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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...

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Autores principales: Arrieta-Cruz, Isabel, Torres-Ávila, Blanca Samara, Martínez-Coria, Hilda, López-Valdés, Héctor Eduardo, Gutiérrez-Juárez, Roger
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
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.
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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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