An enriched environment re-establishes metabolic homeostasis by reducing obesity-induced inflammation Article Swipe
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· 2022
· Open Access
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· DOI: https://doi.org/10.1242/dmm.048936
Obesity can lead to chronic inflammation in different tissues, generating insulin and leptin resistance and alterations in glucose and lipid metabolism, favoring the development of degenerative diseases, including type II diabetes. Congruently, the inflammatory signaling inhibition prevents the development of obesity and restores insulin sensitivity. Via the enhancement of central nervous system activity, an enriched environment (EE) has beneficial effects on learning and memory as well as on immune cell functions and inflammation in different disease models. Here, we explored whether an EE can restore energy balance in obese mice that previously presented metabolic alterations. We discovered that an EE improved glucose metabolism, increased insulin signaling in liver, and reduced hepatic steatosis and inflammation, and increased lipolysis and browning in the white adipose tissue of high-fat diet (HFD)-fed mice. Finally, we found reduced inflammatory signaling and increased anorexigenic signaling in the hypothalamus of HFD-fed mice exposed to an EE. These data indicate that an EE is able to restore the metabolic imbalance caused by HFD feeding. Thus, we propose EE as a novel therapeutic approach for treating obesity-related metabolic alterations. This article has an associated First Person interview with the first author of the paper.
Related Topics
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1242/dmm.048936
- OA Status
- gold
- Cited By
- 15
- References
- 104
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4210778133
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4210778133Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1242/dmm.048936Digital Object Identifier
- Title
-
An enriched environment re-establishes metabolic homeostasis by reducing obesity-induced inflammationWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2022Year of publication
- Publication date
-
2022-02-03Full publication date if available
- Authors
-
Sol Díaz de León‐Guerrero, Jonathan Salazar‐León, Karla F. Meza‐Sosa, David Valle‐García, Diana Aguilar‐León, Gustavo Pedraza‐Alva, Leonor Pérez-Martı́nezList of authors in order
- Landing page
-
https://doi.org/10.1242/dmm.048936Publisher landing page
- Open access
-
YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://doi.org/10.1242/dmm.048936Direct OA link when available
- Concepts
-
Endocrinology, Inflammation, Internal medicine, Steatosis, Insulin resistance, Adipose tissue, Lipolysis, Glucose homeostasis, Leptin, White adipose tissue, Biology, Carbohydrate metabolism, Lipid metabolism, Insulin, Obesity, MedicineTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
15Total citation count in OpenAlex
- Citations by year (recent)
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2025: 4, 2024: 4, 2023: 5, 2022: 2Per-year citation counts (last 5 years)
- References (count)
-
104Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.obese | 89 |
| abstract_inverted_index.white | 122 |
| abstract_inverted_index.Person | 187 |
| abstract_inverted_index.author | 192 |
| abstract_inverted_index.caused | 163 |
| abstract_inverted_index.energy | 86 |
| abstract_inverted_index.immune | 69 |
| abstract_inverted_index.leptin | 13 |
| abstract_inverted_index.liver, | 108 |
| abstract_inverted_index.memory | 64 |
| abstract_inverted_index.paper. | 195 |
| abstract_inverted_index.system | 52 |
| abstract_inverted_index.tissue | 124 |
| abstract_inverted_index.HFD-fed | 144 |
| abstract_inverted_index.Obesity | 1 |
| abstract_inverted_index.adipose | 123 |
| abstract_inverted_index.article | 182 |
| abstract_inverted_index.balance | 87 |
| abstract_inverted_index.central | 50 |
| abstract_inverted_index.chronic | 5 |
| abstract_inverted_index.disease | 76 |
| abstract_inverted_index.effects | 60 |
| abstract_inverted_index.exposed | 146 |
| abstract_inverted_index.glucose | 18, 102 |
| abstract_inverted_index.hepatic | 111 |
| abstract_inverted_index.insulin | 11, 44, 105 |
| abstract_inverted_index.models. | 77 |
| abstract_inverted_index.nervous | 51 |
| abstract_inverted_index.obesity | 41 |
| abstract_inverted_index.propose | 169 |
| abstract_inverted_index.reduced | 110, 133 |
| abstract_inverted_index.restore | 85, 159 |
| abstract_inverted_index.whether | 81 |
| abstract_inverted_index.ABSTRACT | 0 |
| abstract_inverted_index.Finally, | 130 |
| abstract_inverted_index.approach | 175 |
| abstract_inverted_index.browning | 119 |
| abstract_inverted_index.enriched | 55 |
| abstract_inverted_index.explored | 80 |
| abstract_inverted_index.favoring | 22 |
| abstract_inverted_index.feeding. | 166 |
| abstract_inverted_index.high-fat | 126 |
| abstract_inverted_index.improved | 101 |
| abstract_inverted_index.indicate | 152 |
| abstract_inverted_index.learning | 62 |
| abstract_inverted_index.prevents | 37 |
| abstract_inverted_index.restores | 43 |
| abstract_inverted_index.tissues, | 9 |
| abstract_inverted_index.treating | 177 |
| abstract_inverted_index.(HFD)-fed | 128 |
| abstract_inverted_index.activity, | 53 |
| abstract_inverted_index.diabetes. | 31 |
| abstract_inverted_index.different | 8, 75 |
| abstract_inverted_index.diseases, | 27 |
| abstract_inverted_index.functions | 71 |
| abstract_inverted_index.imbalance | 162 |
| abstract_inverted_index.including | 28 |
| abstract_inverted_index.increased | 104, 116, 137 |
| abstract_inverted_index.interview | 188 |
| abstract_inverted_index.lipolysis | 117 |
| abstract_inverted_index.metabolic | 94, 161, 179 |
| abstract_inverted_index.presented | 93 |
| abstract_inverted_index.signaling | 35, 106, 135, 139 |
| abstract_inverted_index.steatosis | 112 |
| abstract_inverted_index.associated | 185 |
| abstract_inverted_index.beneficial | 59 |
| abstract_inverted_index.discovered | 97 |
| abstract_inverted_index.generating | 10 |
| abstract_inverted_index.inhibition | 36 |
| abstract_inverted_index.previously | 92 |
| abstract_inverted_index.resistance | 14 |
| abstract_inverted_index.alterations | 16 |
| abstract_inverted_index.development | 24, 39 |
| abstract_inverted_index.enhancement | 48 |
| abstract_inverted_index.environment | 56 |
| abstract_inverted_index.metabolism, | 21, 103 |
| abstract_inverted_index.therapeutic | 174 |
| abstract_inverted_index.Congruently, | 32 |
| abstract_inverted_index.alterations. | 95, 180 |
| abstract_inverted_index.anorexigenic | 138 |
| abstract_inverted_index.degenerative | 26 |
| abstract_inverted_index.hypothalamus | 142 |
| abstract_inverted_index.inflammation | 6, 73 |
| abstract_inverted_index.inflammatory | 34, 134 |
| abstract_inverted_index.sensitivity. | 45 |
| abstract_inverted_index.inflammation, | 114 |
| abstract_inverted_index.obesity-related | 178 |
| cited_by_percentile_year.max | 98 |
| cited_by_percentile_year.min | 94 |
| countries_distinct_count | 1 |
| institutions_distinct_count | 7 |
| sustainable_development_goals[0].id | https://metadata.un.org/sdg/3 |
| sustainable_development_goals[0].score | 0.5199999809265137 |
| sustainable_development_goals[0].display_name | Good health and well-being |
| citation_normalized_percentile.value | 0.89074246 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | True |