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Fatty Liver and Fatty Heart—Where do They Stand in the AMIS Syndrome?
Meal-induced insulin sensitization (MIS) refers to the augmented glucose uptake response to insulin following a meal. Absence of MIS (AMIS) causes significant decrease in post-meal glucose disposal leading to postprandial hyperglycemia, hyperinsulinemia, hyperlipidemia, adiposity, increased free rad...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4939563/ https://www.ncbi.nlm.nih.gov/pubmed/27417789 http://dx.doi.org/10.3390/healthcare3030666 |
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author | Lautt, W. Wayne Ming, Zhi Legare, Dallas J. Chowdhury, Kawshik K. Hatch, Grant M. Wang, Hui Helen |
author_facet | Lautt, W. Wayne Ming, Zhi Legare, Dallas J. Chowdhury, Kawshik K. Hatch, Grant M. Wang, Hui Helen |
author_sort | Lautt, W. Wayne |
collection | PubMed |
description | Meal-induced insulin sensitization (MIS) refers to the augmented glucose uptake response to insulin following a meal. Absence of MIS (AMIS) causes significant decrease in post-meal glucose disposal leading to postprandial hyperglycemia, hyperinsulinemia, hyperlipidemia, adiposity, increased free radical stress, and a cluster of progressive metabolic, vascular, and cardiac dysfunctions referred to as the AMIS syndrome. We tested the hypothesis that fat accumulation in the liver and heart is part of the AMIS syndrome. Questions examined in the study: (1) Is prediabetic fat accumulation in the heart and liver a component of the AMIS syndrome? (2) Is fatty liver a cause or consequence of peripheral insulin resistance? (3) Is early cardiac dysfunction in the AMIS syndrome attributable to fat accumulation in the heart? and (4) Can the synergistic antioxidant cocktail SAMEC (S-adenosylmethionine, vitamin E, and vitamin C), known to benefit MIS, affect cardiac and hepatic triglyceride levels? Four animal models of AMIS were used in aged male Sprague-Dawley rats (52 weeks ± sucrose ± SAMEC), compared with young controls (nine weeks). Fat accumulation in the heart was not significant and therefore cannot account for the early cardiac dysfunction. Hepatic triglycerides increased only in the most severe AMIS model but the small changes correlated with the much more rapidly developing peripheral adiposity. Systemic adiposity represents an early stage, whereas accumulation of cardiac and hepatic triglycerides represents a late stage of the prediabetic AMIS syndrome. Fat accumulation in the liver is a consequence, not a cause, of AMIS. SAMEC protected against the sucrose effects on whole body adiposity and hepatic lipid accumulation. |
format | Online Article Text |
id | pubmed-4939563 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-49395632016-07-12 Fatty Liver and Fatty Heart—Where do They Stand in the AMIS Syndrome? Lautt, W. Wayne Ming, Zhi Legare, Dallas J. Chowdhury, Kawshik K. Hatch, Grant M. Wang, Hui Helen Healthcare (Basel) Article Meal-induced insulin sensitization (MIS) refers to the augmented glucose uptake response to insulin following a meal. Absence of MIS (AMIS) causes significant decrease in post-meal glucose disposal leading to postprandial hyperglycemia, hyperinsulinemia, hyperlipidemia, adiposity, increased free radical stress, and a cluster of progressive metabolic, vascular, and cardiac dysfunctions referred to as the AMIS syndrome. We tested the hypothesis that fat accumulation in the liver and heart is part of the AMIS syndrome. Questions examined in the study: (1) Is prediabetic fat accumulation in the heart and liver a component of the AMIS syndrome? (2) Is fatty liver a cause or consequence of peripheral insulin resistance? (3) Is early cardiac dysfunction in the AMIS syndrome attributable to fat accumulation in the heart? and (4) Can the synergistic antioxidant cocktail SAMEC (S-adenosylmethionine, vitamin E, and vitamin C), known to benefit MIS, affect cardiac and hepatic triglyceride levels? Four animal models of AMIS were used in aged male Sprague-Dawley rats (52 weeks ± sucrose ± SAMEC), compared with young controls (nine weeks). Fat accumulation in the heart was not significant and therefore cannot account for the early cardiac dysfunction. Hepatic triglycerides increased only in the most severe AMIS model but the small changes correlated with the much more rapidly developing peripheral adiposity. Systemic adiposity represents an early stage, whereas accumulation of cardiac and hepatic triglycerides represents a late stage of the prediabetic AMIS syndrome. Fat accumulation in the liver is a consequence, not a cause, of AMIS. SAMEC protected against the sucrose effects on whole body adiposity and hepatic lipid accumulation. MDPI 2015-08-11 /pmc/articles/PMC4939563/ /pubmed/27417789 http://dx.doi.org/10.3390/healthcare3030666 Text en © 2015 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 license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Lautt, W. Wayne Ming, Zhi Legare, Dallas J. Chowdhury, Kawshik K. Hatch, Grant M. Wang, Hui Helen Fatty Liver and Fatty Heart—Where do They Stand in the AMIS Syndrome? |
title | Fatty Liver and Fatty Heart—Where do They Stand in the AMIS Syndrome? |
title_full | Fatty Liver and Fatty Heart—Where do They Stand in the AMIS Syndrome? |
title_fullStr | Fatty Liver and Fatty Heart—Where do They Stand in the AMIS Syndrome? |
title_full_unstemmed | Fatty Liver and Fatty Heart—Where do They Stand in the AMIS Syndrome? |
title_short | Fatty Liver and Fatty Heart—Where do They Stand in the AMIS Syndrome? |
title_sort | fatty liver and fatty heart—where do they stand in the amis syndrome? |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4939563/ https://www.ncbi.nlm.nih.gov/pubmed/27417789 http://dx.doi.org/10.3390/healthcare3030666 |
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