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Kale supplementation during high fat feeding improves metabolic health in a mouse model of obesity and insulin resistance
Cruciferous vegetables have been widely studied for cancer prevention and cardiovascular health. Broccoli is the cruciferous vegetable whose phytochemistry and physiological effects have been most extensively studied. Kale (Brassica oleracea var. acephala) appears on lists of ‘healthiest, nutrient d...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8386848/ https://www.ncbi.nlm.nih.gov/pubmed/34432833 http://dx.doi.org/10.1371/journal.pone.0256348 |
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author | Raychaudhuri, Samnhita Fan, Si Kraus, Olivia Shahinozzaman, Md. Obanda, Diana N. |
author_facet | Raychaudhuri, Samnhita Fan, Si Kraus, Olivia Shahinozzaman, Md. Obanda, Diana N. |
author_sort | Raychaudhuri, Samnhita |
collection | PubMed |
description | Cruciferous vegetables have been widely studied for cancer prevention and cardiovascular health. Broccoli is the cruciferous vegetable whose phytochemistry and physiological effects have been most extensively studied. Kale (Brassica oleracea var. acephala) appears on lists of ‘healthiest, nutrient dense foods’ but, there is paucity of data on kale as a functional food. In a 12-week study, we tested the effect of curly green kale on high fat diet (HFD) induced obesity and insulin resistance, lipid metabolism, endotoxemia and inflammation in C57BL/6J mice fed isocaloric diets. Kale supplementation did not attenuate HFD diet induced fat accumulation and insulin resistance (P = ns; n = 9) but, it lowered serum triglycerides, low density lipoprotein (LPL) cholesterol and prevented HFD induced increases in systemic endotoxemia and inflammation (serum LPS and Ccl2) (P<0.01; n = 9). In adipose tissue, kale enhanced the expression of genes involved in adipogenesis (P<0.01; n = 9), reduced the appearance of histologic markers of inflammation, downregulated both the gene expression and protein expression of the adipose tissue specific inflammation markers CD11c and F4/80 (P<0.001; n = 9) and reduced the gene expression of a battery of chemokine C-C motif ligands (Ccl2, Ccl6, Ccl7, Ccl8, Ccl9) and chemokine C-C motif receptors (Ccr2, Ccr3, Ccr5). We conclude that kale vegetable protects against HFD diet induced dysfunction through mechanisms involving lipid metabolism, endotoxemia and inflammation. |
format | Online Article Text |
id | pubmed-8386848 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-83868482021-08-26 Kale supplementation during high fat feeding improves metabolic health in a mouse model of obesity and insulin resistance Raychaudhuri, Samnhita Fan, Si Kraus, Olivia Shahinozzaman, Md. Obanda, Diana N. PLoS One Research Article Cruciferous vegetables have been widely studied for cancer prevention and cardiovascular health. Broccoli is the cruciferous vegetable whose phytochemistry and physiological effects have been most extensively studied. Kale (Brassica oleracea var. acephala) appears on lists of ‘healthiest, nutrient dense foods’ but, there is paucity of data on kale as a functional food. In a 12-week study, we tested the effect of curly green kale on high fat diet (HFD) induced obesity and insulin resistance, lipid metabolism, endotoxemia and inflammation in C57BL/6J mice fed isocaloric diets. Kale supplementation did not attenuate HFD diet induced fat accumulation and insulin resistance (P = ns; n = 9) but, it lowered serum triglycerides, low density lipoprotein (LPL) cholesterol and prevented HFD induced increases in systemic endotoxemia and inflammation (serum LPS and Ccl2) (P<0.01; n = 9). In adipose tissue, kale enhanced the expression of genes involved in adipogenesis (P<0.01; n = 9), reduced the appearance of histologic markers of inflammation, downregulated both the gene expression and protein expression of the adipose tissue specific inflammation markers CD11c and F4/80 (P<0.001; n = 9) and reduced the gene expression of a battery of chemokine C-C motif ligands (Ccl2, Ccl6, Ccl7, Ccl8, Ccl9) and chemokine C-C motif receptors (Ccr2, Ccr3, Ccr5). We conclude that kale vegetable protects against HFD diet induced dysfunction through mechanisms involving lipid metabolism, endotoxemia and inflammation. Public Library of Science 2021-08-25 /pmc/articles/PMC8386848/ /pubmed/34432833 http://dx.doi.org/10.1371/journal.pone.0256348 Text en © 2021 Raychaudhuri et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Raychaudhuri, Samnhita Fan, Si Kraus, Olivia Shahinozzaman, Md. Obanda, Diana N. Kale supplementation during high fat feeding improves metabolic health in a mouse model of obesity and insulin resistance |
title | Kale supplementation during high fat feeding improves metabolic health in a mouse model of obesity and insulin resistance |
title_full | Kale supplementation during high fat feeding improves metabolic health in a mouse model of obesity and insulin resistance |
title_fullStr | Kale supplementation during high fat feeding improves metabolic health in a mouse model of obesity and insulin resistance |
title_full_unstemmed | Kale supplementation during high fat feeding improves metabolic health in a mouse model of obesity and insulin resistance |
title_short | Kale supplementation during high fat feeding improves metabolic health in a mouse model of obesity and insulin resistance |
title_sort | kale supplementation during high fat feeding improves metabolic health in a mouse model of obesity and insulin resistance |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8386848/ https://www.ncbi.nlm.nih.gov/pubmed/34432833 http://dx.doi.org/10.1371/journal.pone.0256348 |
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