The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
n-3 Fatty Acids Preserve Insulin Sensitivity In Vivo in a Peroxisome Proliferator–Activated Receptor-α–Dependent Manner
Open accessAbstract
Recent studies have suggested that n-3 fatty acids, abundant in fish oil, protect against high-fat diet–induced insulin resistance through peroxisome proliferator–activated receptor (PPAR)-α activation and a subsequent decrease in intracellular lipid abundance. To directly test this hypothesis, we fed PPAR-α null and wild-type mice for 2 weeks with isocaloric high-fat diets containing 27% fat from either safflower oil or safflower oil with an 8% fish oil replacement (fish oil diet). In both genotypes the safflower oil diet blunted insulin-mediated suppression of hepatic glucose production (P < 0.02 vs. genotype control) and PEPCK gene expression. Feeding wild-type mice a fish oil diet restored hepatic insulin sensitivity (hepatic glucose production [HGP], P < 0.002 vs. wild-type mice fed safflower oil), whereas in contrast, in PPAR-α null mice failed to counteract hepatic insulin resistance (HGP, P = NS vs. PPAR-α null safflower oil–fed mice). In PPAR-α null mice fed the fish oil diet, safflower oil plus fish oil, hepatic insulin resistance was dissociated from increases in hepatic triacylglycerol and acyl-CoA but accompanied by a more than threefold increase in hepatic diacylglycerol concentration (P < 0.0001 vs. genotype control). These data support the hypothesis that n-3 fatty acids protect from high-fat diet–induced hepatic insulin resistance in a PPAR-α–and diacylglycerol-dependent manner.
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Citations
Cites
Cellular mechanisms of insulin resistance
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Self-citationThe adipocyte-secreted protein Acrp30 enhances hepatic insulin action
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Impaired Mitochondrial Activity in the Insulin-Resistant Offspring of Patients with Type 2 Diabetes
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Self-citationMechanism of hepatic insulin resistance in non-alcoholic fatty liver disease
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Self-citationSkeletal muscle triglyceride levels are inversely related to insulin action
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Cited by
Macrophages, inflammation, and insulin resistance
Olefsky, J. M., & Glass, C. K. (2010) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021909-135846 · Cited by 2,733
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“After 15 weeks on HFD, WT and GPR120 KO mice were switched to an isocaloric HFD-containing 27% menhaden fish oil replacement (wt/wt; menhaden fish oil: 16% EPA (C20:5n3), 9%, DHA (C22:6n3), Research Diet) (Jucker et al., 1999; Neschen et al., 2007) and fed for 5 weeks.”
Lipid-induced insulin resistance: unravelling the mechanism
Samuel, V. T., Petersen, K. F., & Shulman, G. I. (2010) · The Lancet · doi:10.1016/s0140-6736(10)60408-4 · Cited by 1,189
Self-citationGrygiel-Górniak, B. (2014) · Nutrition Journal · doi:10.1186/1475-2891-13-17 · Cited by 1,079
A Gpr120-selective agonist improves insulin resistance and chronic inflammation in obese mice
Oh, D. Y., Walenta, E., Akiyama, T. E., Lagakos, W. S., Lackey, D., Pessentheiner, A. R., Sasik, R., Hah, N., Chi, T. J., Cox, J. M., et al. (2014) · Nature Medicine · doi:10.1038/nm.3614 · Cited by 391
Metadata
- Authors
- Neschen, S., Morino, K., Dong, J., Wang-Fischer, Y., Cline, G. W., Romanelli, A. J., Rossbacher, J. C., Moore, I. K., Regittnig, W., Munoz, D. S., Kim, J. H., & Shulman, G. I.
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2007-04-01
- Volume
- 56
- Issue
- 4
- Pages
- 1034-1041
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2113717007
- Cited by
- 233
- References
- 16
- FWCI
- 11.83
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Neschen, S., Morino, K., Dong, J., Wang-Fischer, Y., Cline, G. W., Romanelli, A. J., Rossbacher, J. C., Moore, I. K., Regittnig, W., Munoz, D. S., Kim, J. H., & Shulman, G. I. (2007). n-3 Fatty Acids Preserve Insulin Sensitivity In Vivo in a Peroxisome Proliferator–Activated Receptor-α–Dependent Manner. Diabetes. https://doi.org/10.2337/db06-1206
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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