The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Weight-Reducing Effects of the Plasma Protein Encoded by the obese Gene
Abstract
The gene product of the ob locus is important in the regulation of body weight. The ob product was shown to be present as a 16-kilodalton protein in mouse and human plasma but was undetectable in plasma from C57BL/6J ob / ob mice. Plasma levels of this protein were increased in diabetic ( db ) mice, a mutant thought to be resistant to the effects of ob . Daily intraperitoneal injections of either mouse or human recombinant OB protein reduced the body weight of ob / ob mice by 30 percent after 2 weeks of treatment with no apparent toxicity but had no effect on db / db mice. The protein reduced food intake and increased energy expenditure in ob / ob mice. Injections of wild-type mice twice daily with the mouse protein resulted in a sustained 12 percent weight loss, decreased food intake, and a reduction of body fat from 12.2 to 0.7 percent. These data suggest that the OB protein serves an endocrine function to regulate body fat stores.
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In the citing paper
“Among the most often used genetic models of MASLD are mice genetically deficient for leptin (ob/ob) or the leptin receptor (db/db) (216-219).”
From Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) (2023) · cites this paper as [217]
In the citing paper
“The gene is disrupted in the 2 available alleles of ob; in the original C57/Bl6J ob/ob mutation, a nonsense mutation disrupts protein function, whereas in the second coisogenic ob 2j mutation, a retroviral insertion abrogrates expression of the coding sequence altogether (2,21).”
From Leptin at 14 y of age: an ongoing story (2009) · cites this paper as [2]
In the citing paper
“The failure of recombinant leptin to alter food intake or weight in db mice established the specificity of the effect and essentially excluded the possibility that the protein reduced weight as a result of an aversive effect (2).”
From Leptin at 14 y of age: an ongoing story (2009) · cites this paper as [2]
In the citing paper
“Leptin circulates in the plasma of all mammals tested, including humans and rodents, as an '16-kD protein with a single disulfide bond that is required for bioactivity (2).”
From Leptin at 14 y of age: an ongoing story (2009) · cites this paper as [2]
In the citing paper
“infusions of low-dose leptin centrally replicate all the effects of peripheral leptin even at intracerebroventricular doses that do not alter plasma leptin concentrations (2).”
From Leptin at 14 y of age: an ongoing story (2009) · cites this paper as [2]
In the citing paper
“Administration of either peptide into the brain reduces food intake and body weight (30, 76, 200)”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [76]
In the citing paper
“despite clear evidence that ob/ob mice are more sensitive to leptin than normal mice (30, 76).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [76]
Citations
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Flagged first, then by citations
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Cited by
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Items 201–219 of 219
Leptin, neuroinflammation and obesity
Dragano, N. R. V., Haddad-Tovolli, R., & Velloso, L. A. (2017) · Frontiers of hormone research · doi:10.1159/000452908 · Cited by 45
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Effects of nutrition on neuro-endocrine stress responses
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The Neuronal Actions of Leptin and the Implications for Treating Alzheimer’s Disease
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Adipokines in healthy skeletal muscle and metabolic disease
Coles, C. A. (2016) · Advances in experimental medicine and biology · doi:10.1007/978-3-319-27511-6_6 · Cited by 39
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Leptin Deficiency Per Se Dictates Body Composition and Insulin Action in ob/ob Mice
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Metreleptin and generalized lipodystrophy and evolving therapeutic perspectives
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Central Control of Glucose Homeostasis
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Badhwar, R., Kaur, G., Popli, H., Yadav, D., & Buttar, H. S. (2020) · Pathophysiology of Obesity-Induced Health Complications · doi:10.1007/978-3-030-35358-2_19 · Cited by 3
Metadata
- Authors
- Halaas, J. L., Gajiwala, K. S., Maffei, M., Cohen, S. L., Chait, B. T., Rabinowitz, D., Lallone, R. L., Burley, S. K., & Friedman, J. M.
- Affiliations
- Howard Hughes Medical Institute (US)
- Rockefeller University (US)
- Columbia University (US)
- Brookwood Biomedical Center, Birmingham, AL 35209, USA.
- Venue
- Science
- Published
- 1995-07-28
- Volume
- 269
- Issue
- 5223
- Pages
- 543-546
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2014093920
- Cited by
- 4,451
- References
- 10
- Citations by year
- 2026: 28 · 2025: 32 · 2024: 50 · 2023: 39 · 2022: 68 · 2021: 104 · 2020: 73 · 2019: 115 · 2018: 84 · 2017: 100 · 2016: 121 · 2015: 112 · 2014: 167 · 2013: 142 · 2012: 158
- FWCI
- 105.95
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Rutgers University Community Repository (Rutgers University) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-41096, R01DK041096)
- National Center for Research Resources (RR00862, P41RR000862)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Pharmacology (medical) › Pharmacology and Obesity Treatment
- Keywords
- obese gene, leptin, ob/ob mice, db/db mice, body weight regulation, weight loss, dietary intake, energy expenditure, fat mass, plasma leptin, diabetes mellitus
- MeSH terms
- Adipose Tissue, Animals, Blood Glucose, Body Composition, Diabetes Mellitus, Eating, Energy Metabolism, Female, Humans, Mice, Inbred C57BL, Mice, Obese, Obesity, Proteins, Recombinant Proteins, Weight Loss, Leptin, Mice
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