HAL Id: hal-02739867
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EPA prevents insulin resistance and glucose intolerance
in mice fed a high fat-high sucrose diet
Alexandre Pinel, Jean-Paul Rigaudière, Elodie Pitois, Chrystele Jouve, Béatrice Morio, Frédéric Capel
To cite this version:
Alexandre Pinel, Jean-Paul Rigaudière, Elodie Pitois, Chrystele Jouve, Béatrice Morio, et al.. EPA prevents insulin resistance and glucose intolerance in mice fed a high fat-high sucrose diet. 12. Euro-pean Nutrition Conference FENS 2015, Oct 2015, Berlin, Germany. KARGER, Annals of Nutrition and Metabolism, 67, 601 p., 2015, 12th European Nutrition Conference (FENS). �hal-02739867�
0 2 4 6 8 10 12 14 16 18 20 C22.6.n.3 0 0,5 1 1,5 2 2,5 3 3,5 4 4,5 5 C18.3.n.3 C20.5.n.3 C22.5.n.3
Ctrl HF ALA EPA DHA
bc b
a
c b
A. Pinel1,2, J-P. Rigaudière1,2, E.Pitois1,2, C. Jouve1,2, B. Morio1,2, F. Capel1,2
1Institut National de la Recherche Agronomique, centre de Clermont-Ferrand Theix Lyon, Unité de Nutrition Humaine UMR1019.
2Laboratoire de Nutrition Humaine, Equipe CHLEO (Contrôle de l’Homéostasie Lipido-énergétique et Obésité), 63009 Clermont Ferrand Cedex 1. 3INRA, UMR 1397, Laboratoire CarMeN, Université Lyon 1, INSERM U1060, INSA de Lyon, Université Lyon-Sud Rockefeller et Charles Merieux,
Lyon, France.
Results:
Conclusion : Materials & Methods :
Introduction:
Objectives:
Insulin resistance (IR) is a key feature of obesity. IR favors the progression of metabolic syndrome (MetS), increases the risk of type 2 diabetes and cardiovascular diseases. IR results from metabolic dysfunctions caused by ectopic fat depots in the liver and skeletal muscle when adipose tissue storage capacity is exceeded. Nutritional strategies using n-3 PUFA were proposed to prevent IR and MetS associated to obesity by unclear mechanisms.
The aim of the present work was to compare the effect of ALA, EPA and DHA on insulin resistance and metabolic dysfunctions during a high fat (HF)-high sucrose (HS) challenge.
C57BL6 and Ob/Ob mice were fed a HF (45% energy)-HS (17% energy) diet without or with 1% energy replaced by ALA, EPA or DHA for 16 and 6 weeks respectively. IR was evaluated by intraperitoneal (ip) injection of insulin followed by monitoring of glycaemia over 2 hours. Glucose tolerance was similarly assessed using glucose injection. Fatty acid composition of tissues was determined by gas chromatography.
Long chain omega 3 fatty acids have distinct effects on IR and glucose tolerance. By contrast with ALA and DHA, EPA has interesting
protective effect against several key parameters of MetS. 20,00 22,00 24,00 26,00 28,00 30,00 START 5 9 13 Ctrl HF ALA EPA DHA B ody Wei ght ( g) Time (weeks)
Figure 1. Body weight of mice during HF/HS diet
c c bc b a c c b d a e c b d a % of t ot al f at ty aci ds % of t ot al f at ty aci ds
(% of total fatty acids)
CTRL HF ALA EPA DHA
C18: 3 n-3 0,45 ± 0,05a 0,31 ± 0,05c 0,63 ± 0,03b 0,31 ± 0,04c 0,32 ± 0,04c
C20: 5 n-3 0,37 ± 0,02a 0,39 ± 0,05a 0,77 ± 0,06a 4,84 ± 0,26b 2,84 ± 0,36c
C22:5 n-3 0,24 ± 0,01a 0,26 ± 0,02a 0,35 ± 0,01b 0,82 ± 0,04c 0,23 ± 0,01a
C22: 6 n-3 5,19 ± 0,17a 6,00 ± 0,27a 6,95 ± 0,19b 8,07 ± 0,31c 11,65 ± 0,51d
Figure 4. n-3PUFA enrichment in the adipose
tissue Figure 5. n-3PUFA enrichment in the liver
90 140 190 240 290 340 390 440 490 0 50 100 150 G lyce m ia (m g/ dL ) Time (min) Ctrl HF ALA EPA DHA a a ab bc c
Figure 3. ip-Glucose tolerance test.
A re a un der t he curve ( A U )
CTRL HF ALA EPA DHA
Chol
(g/L) 0,72±0,03c 0,92±0,04a 0,83±0,08ab 0,73±0,04c 0,74±0,02bc NEFA
(g/L) 0,30±0,01ab 0,27±0,01bc 0,37±0,03a 0,22±0,01c 0,31±0,01ab
Table 1. plasma concentration of cholesterol (Chol) and non esterified fatty acids (NEFA)
50 60 70 80 90 100 110 0 20 40 60 80 100 120 G lyce m ia (% of b asal ) Time (min) Ctrl HF ALA EPA DHA
Table 2. n-3 PUFA incorporation into plasma a b b a a 0 20 40 60 80 100
Ctrl HF ALA EPA DHA
A re a un der t he curve ( A U )
Figure 2. ip-insulin tolerance test.
0 0,2 0,4 0,6 0,8 1 1,2 C20:5 n-3 C22:5 n-3 C22:6 n-3
HF ALA DHA EPA
0 5 10 15 20 25 30 35 40 45 50