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The Role of the Adrenal-Gut-Brain Axis on Comorbid Depressive Disorder Development in Diabetes
Diabetic patients are more affected by depression than non-diabetics, and this is related to greater treatment resistance and associated with poorer outcomes. This increase in the prevalence of depression in diabetics is also related to hyperglycemia and hypercortisolism. In diabetics, the hyperacti...
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Published in: | Biomolecules (Basel, Switzerland) Switzerland), 2023-10, Vol.13 (10), p.1504 |
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description | Diabetic patients are more affected by depression than non-diabetics, and this is related to greater treatment resistance and associated with poorer outcomes. This increase in the prevalence of depression in diabetics is also related to hyperglycemia and hypercortisolism. In diabetics, the hyperactivity of the HPA axis occurs in parallel to gut dysbiosis, weakness of the intestinal permeability barrier, and high bacterial-product translocation into the bloodstream. Diabetes also induces an increase in the permeability of the blood-brain barrier (BBB) and Toll-like receptor 4 (TLR4) expression in the hippocampus. Furthermore, lipopolysaccharide (LPS)-induced depression behaviors and neuroinflammation are exacerbated in diabetic mice. In this context, we propose here that hypercortisolism, in association with gut dysbiosis, leads to an exacerbation of hippocampal neuroinflammation, glutamatergic transmission, and neuronal apoptosis, leading to the development and aggravation of depression and to resistance to treatment of this mood disorder in diabetic patients. |
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This increase in the prevalence of depression in diabetics is also related to hyperglycemia and hypercortisolism. In diabetics, the hyperactivity of the HPA axis occurs in parallel to gut dysbiosis, weakness of the intestinal permeability barrier, and high bacterial-product translocation into the bloodstream. Diabetes also induces an increase in the permeability of the blood-brain barrier (BBB) and Toll-like receptor 4 (TLR4) expression in the hippocampus. Furthermore, lipopolysaccharide (LPS)-induced depression behaviors and neuroinflammation are exacerbated in diabetic mice. In this context, we propose here that hypercortisolism, in association with gut dysbiosis, leads to an exacerbation of hippocampal neuroinflammation, glutamatergic transmission, and neuronal apoptosis, leading to the development and aggravation of depression and to resistance to treatment of this mood disorder in diabetic patients.</description><identifier>ISSN: 2218-273X</identifier><identifier>EISSN: 2218-273X</identifier><identifier>DOI: 10.3390/biom13101504</identifier><identifier>PMID: 37892186</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Adrenal glands ; Animals ; Apoptosis ; Bacteria ; Blood-brain barrier ; Brain-Gut Axis ; Care and treatment ; Chronic illnesses ; Comorbidity ; Complications and side effects ; Cushing Syndrome ; depression ; Depression, Mental ; Depressive Disorder ; Development and progression ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental ; Diabetics ; Digestive system ; Disease ; Dysbacteriosis ; Dysbiosis ; Emotional disorders ; Enzymes ; Expenditures ; Feedback ; Gastrointestinal tract ; glucocorticoids ; Glutamatergic transmission ; gut microbiota ; Hippocampus ; Homeostasis ; Hormones ; Humans ; Hyperactivity ; Hyperglycemia ; Hypothalamic-pituitary-adrenal axis ; Hypothalamo-Hypophyseal System - physiology ; Hypothalamus ; Inflammation ; Lipopolysaccharides ; Membrane permeability ; Mental depression ; Metabolism ; Metabolites ; Mice ; Microbiota ; Mood disorders ; Neuroinflammatory Diseases ; Permeability ; Pituitary gland ; Pituitary-Adrenal System - physiology ; Probiotics ; Proteins ; Psychological aspects ; Review ; Risk factors ; TLR4 ; TLR4 protein ; Toll-like receptors ; Treatment resistance ; treatment-resistant depression</subject><ispartof>Biomolecules (Basel, Switzerland), 2023-10, Vol.13 (10), p.1504</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 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 (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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This increase in the prevalence of depression in diabetics is also related to hyperglycemia and hypercortisolism. In diabetics, the hyperactivity of the HPA axis occurs in parallel to gut dysbiosis, weakness of the intestinal permeability barrier, and high bacterial-product translocation into the bloodstream. Diabetes also induces an increase in the permeability of the blood-brain barrier (BBB) and Toll-like receptor 4 (TLR4) expression in the hippocampus. Furthermore, lipopolysaccharide (LPS)-induced depression behaviors and neuroinflammation are exacerbated in diabetic mice. In this context, we propose here that hypercortisolism, in association with gut dysbiosis, leads to an exacerbation of hippocampal neuroinflammation, glutamatergic transmission, and neuronal apoptosis, leading to the development and aggravation of depression and to resistance to treatment of this mood disorder in diabetic patients.