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A Synergistic, Balanced Antioxidant Cocktail, Protects Aging Rats from Insulin Resistance and Absence of Meal-Induced Insulin Sensitization (AMIS) Syndrome
A series of in vivo and in vitro studies using animal and human models in the past 15 years have demonstrated that approximately 55% (~66% in humans) of the glucose disposal effect of an i.v. injection of insulin in the fed state is dependent on the action of a second hormone, hepatic insulin sensit...
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/PMC6272698/ https://www.ncbi.nlm.nih.gov/pubmed/25569521 http://dx.doi.org/10.3390/molecules20010669 |
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author | Wang, Hui Helen Chowdhury, Kawshik K. Lautt, W. Wayne |
author_facet | Wang, Hui Helen Chowdhury, Kawshik K. Lautt, W. Wayne |
author_sort | Wang, Hui Helen |
collection | PubMed |
description | A series of in vivo and in vitro studies using animal and human models in the past 15 years have demonstrated that approximately 55% (~66% in humans) of the glucose disposal effect of an i.v. injection of insulin in the fed state is dependent on the action of a second hormone, hepatic insulin sensitizing substance (HISS), which is released from the liver and stimulates glucose uptake in muscle, heart and kidneys. Sensitization of the insulin response by a meal through release of HISS is called meal-induced insulin sensitization (MIS). Absence of HISS action results in postprandial hyperglycemia, hyperinsulinemia, hyperlipidemia, adiposity, increased free radical stress and a cluster of progressive metabolic and cardiovascular dysfunctions referred to as the AMIS (absence of meal-induced insulin sensitization) syndrome. Reduced HISS release accounts for the insulin resistance that occurs with aging and is made worse by physical inactivity and diets high in sucrose or fat. This brief review provides an update of major metabolic disturbances associated with aging due to reduction of HISS release, and the protection against these pathological changes in aging animals using a balanced synergistic antioxidant cocktail SAMEC (S-adenosylmethionine, vitamins E and C). The synergy amongst the components is consistent with the known benefits of antioxidants supplied by a mixed diet and acting through diverse mechanisms. Using only three constituents, SAMEC appears suitable as an antioxidant specifically targeting the AMIS syndrome. |
format | Online Article Text |
id | pubmed-6272698 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-62726982018-12-28 A Synergistic, Balanced Antioxidant Cocktail, Protects Aging Rats from Insulin Resistance and Absence of Meal-Induced Insulin Sensitization (AMIS) Syndrome Wang, Hui Helen Chowdhury, Kawshik K. Lautt, W. Wayne Molecules Review A series of in vivo and in vitro studies using animal and human models in the past 15 years have demonstrated that approximately 55% (~66% in humans) of the glucose disposal effect of an i.v. injection of insulin in the fed state is dependent on the action of a second hormone, hepatic insulin sensitizing substance (HISS), which is released from the liver and stimulates glucose uptake in muscle, heart and kidneys. Sensitization of the insulin response by a meal through release of HISS is called meal-induced insulin sensitization (MIS). Absence of HISS action results in postprandial hyperglycemia, hyperinsulinemia, hyperlipidemia, adiposity, increased free radical stress and a cluster of progressive metabolic and cardiovascular dysfunctions referred to as the AMIS (absence of meal-induced insulin sensitization) syndrome. Reduced HISS release accounts for the insulin resistance that occurs with aging and is made worse by physical inactivity and diets high in sucrose or fat. This brief review provides an update of major metabolic disturbances associated with aging due to reduction of HISS release, and the protection against these pathological changes in aging animals using a balanced synergistic antioxidant cocktail SAMEC (S-adenosylmethionine, vitamins E and C). The synergy amongst the components is consistent with the known benefits of antioxidants supplied by a mixed diet and acting through diverse mechanisms. Using only three constituents, SAMEC appears suitable as an antioxidant specifically targeting the AMIS syndrome. MDPI 2015-01-06 /pmc/articles/PMC6272698/ /pubmed/25569521 http://dx.doi.org/10.3390/molecules20010669 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 | Review Wang, Hui Helen Chowdhury, Kawshik K. Lautt, W. Wayne A Synergistic, Balanced Antioxidant Cocktail, Protects Aging Rats from Insulin Resistance and Absence of Meal-Induced Insulin Sensitization (AMIS) Syndrome |
title | A Synergistic, Balanced Antioxidant Cocktail, Protects Aging Rats from Insulin Resistance and Absence of Meal-Induced Insulin Sensitization (AMIS) Syndrome |
title_full | A Synergistic, Balanced Antioxidant Cocktail, Protects Aging Rats from Insulin Resistance and Absence of Meal-Induced Insulin Sensitization (AMIS) Syndrome |
title_fullStr | A Synergistic, Balanced Antioxidant Cocktail, Protects Aging Rats from Insulin Resistance and Absence of Meal-Induced Insulin Sensitization (AMIS) Syndrome |
title_full_unstemmed | A Synergistic, Balanced Antioxidant Cocktail, Protects Aging Rats from Insulin Resistance and Absence of Meal-Induced Insulin Sensitization (AMIS) Syndrome |
title_short | A Synergistic, Balanced Antioxidant Cocktail, Protects Aging Rats from Insulin Resistance and Absence of Meal-Induced Insulin Sensitization (AMIS) Syndrome |
title_sort | synergistic, balanced antioxidant cocktail, protects aging rats from insulin resistance and absence of meal-induced insulin sensitization (amis) syndrome |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6272698/ https://www.ncbi.nlm.nih.gov/pubmed/25569521 http://dx.doi.org/10.3390/molecules20010669 |
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