Bromocriptine Administration Reduces Hyperphagia and Adiposity and Differentially Affects Dopamine D2 Receptor and Transporter Binding in Leptin-Receptor-Deficient Zucker Rats and Rats with Diet-Induced Obesity
Open accessAbstract
Background: The dopamine (DA) D 2 receptor (D2R) agonist bromocriptine (BC) decreases body fat in animal and human models and increases lean muscle mass, improves glucose intolerance and insulin resistance, and reduces triglycerides and free fatty acids. We have previously shown a negative correlation between D2R and body weight in obese individuals and in rodents, and that chronic food restriction increases D2R binding in genetically obese rats. The purpose of this study was to assess whether the antiobesity and metabolic effects of BC are related to changes in midbrain DA and D2R activity by measuring D2R and DA transporter (DAT) binding in a genetic (leptin-receptor-deficient) and environmental (diet-induced) rodent obesity model. Methods: Obese (fa/fa) (leptin-receptor-deficient), lean (FA/FA) Zucker rats and rats with diet-induced obesity (DIO) were treated with 10 mg/kg BC for 4 weeks. Body weight, food intake, locomotor activity and blood glucose levels were measured along with D2R- and DAT-binding levels using in vitro receptor autoradiography. Results: BC decreased food intake and body fat and increased locomotor activity in both the (fa/fa) and DIO rats. Furthermore, BC increased D2R binding in (fa/fa) but not in DIO rats. Finally, BC increased DAT binding in DIO rats but not in the (fa/fa) rats. Conclusion: These observations are all consistent with the existence of unique leptin-DA interactions and the hypothesis that there is hyposensitivity of the DA system in obesity.
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Dysfunction in OFC and ACC results in compulsivity, and this might be part of the mechanism by which low-striatal D2R signalling facilitates hyperphagia.
“Given that dysfunction in OFC and ACC results in compulsivity (see review (85)), this might be part of the mechanism by which low-striatal D2R signalling facilitates hyperphagia (86,87).”
From Obesity and addiction: Neurobiological overlaps (2013) · cites this paper as [86]
Given that dysfunction in OFC and ACC results in compulsivity, this might be part of the mechanism by which low striatal D2R signaling facilitates hyperphagia.
“Given that dysfunction in OFC and ACC results in compulsivity [see review (Fineberg et al 2009)], this might be part of the mechanism by which low striatal D2R signaling facilitates hyperphagia (Davis et al 2009).”
From Food and Drug Reward: Overlapping Circuits in Human Obesity and Addiction (2011) · cites this paper as Davis et al 2009
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- Authors
- Davis, L. M., Michaelides, M., Cheskin, L. J., Moran, T. H., Aja, S., Watkins, P. A., Pei, Z., Contoreggi, C., McCullough, K., Hope, B., Wang, G. J., Volkow, N. D., & Thanos, P. K.
- Affiliations
- Johns Hopkins University (US)
- National Institutes of Health (US)
- Kennedy Krieger Institute (US)
- ORCID
- Venue
- Neuroendocrinology
- Publisher
- S. Karger AG
- Published
- 2008-11-04
- Volume
- 89
- Issue
- 2
- Pages
- 152-162
- ISSN
- 0028-3835 (ISSN-L)
- 1423-0194
- PMC
- PMC2681080
- OpenAlex
- W2101077649
- Cited by
- 82
- References
- 91
- Citations by year
- 2025: 3 · 2024: 2 · 2023: 7 · 2022: 6 · 2021: 3 · 2020: 3 · 2019: 3 · 2018: 8 · 2017: 6 · 2016: 6 · 2015: 4 · 2014: 6 · 2013: 5 · 2012: 6
- FWCI
- 2.08
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neuroendocrinology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- Johns Hopkins Bloomberg School of Public Health
- National Institute on Alcohol Abuse and Alcoholism (Z01AA000551)
- National Institute of Diabetes and Digestive and Kidney Diseases (R56DK019302, R01DK019302)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Pharmacology › Pharmacology and Obesity Treatment
- Keywords
- bromocriptine, dopamine D2 receptor, dopamine transporter, leptin receptor deficiency, diet-induced obesity, hyperphagia, adiposity, dietary intake, locomotor activity, midbrain dopamine system, anti-obesity drugs, Zucker rats
- MeSH terms
- Animals, Bromocriptine, Diet, Eating, Hyperphagia, Male, Motor Activity, Obesity, Rats, Zucker, Receptors, Dopamine D2, Dopamine Agonists, Adiposity, Dopamine Plasma Membrane Transport Proteins, Rats, Receptors, Leptin
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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