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Neuropeptides in Endocrine, Metabolic and Neuroimmune Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 3942

Special Issue Editor

Special Issue Information

Dear Colleague,

Neuropeptides are short-chain amino acids produced by neurons and the most abundant chemical messengers in the brain. These small molecules are biologically active at very low concentration and exert a broad range of effects in the central nervous system, including regulatory functions in the endocrine and immune system.

Studies to date suggest that dysregulated activities of neuropeptide-expressing neurons or altered levels of neuropeptides in the brain contribute to the onset and/or development of neuroendocrine, metabolic or neuroimmune disorders. However, in many cases, a causal relationship has not been clearly identified. In contrast, a number of studies have determined that certain dietary, lifestyle, environmental, and genetic factors that trigger the above disorders also impact different neuropeptide systems.

Therefore, the purpose of this Special Issue is to shed more light into our understanding of how currently known neuropeptide systems contribute to the onset of and/or are dysregulated by pathological conditions of the endocrine and immune system. Original contributions and review articles addressing the role of neuropeptides in the onset and pathogenesis of auto-immune conditions affecting the CNS or involving HPA axis dysfunctions will also be considered

Dr. Alessandro Castorina
Guest Editor

Manuscript Submission Information

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Keywords

  • neuropeptide
  • autoimmune disease
  • metabolic syndrome
  • stress
  • multiple sclerosis
  • diabetes
  • metabolic syndrome
  • prolactinoma
  • Cushing’s disease
  • acromegaly

Published Papers (1 paper)

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Research

30 pages, 36061 KiB  
Article
Metformin Treatment Attenuates Brain Inflammation and Rescues PACAP/VIP Neuropeptide Alterations in Mice Fed a High-Fat Diet
by Mawj Mandwie, Jocelyn Karunia, Aram Niaz, Kevin A. Keay, Giuseppe Musumeci, Claire Rennie, Kristine McGrath, Ghaith Al-Badri and Alessandro Castorina
Int. J. Mol. Sci. 2021, 22(24), 13660; https://doi.org/10.3390/ijms222413660 - 20 Dec 2021
Cited by 13 | Viewed by 3367
Abstract
High-fat diet (HFD)-induced comorbid cognitive and behavioural impairments are thought to be the result of persistent low-grade neuroinflammation. Metformin, a first-line medication for the treatment of type-2 diabetes, seems to ameliorate these comorbidities, but the underlying mechanism(s) are not clear. Pituitary adenylate cyclase-activating [...] Read more.
High-fat diet (HFD)-induced comorbid cognitive and behavioural impairments are thought to be the result of persistent low-grade neuroinflammation. Metformin, a first-line medication for the treatment of type-2 diabetes, seems to ameliorate these comorbidities, but the underlying mechanism(s) are not clear. Pituitary adenylate cyclase-activating peptide (PACAP) and vasoactive intestinal peptide (VIP) are neuroprotective peptides endowed with anti-inflammatory properties. Alterations to the PACAP/VIP system could be pivotal during the development of HFD-induced neuroinflammation. To unveil the pathogenic mechanisms underlying HFD-induced neuroinflammation and assess metformin’s therapeutic activities, (1) we determined if HFD-induced proinflammatory activity was present in vulnerable brain regions associated with the development of comorbid behaviors, (2) investigated if the PACAP/VIP system is altered by HFD, and (3) assessed if metformin rescues such diet-induced neurochemical alterations. C57BL/6J male mice were divided into two groups to receive either standard chow (SC) or HFD for 16 weeks. A further HFD group received metformin (HFD + M) (300 mg/kg BW daily for 5 weeks) via oral gavage. Body weight, fasting glucose, and insulin levels were measured. After 16 weeks, the proinflammatory profile, glial activation markers, and changes within the PI3K/AKT intracellular pathway and the PACAP/VIP system were evaluated by real-time qPCR and/or Western blot in the hypothalamus, hippocampus, prefrontal cortex, and amygdala. Our data showed that HFD causes widespread low-grade neuroinflammation and gliosis, with regional-specific differences across brain regions. HFD also diminished phospho-AKT(Ser473) expression and caused significant disruptions to the PACAP/VIP system. Treatment with metformin attenuated these neuroinflammatory signatures and reversed PI3K/AKT and PACAP/VIP alterations caused by HFD. Altogether, our findings demonstrate that metformin treatment rescues HFD-induced neuroinflammation in vulnerable brain regions, most likely by a mechanism involving the reinstatement of PACAP/VIP system homeostasis. Data also suggests that the PI3K/AKT pathway, at least in part, mediates some of metformin’s beneficial effects. Full article
(This article belongs to the Special Issue Neuropeptides in Endocrine, Metabolic and Neuroimmune Disorders)
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