rocha H; Newborn Screening, Metabolism and Genetics Unit, Human Genetics Department, National Institute of Health Doutor Ricardo Jorge, 4000-053 Porto, Portugal.
Gaspar TB; Institute for Research and Innovation in Health Sciences (i3S), University of Porto, 4200-135 Porto, Portugal; Cancer Signalling and Metabolism Group, Institute of Molecular Pathology and Immunology of the University of Porto (Ipatimup), 4200-135 Porto, Portugal; Medical Faculty of University of Porto (FMUP), 4200-139 Porto, Portugal; Abel Salazar Biomedical Sciences Institute (ICBAS), University of Porto, 4050-313 Porto, Portugal.
Gärtner F; Institute for Research and Innovation in Health Sciences (i3S), University of Porto, 4200-135 Porto, Portugal; Department of Molecular Pathology and Immunology, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, 4050-313, Porto, Portugal; Glycobiology in Cancer Group, Institute of Molecular Pathology and Immunology of University of Porto (Ipatimup), University of Porto, 4200-135 Porto, Portugal.
Correia R; HEMS - Histology and Electron Microscopy Institute for Research and Innovation in Health Sciences (i3S), University of Porto, 4200-135, Porto, Portugal,; Ipatimup - Institute of Molecular Pathology and Immunology of the University of Porto, 4200-135 Porto, Portugal.
Martins MJ; Institute for Research and Innovation in Health Sciences (i3S), University of Porto, 4200-135 Porto, Portugal; Department of Biomedicine, Biochemistry Unit, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal.
Guimarães T; Department of Biomedicine, Biochemistry Unit, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal; Department of Clinical Pathology, São João Hospital Centre, EPE, 4200-319 Porto, Portugal.
Martins S; Department of Clinical Pathology, São João Hospital Centre, EPE, 4200-319 Porto, Portugal; EPIUnit, Institute of Public Health, University of Porto, 4050-091 Porto, Portugal.
Oliveira PJ; CNC - Center for Neuroscience and Cell Biology, UC-Biotech, University of Coimbra, 3060-197 Cantanhede, Portugal.
Ascensão A; Laboratory of Metabolism and Exercise (LaMetEx), Research Centre in Physical Activity, Health and Leisure (CIAFEL), Faculty of Sport, University of Porto, 4200-450, Porto, Portugal.
Magalhães J; Laboratory of Metabolism and Exercise (LaMetEx), Research Centre in Physical Activity, Health and Leisure (CIAFEL), Faculty of Sport, University of Porto, 4200-450, Porto, Portugal.
Źródło:
Metabolism: clinical and experimental [Metabolism] 2021 Mar; Vol. 116, pp. 154704. Date of Electronic Publication: 2021 Jan 07.
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Publication: New York, NY : Elsevier Inc.
Original Publication: New York, Grune & Stratton.
MeSH Terms:
Diet, High-Fat*/adverse effects
Liver/*metabolism
Mitochondria, Liver/*metabolism
Physical Conditioning, Animal/*physiology
Prenatal Exposure Delayed Effects/*metabolism
Sucrose/*administration & dosage
Animals ; Cell Respiration/drug effects ; Diabetes, Gestational/metabolism ; Diabetes, Gestational/physiopathology ; Dietary Carbohydrates/adverse effects ; Female ; Lipid Metabolism/drug effects ; Male ; Maternal Nutritional Physiological Phenomena ; Mitochondria, Liver/drug effects ; Mothers ; Pregnancy ; Prenatal Exposure Delayed Effects/physiopathology ; Rats ; Rats, Sprague-Dawley
Contributed Indexing:
Keywords: Fetal programming; Gestational diabetes; Liver mitochondria; Physical activity; Pregnancy
Substance Nomenclature:
0 (Dietary Carbohydrates)
57-50-1 (Sucrose)
Entry Date(s):
Date Created: 20210109 Date Completed: 20210224 Latest Revision: 20210224
Update Code:
20240105
DOI:
10.1016/j.metabol.2021.154704
PMID:
33421507
Czasopismo naukowe
Background: Maternal high-caloric nutrition and related gestational diabetes mellitus (GDM) are associated with a high-risk for developing metabolic complications later in life and in their offspring. In contrast, exercise is recognized as a non-pharmacological strategy against metabolic dysfunctions associated to lifestyle disorders. Therefore, we investigated whether gestational exercise delays the development of metabolic alterations in GDM mothers later in life, but also protects 6-week-old male offspring from adverse effects of maternal diet.
Methods: Female Sprague-Dawley rats were fed with either control (C) or high-fat high-sucrose (HFHS) diet to induce GDM and submitted to gestational exercise during the 3 weeks of pregnancy. Male offspring were sedentary and fed with C-diet.
Results: Sedentary HFHS-fed dams exhibited increased gestational body weight gain (p < 0.01) and glucose intolerance (p < 0.01), characteristic of GDM. Their offspring had normal glucose metabolism, but increased early-age body weight, which was reverted by gestational exercise. Gestational exercise also reduced offspring hepatic triglycerides accumulation (p < 0.05) and improved liver mitochondrial respiration capacity (p < 0.05), contributing to the recovery of liver bioenergetics compromised by maternal HFHS diet. Interestingly, liver mitochondrial respiration remained increased by gestational exercise in HFHS-fed dams despite prolonged HFHS consumption and exercise cessation.
Conclusions: Gestational exercise can result in liver mitochondrial adaptations in GDM animals, which can be preserved even after the exercise program cessation. Exposure to maternal GDM programs liver metabolic setting of male offspring, whereas gestational exercise appears as an important preventive tool against maternal diet-induced metabolic alterations.
Competing Interests: Declaration of competing interest No conflict of interest.
(Copyright © 2021. Published by Elsevier Inc.)

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