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Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high-fat-fed rats: role of apoptosis, adiponectin and tumour necrosis factor-alpha.
Br J Nutr. 2007 Feb; 97(2):389-98.BJ

Abstract

n-3 PUFA have shown potential anti-obesity and insulin-sensitising properties. However, the mechanisms involved are not clearly established. The aim of the present study was to assess the effects of EPA administration, one of the n-3 PUFA, on body-weight gain and adiposity in rats fed on a standard or a high-fat (cafeteria) diet. The actions on white adipose tissue lipolysis, apoptosis and on several genes related to obesity and insulin resistance were also studied. Control and cafeteria-induced overweight male Wistar rats were assigned into two subgroups, one of them daily received EPA ethyl ester (1 g/kg) for 5 weeks by oral administration. The high-fat diet induced a very significant increase in both body weight and fat mass. Rats fed with the cafeteria diet and orally treated with EPA showed a marginally lower body-weight gain (P = 0.09), a decrease in food intake (P < 0.01) and an increase in leptin production (P < 0.05). EPA administration reduced retroperitoneal adipose tissue weight (P < 0.05) which could be secondary to the inhibition of the adipogenic transcription factor PPARgamma gene expression (P < 0.001), and also to the increase in apoptosis (P < 0.05) found in rats fed with a control diet. TNFalpha gene expression was significantly increased (P < 0.05) by the cafeteria diet, while EPA treatment was able to prevent (P < 0.01) the rise in this inflammatory cytokine. Adiposity-corrected adiponectin plasma levels were increased by EPA. These actions on both TNFalpha and adiponectin could explain the beneficial effects of EPA on insulin resistance induced by the cafeteria diet.

Authors+Show Affiliations

Department of Physiology and Nutrition, University of Navarra, 31008 Pamplona, Spain.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17298710

Citation

Pérez-Matute, Patricia, et al. "Eicosapentaenoic Acid Actions On Adiposity and Insulin Resistance in Control and High-fat-fed Rats: Role of Apoptosis, Adiponectin and Tumour Necrosis Factor-alpha." The British Journal of Nutrition, vol. 97, no. 2, 2007, pp. 389-98.
Pérez-Matute P, Pérez-Echarri N, Martínez JA, et al. Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high-fat-fed rats: role of apoptosis, adiponectin and tumour necrosis factor-alpha. Br J Nutr. 2007;97(2):389-98.
Pérez-Matute, P., Pérez-Echarri, N., Martínez, J. A., Marti, A., & Moreno-Aliaga, M. J. (2007). Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high-fat-fed rats: role of apoptosis, adiponectin and tumour necrosis factor-alpha. The British Journal of Nutrition, 97(2), 389-98.
Pérez-Matute P, et al. Eicosapentaenoic Acid Actions On Adiposity and Insulin Resistance in Control and High-fat-fed Rats: Role of Apoptosis, Adiponectin and Tumour Necrosis Factor-alpha. Br J Nutr. 2007;97(2):389-98. PubMed PMID: 17298710.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high-fat-fed rats: role of apoptosis, adiponectin and tumour necrosis factor-alpha. AU - Pérez-Matute,Patricia, AU - Pérez-Echarri,Nerea, AU - Martínez,J Alfredo, AU - Marti,Amelia, AU - Moreno-Aliaga,María J, PY - 2007/2/15/pubmed PY - 2007/6/20/medline PY - 2007/2/15/entrez SP - 389 EP - 98 JF - The British journal of nutrition JO - Br. J. Nutr. VL - 97 IS - 2 N2 - n-3 PUFA have shown potential anti-obesity and insulin-sensitising properties. However, the mechanisms involved are not clearly established. The aim of the present study was to assess the effects of EPA administration, one of the n-3 PUFA, on body-weight gain and adiposity in rats fed on a standard or a high-fat (cafeteria) diet. The actions on white adipose tissue lipolysis, apoptosis and on several genes related to obesity and insulin resistance were also studied. Control and cafeteria-induced overweight male Wistar rats were assigned into two subgroups, one of them daily received EPA ethyl ester (1 g/kg) for 5 weeks by oral administration. The high-fat diet induced a very significant increase in both body weight and fat mass. Rats fed with the cafeteria diet and orally treated with EPA showed a marginally lower body-weight gain (P = 0.09), a decrease in food intake (P < 0.01) and an increase in leptin production (P < 0.05). EPA administration reduced retroperitoneal adipose tissue weight (P < 0.05) which could be secondary to the inhibition of the adipogenic transcription factor PPARgamma gene expression (P < 0.001), and also to the increase in apoptosis (P < 0.05) found in rats fed with a control diet. TNFalpha gene expression was significantly increased (P < 0.05) by the cafeteria diet, while EPA treatment was able to prevent (P < 0.01) the rise in this inflammatory cytokine. Adiposity-corrected adiponectin plasma levels were increased by EPA. These actions on both TNFalpha and adiponectin could explain the beneficial effects of EPA on insulin resistance induced by the cafeteria diet. SN - 0007-1145 UR - https://www.unboundmedicine.com/medline/citation/17298710/Eicosapentaenoic_acid_actions_on_adiposity_and_insulin_resistance_in_control_and_high_fat_fed_rats:_role_of_apoptosis_adiponectin_and_tumour_necrosis_factor_alpha_ L2 - https://www.cambridge.org/core/product/identifier/S0007114507207627/type/journal_article DB - PRIME DP - Unbound Medicine ER -