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Seafood intake and the development of obesity, insulin resistance and type 2 diabetes
We provide an overview of studies on seafood intake in relation to obesity, insulin resistance and type 2 diabetes. Overweight and obesity development is for most individuals the result of years of positive energy balance. Evidence from intervention trials and animal studies suggests that frequent i...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cambridge University Press
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6536831/ https://www.ncbi.nlm.nih.gov/pubmed/30728086 http://dx.doi.org/10.1017/S0954422418000240 |
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author | Liaset, Bjørn Øyen, Jannike Jacques, Hélène Kristiansen, Karsten Madsen, Lise |
author_facet | Liaset, Bjørn Øyen, Jannike Jacques, Hélène Kristiansen, Karsten Madsen, Lise |
author_sort | Liaset, Bjørn |
collection | PubMed |
description | We provide an overview of studies on seafood intake in relation to obesity, insulin resistance and type 2 diabetes. Overweight and obesity development is for most individuals the result of years of positive energy balance. Evidence from intervention trials and animal studies suggests that frequent intake of lean seafood, as compared with intake of terrestrial meats, reduces energy intake by 4–9 %, sufficient to prevent a positive energy balance and obesity. At equal energy intake, lean seafood reduces fasting and postprandial risk markers of insulin resistance, and improves insulin sensitivity in insulin-resistant adults. Energy restriction combined with intake of lean and fatty seafood seems to increase weight loss. Marine n-3 PUFA are probably of importance through n-3 PUFA-derived lipid mediators such as endocannabinoids and oxylipins, but other constituents of seafood such as the fish protein per se, trace elements or vitamins also seem to play a largely neglected role. A high intake of fatty seafood increases circulating levels of the insulin-sensitising hormone adiponectin. As compared with a high meat intake, high intake of seafood has been reported to reduce plasma levels of the hepatic acute-phase protein C-reactive protein level in some, but not all studies. More studies are needed to confirm the dietary effects on energy intake, obesity and insulin resistance. Future studies should be designed to elucidate the potential contribution of trace elements, vitamins and undesirables present in seafood, and we argue that stratification into responders and non-responders in randomised controlled trials may improve the understanding of health effects from intake of seafood. |
format | Online Article Text |
id | pubmed-6536831 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Cambridge University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-65368312019-06-10 Seafood intake and the development of obesity, insulin resistance and type 2 diabetes Liaset, Bjørn Øyen, Jannike Jacques, Hélène Kristiansen, Karsten Madsen, Lise Nutr Res Rev Review Article We provide an overview of studies on seafood intake in relation to obesity, insulin resistance and type 2 diabetes. Overweight and obesity development is for most individuals the result of years of positive energy balance. Evidence from intervention trials and animal studies suggests that frequent intake of lean seafood, as compared with intake of terrestrial meats, reduces energy intake by 4–9 %, sufficient to prevent a positive energy balance and obesity. At equal energy intake, lean seafood reduces fasting and postprandial risk markers of insulin resistance, and improves insulin sensitivity in insulin-resistant adults. Energy restriction combined with intake of lean and fatty seafood seems to increase weight loss. Marine n-3 PUFA are probably of importance through n-3 PUFA-derived lipid mediators such as endocannabinoids and oxylipins, but other constituents of seafood such as the fish protein per se, trace elements or vitamins also seem to play a largely neglected role. A high intake of fatty seafood increases circulating levels of the insulin-sensitising hormone adiponectin. As compared with a high meat intake, high intake of seafood has been reported to reduce plasma levels of the hepatic acute-phase protein C-reactive protein level in some, but not all studies. More studies are needed to confirm the dietary effects on energy intake, obesity and insulin resistance. Future studies should be designed to elucidate the potential contribution of trace elements, vitamins and undesirables present in seafood, and we argue that stratification into responders and non-responders in randomised controlled trials may improve the understanding of health effects from intake of seafood. Cambridge University Press 2019-06 /pmc/articles/PMC6536831/ /pubmed/30728086 http://dx.doi.org/10.1017/S0954422418000240 Text en © The Authors 2019 http://creativecommons.org/licenses/by/4.0/ This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Liaset, Bjørn Øyen, Jannike Jacques, Hélène Kristiansen, Karsten Madsen, Lise Seafood intake and the development of obesity, insulin resistance and type 2 diabetes |
title | Seafood intake and the development of obesity, insulin resistance and type 2 diabetes |
title_full | Seafood intake and the development of obesity, insulin resistance and type 2 diabetes |
title_fullStr | Seafood intake and the development of obesity, insulin resistance and type 2 diabetes |
title_full_unstemmed | Seafood intake and the development of obesity, insulin resistance and type 2 diabetes |
title_short | Seafood intake and the development of obesity, insulin resistance and type 2 diabetes |
title_sort | seafood intake and the development of obesity, insulin resistance and type 2 diabetes |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6536831/ https://www.ncbi.nlm.nih.gov/pubmed/30728086 http://dx.doi.org/10.1017/S0954422418000240 |
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