ReviewEndocrinology2021
Obesity, POMC, and POMC-processing Enzymes: Surprising Results From Animal Models.
Review in Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Classification of Congenital Leptin Deficiency.The Journal of clinical endocrinology and metabolism · 2024Pooled it
- Nutraceuticals as modulators of genetic, epigenetic and hormonal factors in obesity.European journal of clinical nutrition · 2026Review
- Update on Obesity and Its Relationship to Atherosclerotic Cardiovascular Disease and Associated Risk Factors.Journal of clinical medicine · 2026Review
- Genetic variability in the leptin-melanocortin pathway and its role in weight loss.Molecular metabolism · 2026Review
- Article
- Modulating food intake by nasal application of peptides targeting melanocortin 4 receptor and ghrelin receptor systems.Brain communications · 2026Article
- Integrated Genetic and Protein Mechanisms Underlying Glucagon-like Peptide-1 Receptor Agonists in Treating Diabetes Mellitus and Weight Loss.Current issues in molecular biology · 2025Article
- Identification of SEC16B as a novel regulator of glucose homeostasis.Diabetologia · 2025Article
- Navigating the Strengths and Constraints of Mouse Models in Obesity Research.Endocrinology · 2025Review
- Neuroendocrinology and the Genetics of Obesity.Endocrinology · 2025Review
- RAF1 in AgRP neurons involved in the regulation of energy metabolismJournal of biomedical research · 2025Article
- Deep Learning-Based Drug Compounds Discovery for Gynecomastia.Biomedicines · 2025Article
- Article
- Effects of Chitosan andBiomedicines · 2024Article
- Marchf6: A guardian against cytosol-spilled POMC-induced ferroptosis.Molecules and cells · 2024Article
- A comprehensive review of genetic causes of obesity.World journal of pediatrics : WJP · 2024Review
- Review
- The Role of Adipokines in Health and Disease.Biomedicines · 2023Review
- Maternal glucose intolerance during pregnancy affects offspring POMC expression and results in adult metabolic alterations in a sex-dependent manner.Frontiers in endocrinology · 2023Article
- Unraveling the roles of endoplasmic reticulum-associated degradation in metabolic disorders.Frontiers in endocrinology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Peptides derived from proopiomelanocortin (POMC) are well-established neuropeptides and peptide hormones that perform multiple functions, including regulation of body weight. In humans and some animals, these peptides include α- and β-melanocyte-stimulating hormone (MSH). In certain rodent species, no β-MSH is produced from POMC because of a change in the cleavage site. Enzymes that convert POMC into MSH include prohormone convertases (PCs), carboxypeptidases (CPs), and peptidyl-α-amidating monooxygenase (PAM). Humans and mice with inactivating mutations in either PC1/3 or carboxypeptidase E (CPE) are obese, which was assumed to result from defective processing of POMC into MSH. However, recent studies have shown that selective loss of either PC1/3 or CPE in POMC-expressing cells does not cause obesity. These findings suggest that defects in POMC processing cannot alone account for the obesity observed in global PC1/3 or CPE mutants. We propose that obesity in animals lacking PC1/3 or CPE activity depends, at least in part, on deficient processing of peptides in non-POMC-expressing cells either in the brain and/or the periphery. Genetic background may also contribute to the manifestation of obesity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.