Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?
The metabolic syndrome (MetS) is manifested by a lipid triad which includes elevated serum triglycerides, small LDL particles, and low high-density lipoprotein (HDL) cholesterol, by central obesity (central adiposity), insulin resistance, glucose intolerance and elevated blood pressure, and it is as...
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| Format: | Online |
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Termedia Publishing House
2011
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/ |
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pubmed-32586892012-01-30 Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet? Seneff, Stephanie Wainwright, Glyn Mascitelli, Luca Review Paper The metabolic syndrome (MetS) is manifested by a lipid triad which includes elevated serum triglycerides, small LDL particles, and low high-density lipoprotein (HDL) cholesterol, by central obesity (central adiposity), insulin resistance, glucose intolerance and elevated blood pressure, and it is associated with an increased risk of type 2 diabetes and coronary heart disease. We have developed a new hypothesis regarding MetS as a consequence of a high intake in carbohydrates and food with a high glycemic index, particularly fructose, and relatively low intake of cholesterol and saturated fat. We support our arguments through animal studies which have shown that exposure of the liver to increased quantities of fructose leads to rapid stimulation of lipogenesis and accumulation of triglycerides. The adipocytes store triglycerides in lipid droplets, leading to adipocyte hypertrophy. Adipocyte hypertrophy is associated with macrophage accumulation in adipose tissue. An important modulator of obesity-associated macrophage responses in white adipose tissue is the death of adipocytes. Excess exposure to fructose intake determines the liver to metabolize high doses of fructose, producing increased levels of fructose end products, like glyceraldehyde and dihydroxyacetone phosphate, that can converge with the glycolytic pathway. Fructose also leads to increased levels of advanced glycation end products. The macrophages exposed to advanced glycation end products become dysfunctional and, on entry into the artery wall, contribute to plaque formation and thrombosis. Termedia Publishing House 2011-02 2011-03-08 /pmc/articles/PMC3258689/ /pubmed/22291727 http://dx.doi.org/10.5114/aoms.2011.20598 Text en Copyright © 2011 Termedia & Banach http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Seneff, Stephanie Wainwright, Glyn Mascitelli, Luca |
| spellingShingle |
Seneff, Stephanie Wainwright, Glyn Mascitelli, Luca Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet? |
| author_facet |
Seneff, Stephanie Wainwright, Glyn Mascitelli, Luca |
| author_sort |
Seneff, Stephanie |
| title |
Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet? |
| title_short |
Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet? |
| title_full |
Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet? |
| title_fullStr |
Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet? |
| title_full_unstemmed |
Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet? |
| title_sort |
is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet? |
| description |
The metabolic syndrome (MetS) is manifested by a lipid triad which includes elevated serum triglycerides, small LDL particles, and low high-density lipoprotein (HDL) cholesterol, by central obesity (central adiposity), insulin resistance, glucose intolerance and elevated blood pressure, and it is associated with an increased risk of type 2 diabetes and coronary heart disease. We have developed a new hypothesis regarding MetS as a consequence of a high intake in carbohydrates and food with a high glycemic index, particularly fructose, and relatively low intake of cholesterol and saturated fat. We support our arguments through animal studies which have shown that exposure of the liver to increased quantities of fructose leads to rapid stimulation of lipogenesis and accumulation of triglycerides. The adipocytes store triglycerides in lipid droplets, leading to adipocyte hypertrophy. Adipocyte hypertrophy is associated with macrophage accumulation in adipose tissue. An important modulator of obesity-associated macrophage responses in white adipose tissue is the death of adipocytes. Excess exposure to fructose intake determines the liver to metabolize high doses of fructose, producing increased levels of fructose end products, like glyceraldehyde and dihydroxyacetone phosphate, that can converge with the glycolytic pathway. Fructose also leads to increased levels of advanced glycation end products. The macrophages exposed to advanced glycation end products become dysfunctional and, on entry into the artery wall, contribute to plaque formation and thrombosis. |
| publisher |
Termedia Publishing House |
| publishDate |
2011 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/ |
| _version_ |
1611500031453429760 |