ArticleDiabetes2013
Fenretinide treatment prevents diet-induced obesity in association with major alterations in retinoid homeostatic gene expression in adipose, liver, and hypothalamus.
Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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
41 citing papers in PubMed, 69 citations in OpenAlex.
- Genetic underpinnings of type-2 diabetes (T2D) with colorectal cancer (CRC): In-silico discovery of common molecular signatures, pathogenetic processes and therapeutic candidates.Journal, genetic engineering & biotechnology · 2026Article
- High-throughput in vitro drug screening and in vivo studies identify fenretinide as a brain-penetrant DMG therapeutic.Neuro-oncology · 2025Article
- Retinoid dynamics in vision: from visual cycle biology to retina disease treatments.Pharmacology & therapeutics · 2025Review
- Hydroxysteroid 17β-dehydrogenase 13 (Hsd17b13) knockdown attenuates liver steatosis in high-fat diet obese mice.Experimental physiology · 2025Article
- A New Strategy for Obesity Treatment: Revealing the Frontiers of Anti-obesity Medications.Current molecular medicine · 2025Review
- Retinoids and retinoid-binding proteins: Unexpected roles in metabolic disease.Current topics in developmental biology · 2025Review
- Immunometabolic effects ofImmunometabolism (Cobham, Surrey) · 2024Review
- Attempts to Improve Lipophilic Drugs' Solubility and Bioavailability: A Focus on Fenretinide.Pharmaceutics · 2024Review
- Control by the brain of vitamin A homeostasis.iScience · 2023Article
- ORMDL in metabolic health and disease.Pharmacology & therapeutics · 2023Review
- Fenretinide inhibits obesity and fatty liver disease but induces Smpd3 to increase serum ceramides and worsen atherosclerosis in LDLRScientific reports · 2023Article
- Retinoic Acid: Sexually Dimorphic, Anti-Insulin and Concentration-Dependent Effects on Energy.Nutrients · 2022Review
- Retinoid Homeostasis and Beyond: How Retinol Binding Protein 4 Contributes to Health and Disease.Nutrients · 2022Review
- Regulatory network and interplay of hepatokines, stellakines, myokines and adipokines in nonalcoholic fatty liver diseases and nonalcoholic steatohepatitis.Frontiers in endocrinology · 2022Review
- The antioxidant tempol transforms gut microbiome to resist obesity in female C3H mice fed a high fat diet.Free radical biology & medicine · 2022Article
- Fenretinide Reduces Intestinal Mucin-2-Positive Goblet Cells in Chronic Alcohol Abuse.Pharmacology · 2022Article
- Dihydroceramide Desaturase Functions as an Inducer and Rectifier of Apoptosis: Effect of Retinol Derivatives, Antioxidants and Phenolic Compounds.Cell biochemistry and biophysics · 2021Article
- Dietary vitamin A supplementation prevents early obesogenic diet-induced microbiota, neuronal and cognitive alterations.International journal of obesity (2005) · 2021Article
- Biological Functions of RBP4 and Its Relevance for Human Diseases.Frontiers in physiology · 2021Review
- Remodeling adipose tissue inflammasome for type 2 diabetes mellitus treatment: Current perspective and translational strategies.Bioengineering & translational medicine · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The synthetic retinoid, Fenretinide (FEN), inhibits obesity and insulin resistance in mice and is in early clinical trials for treatment of insulin resistance in obese humans. We aimed to determine whether alterations in retinoic acid (RA)-responsive genes contribute to the beneficial effects of FEN. We examined the effect of FEN on 3T3-L1 adipocyte differentiation and alterations in gene expression in C57Bl/6 and retinaldehyde dehydrogenase (RALDH) 1 knockout (KO) mice fed a high-fat (HF) diet. FEN completely inhibited adipocyte differentiation by blocking CCAAT/enhancer-binding protein (C/EBP) α/peroxisome proliferator-activated receptor (PPAR) γ-mediated induction of downstream genes and upregulating RA-responsive genes like cellular retinol-binding protein-1. In mice fed an HF diet, RA-responsive genes were markedly increased in adipose, liver, and hypothalamus, with short-term and long-term FEN treatment. In adipose, FEN inhibited the downregulation of PPARγ and improved insulin sensitivity and the levels of adiponectin, resistin, and serum RBP (RBP4). FEN inhibited hyperleptinemia in vivo and leptin expression in adipocytes. Surprisingly, hypothalamic neuropeptide Y expression was completely suppressed, suggesting a central effect of FEN to normalize hyperglycemia. Moreover, FEN induced RA-responsive genes in RALDH1 KO mice, demonstrating that FEN can augment RA signaling when RA synthesis is impaired. We show that FEN-mediated beneficial effects are through alterations in retinoid homeostasis genes, and these are strong candidates as therapeutic targets for the treatment of obesity and insulin resistance.
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.