EPA prevents fat mass expansion and metabolic disturbances in mice fed with a Western diet[S]

Autor: Chrystèle Jouve, Elodie Pitois, Jean-Paul Rigaudière, Brigitte Laillet, Alexandre Pinel, Christophe Montaurier, Sarah De Saint-Vincent, Alain Huertas, Béatrice Morio, Frédéric Capel
Přispěvatelé: Unité de Nutrition Humaine (UNH), Institut National de la Recherche Agronomique (INRA)-Université d'Auvergne - Clermont-Ferrand I (UdA)-Clermont Université, Lesieur
Jazyk: angličtina
Rok vydání: 2016
Předmět:
Leptin
Male
0301 basic medicine
obesity
eicosapentaenoic acid
Erythrocytes
Drug Evaluation
Preclinical

Gene Expression
Mice
Obese

Adipose tissue
Biochemistry
Mice
Endocrinology
insulin resistance
Glucose homeostasis
Phospholipids
Research Articles
Adiposity
2. Zero hunger
Adipogenesis
omega-3 fatty acids
adipose tissue
nutrition
régulation du metabolisme
[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism
Eicosapentaenoic acid
3. Good health
Alimentation et Nutrition
Endocrinologie et métabolisme
lipids (amino acids
peptides
and proteins)

medicine.symptom
medicine.medical_specialty
Adipose Tissue
White

omega-3 polyunsaturated fatty acid
Adipokine
QD415-436
Biology
03 medical and health sciences
Insulin resistance
Adipokines
3T3-L1 Cells
Internal medicine
Glucose Intolerance
medicine
Animals
Food and Nutrition
Endocrinology and metabolism
030109 nutrition & dietetics
Adiponectin
Cell Membrane
Cell Biology
Lipid Metabolism
medicine.disease
Mice
Inbred C57BL

Diet
Western

acide gras polyinsaturé n-3
Anti-Obesity Agents
Weight gain
[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition
Zdroj: Journal of Lipid Research, Vol 57, Iss 8, Pp 1382-1397 (2016)
Journal of Lipid Research 8 (57), 1382-1397. (2016)
Journal of Lipid Research
Journal of Lipid Research, American Society for Biochemistry and Molecular Biology, 2016, 57 (8), pp.1382-1397. ⟨10.1194/jlr.M065458⟩
Journal of Lipid Research, 2016, 57 (8), pp.1382-1397. ⟨10.1194/jlr.M065458⟩
ISSN: 0022-2275
DOI: 10.1194/jlr.M065458⟩
Popis: The authors acknowledge the staff from Auvergne University Experimental Animal Laboratory and Christophe Del’Homme, Philippe Denis, Anne Terisse-Lottier and Alexandre Teynie from the Experimental Animal Facility of the Human Nutrition Unit (INRA of Clermont-Ferrand) for their assistance throughout the animal protocol. We thank Celine Bobby for her help for TaqMan gene expression assays. We gratefully acknowledge financial support and doctoral fellowship (to A.P.) fromLesieur and Avril; Impact of ALA, EPA and DHA on obesity and metabolic complications were studied in mice fed a high-fat high-sucrose diet (HF). HF diets were supplemented with ALA, EPA or DHA (1%w/w) and given to C57BL/6J mice for 16 weeks and to Ob/Ob mice for 6 weeks. In C57BL/6J mice, EPA reduced plasma cholesterol (-20%), limited fat mass accumulation (-23%), adipose cell hypertrophy (-50%), and reduced plasma leptin concentration (-60%), compared to HF fed mice. Furthermore, mice supplemented with EPA exhibited a higher insulin sensitivity (+24%) and glucose tolerance (+20%) compared to HF fed mice. Similar effects were observed in EPA supplemented Ob/Ob mice, although fat mass accumulation was not prevented. By contrast in comparison to HF fed mice, DHA did not prevent fat mass accumulation, increased plasma leptin concentration (+128%) in C57BL/6J mice and did not improve glucose homeostasis in C57BL/6J and Ob/Ob mice. In 3T3-L1 adipocytes, DHA stimulated leptin expression whereas EPA induced adiponectin expression, suggesting that improved leptin / adiponectin balance may contribute to the protective effect of EPA. In conclusion, supplementation with EPA, but not ALA and DHA, could preserve glucose homeostasis in an obesogenic environment and limit fat mass accumulation in the early stage of weight gain.
Databáze: OpenAIRE