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Diet-Induced Metabolic Dysfunction of Hypothalamic Nutrient Sensing in Rodents
A sedentary lifestyle and excessive nutrient intake resulting from the consumption of high-fat and calorie-rich diets are environmental factors contributing to the rapid growth of the current pandemic of type 2 diabetes mellitus (DM2). Fasting hyperglycemia, an established hallmark of DM2, is caused...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8999257/ https://www.ncbi.nlm.nih.gov/pubmed/35409318 http://dx.doi.org/10.3390/ijms23073958 |
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author | Arrieta-Cruz, Isabel Torres-Ávila, Blanca Samara Martínez-Coria, Hilda López-Valdés, Héctor Eduardo Gutiérrez-Juárez, Roger |
author_facet | Arrieta-Cruz, Isabel Torres-Ávila, Blanca Samara Martínez-Coria, Hilda López-Valdés, Héctor Eduardo Gutiérrez-Juárez, Roger |
author_sort | Arrieta-Cruz, Isabel |
collection | PubMed |
description | A sedentary lifestyle and excessive nutrient intake resulting from the consumption of high-fat and calorie-rich diets are environmental factors contributing to the rapid growth of the current pandemic of type 2 diabetes mellitus (DM2). Fasting hyperglycemia, an established hallmark of DM2, is caused by excessive production of glucose by the liver, resulting in the inability of insulin to suppress endogenous glucose production. To prevent inappropriate elevations of circulating glucose resulting from changes in nutrient availability, mammals rely on complex mechanisms for continuously detecting these changes and to respond to them with metabolic adaptations designed to modulate glucose output. The mediobasal hypothalamus (MBH) is the key center where nutritional cues are detected and appropriate modulatory responses are integrated. However, certain environmental factors may have a negative impact on these adaptive responses. For example, consumption of a diet enriched in saturated fat in rodents resulted in the development of a metabolic defect that attenuated these nutrient sensing mechanisms, rendering the animals prone to developing hyperglycemia. Thus, high-fat feeding leads to a state of “metabolic disability” in which animals’ glucoregulatory responses fail. We postulate that the chronic faltering of the hypothalamic glucoregulatory mechanisms contributes to the development of metabolic disease. |
format | Online Article Text |
id | pubmed-8999257 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-89992572022-04-12 Diet-Induced Metabolic Dysfunction of Hypothalamic Nutrient Sensing in Rodents Arrieta-Cruz, Isabel Torres-Ávila, Blanca Samara Martínez-Coria, Hilda López-Valdés, Héctor Eduardo Gutiérrez-Juárez, Roger Int J Mol Sci Review A sedentary lifestyle and excessive nutrient intake resulting from the consumption of high-fat and calorie-rich diets are environmental factors contributing to the rapid growth of the current pandemic of type 2 diabetes mellitus (DM2). Fasting hyperglycemia, an established hallmark of DM2, is caused by excessive production of glucose by the liver, resulting in the inability of insulin to suppress endogenous glucose production. To prevent inappropriate elevations of circulating glucose resulting from changes in nutrient availability, mammals rely on complex mechanisms for continuously detecting these changes and to respond to them with metabolic adaptations designed to modulate glucose output. The mediobasal hypothalamus (MBH) is the key center where nutritional cues are detected and appropriate modulatory responses are integrated. However, certain environmental factors may have a negative impact on these adaptive responses. For example, consumption of a diet enriched in saturated fat in rodents resulted in the development of a metabolic defect that attenuated these nutrient sensing mechanisms, rendering the animals prone to developing hyperglycemia. Thus, high-fat feeding leads to a state of “metabolic disability” in which animals’ glucoregulatory responses fail. We postulate that the chronic faltering of the hypothalamic glucoregulatory mechanisms contributes to the development of metabolic disease. MDPI 2022-04-02 /pmc/articles/PMC8999257/ /pubmed/35409318 http://dx.doi.org/10.3390/ijms23073958 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Arrieta-Cruz, Isabel Torres-Ávila, Blanca Samara Martínez-Coria, Hilda López-Valdés, Héctor Eduardo Gutiérrez-Juárez, Roger Diet-Induced Metabolic Dysfunction of Hypothalamic Nutrient Sensing in Rodents |
title | Diet-Induced Metabolic Dysfunction of Hypothalamic Nutrient Sensing in Rodents |
title_full | Diet-Induced Metabolic Dysfunction of Hypothalamic Nutrient Sensing in Rodents |
title_fullStr | Diet-Induced Metabolic Dysfunction of Hypothalamic Nutrient Sensing in Rodents |
title_full_unstemmed | Diet-Induced Metabolic Dysfunction of Hypothalamic Nutrient Sensing in Rodents |
title_short | Diet-Induced Metabolic Dysfunction of Hypothalamic Nutrient Sensing in Rodents |
title_sort | diet-induced metabolic dysfunction of hypothalamic nutrient sensing in rodents |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8999257/ https://www.ncbi.nlm.nih.gov/pubmed/35409318 http://dx.doi.org/10.3390/ijms23073958 |
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