ArticleEuropean journal of pharmacology2008
Increased adiposity on normal diet, but decreased susceptibility to diet-induced obesity in mu-opioid receptor-deficient mice.
Article in European journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Endogenous opioid receptors and the feast or famine of maladaptive feeding.Nature communications · 2025Review
- The role of mu-opioid receptors in pancreatic islet α-cells.Journal of molecular endocrinology · 2025Article
- The role of mu-opioid receptors in pancreatic islet alpha cells.bioRxiv : the preprint server for biology · 2024Article
- The Impact of Opioid Receptor Gene Polymorphism on Fentanyl and Alfentanil's Analgesic Effects in the Pediatric Perioperative Period.Pharmacogenomics and personalized medicine · 2024Article
- Central effects of opioidergic system on food intake in birds and mammals: a review.Veterinary research communications · 2023Review
- High-Throughput Screening of Mouse Gene Knockouts Identifies Established and Novel High Body Fat Phenotypes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Persistent effects of obesity: a neuroplasticity hypothesis.Annals of the New York Academy of Sciences · 2018Review
- Absence of Role of Dietary Protein Sensing in the Metabolic Benefits of Duodenal-Jejunal Bypass in the Mouse.Scientific reports · 2017Article
- Cognitive and autonomic determinants of energy homeostasis in obesity.Nature reviews. Endocrinology · 2015Review
- Involvement of Endogenous Enkephalins and β-Endorphin in Feeding and Diet-Induced Obesity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015Article
- Rationale and consequences of reclassifying obesity as an addictive disorder: neurobiology, food environment and social policy perspectives.Physiology & behavior · 2012Review
- Mice lacking δ-opioid receptors resist the development of diet-induced obesity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Current research on opioid receptor function.Current drug targets · 2012Review
- Neuro-Genetics of Reward Deficiency Syndrome (RDS) as the Root Cause of "Addiction Transfer": A New Phenomenon Common after Bariatric Surgery.Journal of genetic syndromes & gene therapy · 2011Article
- The μ-opioid receptor variant N190K is unresponsive to peptide agonists yet can be rescued by small-molecule drugs.Molecular pharmacology · 2010Article
- Reversible suppression of food reward behavior by chronic mu-opioid receptor antagonism in the nucleus accumbens.Neuroscience · 2010Article
- Chronic suppression of μ-opioid receptor signaling in the nucleus accumbens attenuates development of diet-induced obesity in rats.International journal of obesity (2005) · 2010Article
- kappa-Opioid receptors control the metabolic response to a high-energy diet in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Mice lacking the G protein gamma3-subunit show resistance to opioids and diet induced obesity.American journal of physiology. Regulatory, integrative and comparative physiology · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The mu-opioid receptor encoded by the Oprm1 gene plays a crucial role in the mediation of food reward and drug-induced positive reinforcement, but its genetic deletion has been shown to provide food intake-independent, partial protection from diet-induced obesity. We hypothesized that mu-opioid receptor-deficient mice would show an even greater, intake-dependent, resistance to high-fat diet-induced obesity if the diet comprises a sweet component. We generated an F2 population by crossing the heterozygous offspring of homozygous female Oprm1(-/-) mice (on a mixed C57BL/6 and BALB/c genetic background) with male inbred C57BL/6 mice. Groups of genotyped wild-type (WT) and homozygous mutant (KO) males and females were fed either control chow or a high caloric palatable diet consisting of sweet, liquid chocolate-flavored Ensure together with a solid high-fat diet. Food intake, body weight, and body composition was measured over a period of 16 weeks. Unexpectedly, male, and to a lesser extent female, KO mice fed chow for the entire period showed progressively increased body weight and adiposity while eating significantly more chow. In contrast, when exposed to the sweet plus high-fat diet, male, and to a lesser extent female, KO mice gained significantly less body weight and fat mass compared to WT mice when using chow fed counterparts for reference values. Male KO mice consumed 33% less of the sweet liquid diet but increased intake of high-fat pellets, so that total calorie intake was not different from WT animals. These results demonstrate a dissociation of the role of mu-opioid receptors in the control of adiposity for different diets and sex. On a bland diet, normal receptor function appears to confer a slightly catabolic predisposition, but on a highly palatable diet, it confers an anabolic metabolic profile, favoring fat accretion. Because of the complexity of mu-opioid gene regulation and tissue distribution, more selective and targeted approaches will be necessary to fully understand the underlying mechanisms.
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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.