</description><subject>Adrenal glands</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Bacteria</subject><subject>Blood-brain barrier</subject><subject>Brain-Gut Axis</subject><subject>Care and treatment</subject><subject>Chronic illnesses</subject><subject>Comorbidity</subject><subject>Complications and side effects</subject><subject>Cushing Syndrome</subject><subject>depression</subject><subject>Depression, Mental</subject><subject>Depressive Disorder</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental</subject><subject>Diabetics</subject><subject>Digestive system</subject><subject>Disease</subject><subject>Dysbacteriosis</subject><subject>Dysbiosis</subject><subject>Emotional disorders</subject><subject>Enzymes</subject><subject>Expenditures</subject><subject>Feedback</subject><subject>Gastrointestinal tract</subject><subject>glucocorticoids</subject><subject>Glutamatergic transmission</subject><subject>gut microbiota</subject><subject>Hippocampus</subject><subject>Homeostasis</subject><subject>Hormones</subject><subject>Humans</subject><subject>Hyperactivity</subject><subject>Hyperglycemia</subject><subject>Hypothalamic-pituitary-adrenal axis</subject><subject>Hypothalamo-Hypophyseal System - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Biomolecules (Basel, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mázala-de-Oliveira, Thalita</au><au>Silva, Bruna Teixeira</au><au>Campello-Costa, Paula</au><au>Carvalho, Vinicius Frias</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Role of the Adrenal-Gut-Brain Axis on Comorbid Depressive Disorder Development in Diabetes</atitle><jtitle>Biomolecules (Basel, Switzerland)</jtitle><addtitle>Biomolecules</addtitle><date>2023-10-01</date><risdate>2023</risdate><volume>13</volume><issue>10</issue><spage>1504</spage><pages>1504-</pages><issn>2218-273X</issn><eissn>2218-273X</eissn><abstract>Diabetic patients are more affected by depression than non-diabetics, and this is related to greater treatment resistance and associated with poorer outcomes. This increase in the prevalence of depression in diabetics is also related to hyperglycemia and hypercortisolism. In diabetics, the hyperactivity of the HPA axis occurs in parallel to gut dysbiosis, weakness of the intestinal permeability barrier, and high bacterial-product translocation into the bloodstream. Diabetes also induces an increase in the permeability of the blood-brain barrier (BBB) and Toll-like receptor 4 (TLR4) expression in the hippocampus. Furthermore, lipopolysaccharide (LPS)-induced depression behaviors and neuroinflammation are exacerbated in diabetic mice. In this context, we propose here that hypercortisolism, in association with gut dysbiosis, leads to an exacerbation of hippocampal neuroinflammation, glutamatergic transmission, and neuronal apoptosis, leading to the development and aggravation of depression and to resistance to treatment of this mood disorder in diabetic patients.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37892186</pmid><doi>10.3390/biom13101504</doi><oa>free_for_read</oa></addata></record> |
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subjects | Adrenal glands Animals Apoptosis Bacteria Blood-brain barrier Brain-Gut Axis Care and treatment Chronic illnesses Comorbidity Complications and side effects Cushing Syndrome depression Depression, Mental Depressive Disorder Development and progression Diabetes Diabetes mellitus Diabetes Mellitus, Experimental Diabetics Digestive system Disease Dysbacteriosis Dysbiosis Emotional disorders Enzymes Expenditures Feedback Gastrointestinal tract glucocorticoids Glutamatergic transmission gut microbiota Hippocampus Homeostasis Hormones Humans Hyperactivity Hyperglycemia Hypothalamic-pituitary-adrenal axis Hypothalamo-Hypophyseal System - physiology Hypothalamus Inflammation Lipopolysaccharides Membrane permeability Mental depression Metabolism Metabolites Mice Microbiota Mood disorders Neuroinflammatory Diseases Permeability Pituitary gland Pituitary-Adrenal System - physiology Probiotics Proteins Psychological aspects Review Risk factors TLR4 TLR4 protein Toll-like receptors Treatment resistance treatment-resistant depression |
title | The Role of the Adrenal-Gut-Brain Axis on Comorbid Depressive Disorder Development in Diabetes |
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