Evidence map›Paper›PMID 38747226›Full record

ReviewCNS & neurological disorders drug targets2024

Obesity and Depression: Common Link and Possible Targets.

Srikanth Jitte, Saritha Keluth, Priya Bisht, Pranay Wal, Sanjiv Singh, Krishna Murti, Nitesh Kumar

Abstract readReview
PubMed Publisher
In one paragraph

Review in CNS & neurological disorders drug targets, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Srikanth JitteDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Hajipur, Vaishali 844102, Bihar, India.
Saritha KeluthDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Hajipur, Vaishali 844102, Bihar, India.
Priya BishtDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Hajipur, Vaishali 844102, Bihar, India.
Pranay WalPSIT- Pranveer Singh Institute of Technology, Pharmacy, Kanpur 209305, Uttar Pradesh, India.
Sanjiv SinghDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Hajipur, Vaishali 844102, Bihar, India.
Krishna MurtiDepartment of Pharmacy Practice, National Institute of Pharmaceutical Education and Research, Hajipur, Vaishali 844102, Bihar, India.
Nitesh KumarDepartment of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Hajipur, Vaishali 844102, Bihar, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Depression is among the main causes of disability, and its protracted manifestations could make it even harder to treat metabolic diseases. Obesity is linked to episodes of depression, which is closely correlated to abdominal adiposity and impaired food quality. The present review is aimed at studying possible links between obesity and depression along with targets to disrupt it. Research output in Pubmed and Scopus were referred for writing this manuscript. Obesity and depression are related, with the greater propensity of depressed people to gain weight, resulting in poor dietary decisions and a sedentary lifestyle. Adipokines, which include adiponectin, resistin, and leptin are secretory products of the adipose tissue. These adipokines are now being studied to learn more about the connection underlying obesity and depression. Ghrelin, a gut hormone, controls both obesity and depression. Additionally, elevated ghrelin levels result in anxiolytic and antidepressant-like effects. The gut microbiota influences the metabolic functionalities of a person, like caloric processing from indigestible nutritional compounds and storage in fatty tissue, that exposes an individual to obesity, and gut microorganisms might connect to the CNS through interconnecting pathways, including neurological, endocrine, and immunological signalling systems. The alteration of brain activity caused by gut bacteria has been related to depressive episodes. Monoamines, including dopamine, serotonin, and norepinephrine, have been widely believed to have a function in emotions and appetite control. Emotional signals stimulate arcuate neurons in the hypothalamus that are directly implicated in mood regulation and eating. The peptide hormone GLP-1(glucagon-like peptide- 1) seems to have a beneficial role as a medical regulator of defective neuroinflammation, neurogenesis, synaptic dysfunction, and neurotransmitter secretion discrepancy in the depressive brain. The gut microbiota might have its action in mood and cognition regulation, in addition to its traditional involvement in GI function regulation. This review addressed the concept that obesity-related low-grade mild inflammation in the brain contributes to chronic depression and cognitive impairments.

Indexed as

DepressionGastrointestinal MicrobiomeObesityAdipokinesAnimalsBrainBrain-Gut AxisGhrelinHumansAdipokinesGhrelinadipose tissuedepressionendocannabinoid systemglucagon-like peptide-1.gut microbiomeObesity

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.