title: Fish oil and argan oil intake differently modulate insulin resistance and glucose intolerance in a rat model of dietary-induced obesity.
abstract: We investigated the potential metabolic benefits of fish oil (FO) or vegetable argan oil (AO) intake in a dietary model of obesity-linked insulin resistance. Rats were fed a standard chow diet (controls), a high-fat/high-sucrose (HFHS) diet, or an HFHS diet in which 6% of the fat was replaced by either FO or AO feeding, respectively. The HFHS diet increased adipose tissue weight and insulin resistance as revealed by increased fasting glucose and exaggerated glycemic and insulin responses to a glucose tolerance test (intraperitoneal glucose tolerance test). Fish oil feeding prevented fat accretion, reduced fasting glycemia, and normalized glycemic or insulin responses to intraperitoneal glucose tolerance test as compared with HFHS diet. Unlike FO consumption, AO intake failed to prevent obesity, yet restored fasting glycemia back to chow-fed control values. Insulin-induced phosphorylation of Akt and Erk in adipose tissues, skeletal muscles, and liver was greatly attenuated in HFHS rats as compared with chow-fed controls. High-fat/high-sucrose diet-induced insulin resistance was also confirmed in isolated hepatocytes. Fish oil intake prevented insulin resistance by improving or fully restoring insulin signaling responses in all tissues and isolated hepatocytes. Argan oil intake also improved insulin-dependent phosphorylations of Akt and Erk; and in adipose tissue, these responses were increased even beyond values observed in chow-fed controls. Taken together, these results strongly support the beneficial action of FO on diet-induced insulin resistance and glucose intolerance, an effect likely explained by the ability of FO to prevent HFHS-induced adiposity. Our data also show for the first time that AO can improve some of the metabolic and insulin signaling abnormalities associated with HFHS feeding.
authors.affiliation: Department of Pharmacology, Université de Montréal, Montréal, Québec, Canada.
authors.forename: Samira
authors.initials: S
authors.lastname: Samane
authors.forename: Raymond
authors.initials: R
authors.lastname: Christon
authors.forename: Luce
authors.initials: L
authors.lastname: Dombrowski
authors.forename: Stéphane
authors.initials: S
authors.lastname: Turcotte
authors.forename: Zoubida
authors.initials: Z
authors.lastname: Charrouf
authors.forename: Charles
authors.initials: C
authors.lastname: Lavigne
authors.forename: Emile
authors.initials: E
authors.lastname: Levy
authors.forename: Hélène
authors.initials: H
authors.lastname: Bachelard
authors.forename: Hamid
authors.initials: H
authors.lastname: Amarouch
authors.forename: André
authors.initials: A
authors.lastname: Marette
authors.forename: Pierre Selim
authors.initials: PS
authors.lastname: Haddad
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004789:Enzyme Activation / Q000502:physiology; D005395:Fish Oils / Q000494:pharmacology*; D018149:Glucose Intolerance / Q000378:metabolism*; D005951:Glucose Tolerance Test; D015151:Immunoblotting; D007328:Insulin / Q000097:blood / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology*; D008099:Liver / Q000378:metabolism; D008297:Male; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D009765:Obesity / Q000097:blood / Q000378:metabolism*; D010938:Plant Oils / Q000494:pharmacology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000502:physiology
chemical_list: D001786:Blood Glucose; D005395:Fish Oils; D007328:Insulin; D010938:Plant Oils; D020928:Mitogen-Activated Protein Kinases