The DOI matches its Crossref record; 248 of the 249 references it cites were found in a registry or an index.
Unraveling the Mechanisms Responsible for the Comorbidity between Metabolic Syndrome and Mental Health Disorders
Open accessAbstract
The increased prevalence and high comorbidity of metabolic syndrome (MetS) and mental health disorders (MHDs) have prompted investigation into the potential contributing mechanisms. There is a bidirectional association between MetS and MHDs including schizophrenia, bipolar disorder, depression, anxiety, attention-deficit/hyperactivity disorder, and autism spectrum disorders. Medication side effects and social repercussions are contributing environmental factors, but there are a number of shared underlying neurological and physiological mechanisms that explain the high comorbidity between these two disorders. Inflammation is a state shared by both disorders, and it contributes to disruptions of neuroregulatory systems (including the serotonergic, dopaminergic, and neuropeptide Y systems) as well as dysregulation of the hypothalamic-pituitary-adrenal axis. MetS in pregnant women also exposes the developing fetal brain to inflammatory factors that predispose the offspring to MetS and psychopathologies. Due to the shared nature of these conditions, treatment should address aspects of both mental health and metabolic disorders. Additionally, interventions that can interrupt the transfer of increased risk of the disorders to the next generation need to be developed.
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“Maternal metabolic disorders including diabetes and obesity can pose another threat to the unborn child as placental dysfunctioning alters the prenatal exposure to nutrients and toxins [312–314].”
From Development of prefrontal cortex (2022) · cites this paper as [313]
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Metadata
- Authors
- Nousen, E. K., Franco, J. G., & Sullivan, E. L.
- Affiliations
- Oregon National Primate Research Center (US)
- Venue
- Neuroendocrinology
- Publisher
- S. Karger AG
- Published
- 2013
- Volume
- 98
- Issue
- 4
- Pages
- 254-266
- ISSN
- 0028-3835 (ISSN-L)
- 1423-0194
- PMC
- PMC4121390
- OpenAlex
- W2040707068
- Cited by
- 123
- References
- 249
- Citations by year
- 2026: 5 · 2025: 15 · 2024: 11 · 2023: 8 · 2022: 14 · 2021: 8 · 2020: 8 · 2019: 9 · 2018: 4 · 2017: 12 · 2016: 14 · 2015: 9 · 2014: 6
- FWCI
- 0.63
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR000128)
- Oregon Clinical and Translational Research Institute
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK079194)
- National Center for Research Resources (P51RR000163)
- National Center for Advancing Translational Sciences
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (L40 HD059242)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- metabolic syndrome, mental illness, comorbidities, inflammation, serotonergic system, dopaminergic system, neuropeptide Y, hypothalamic-pituitary-adrenal axis, maternal metabolic syndrome, fetal brain development, schizophrenia, bipolar disorder, depression, anxiety, attention deficit hyperactivity disorder, autism spectrum disorder, bidirectional relationship
- MeSH terms
- Animals, Mental Disorders, Female, Humans, Metabolic Diseases, Models, Neurological, Pregnancy, Prenatal Exposure Delayed Effects, Comorbidity
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