- Title
- Docosahexaenoic acid-rich fish oil supplementation reduces kinase associated with insulin resistance in overweight and obese midlife adults
- Creator
- Thota, Rohith N.; Rosato, Jessica; Burrows, Tracy L.; Dias, Cintia B.; Abbott, Kylie A.; Martins, Ralph N.; Garg, Manohar L.
- Relation
- Nutrients Vol. 12, Issue 6, no. 1612
- Publisher Link
- http://dx.doi.org/10.3390/nu12061612
- Publisher
- MDPI AG
- Resource Type
- journal article
- Date
- 2020
- Description
- Targeting kinases linked to insulin resistance (IR) and inflammation may help in reducing the risk of type 2 diabetes (T2D) and Alzheimer’s disease (AD) in its early stages. This study aimed to determine whether DHA-rich fish oil supplementation reduces glycogen synthase kinase (GSK-3), which is linked to both IR and AD. Baseline and post-intervention plasma samples from 58 adults with abdominal obesity (Age: 51.7 ± 1.7 years, BMI: 31.9 ± 0.8 kg/m2) were analysed for outcome measures. Participants were allocated to 2 g DHA-rich fish oil capsules (860 mg DHA + 120 mg EPA) (n = 31) or placebo capsules (n = 27) per day for 12 weeks. Compared to placebo, DHA-rich fish oil significantly reduced GSK-3β by −2.3 ± 0.3 ng/mL. An inverse correlation (p < 0.05) was found between baseline insulin and IR and their changes following intervention only in participants with C-reactive protein levels higher than 2.4 mg/L. DHA-rich fish oil reduces GSK-3 and IR, suggesting a potential role of long-chain omega-3 polyunsaturated fatty acids (LCn-3PUFA) in ameliorating AD risk.
- Subject
- long-chain omega-3 polyunsaturated fatty acids; docosahexaenoic acid; insulin resistance; obesity; alzheimer's disease; glycogen synthase kinase-3; SDG 3; Sustainable Development Goals
- Identifier
- http://hdl.handle.net/1959.13/1454854
- Identifier
- uon:45006
- Identifier
- ISSN:2072-6643
- Rights
- © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
- Language
- eng
- Full Text
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