ReviewPhysiology & behavior2008
Unraveling the obesity of OLETF rats.
Review in Physiology & behavior, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 85 citations in OpenAlex.
- Limited Impact of Sodium-Glucose Cotransporter-2 Inhibitors on Appetite and Body Weight: Evidence From Clinical and Rodent Studies.Journal of Korean medical science · 2026Trial
- Exercise duration and detraining influence not only body weight but also histopathological changes in the white adipose tissue of young male OLETF rats as an obesity model.Physiological reports · 2025Article
- Reduced Striatal Dopamine Transporter Availability and Heightened Response to Natural and Pharmacological Stimulation in CCK-1R-Deficient Obese Rats.International journal of molecular sciences · 2023Article
- Mammalian models of diabetes mellitus, with a focus on type 2 diabetes mellitus.Nature reviews. Endocrinology · 2023Review
- Angiotensin receptor blockade with olmesartan alleviates brain pathology in obese OLETF rats.Clinical and experimental pharmacology & physiology · 2023Article
- Rodent Models of Diabetic Retinopathy as a Useful Research Tool to Study Neurovascular Cross-Talk.Biology · 2023Review
- Neurohormonal Changes in the Gut-Brain Axis and Underlying Neuroendocrine Mechanisms following Bariatric Surgery.International journal of molecular sciences · 2022Review
- Effects of long-term childhood exercise and detraining on lipid accumulation in metabolic-related organs.PloS one · 2022Article
- The Use of Natural Compounds as a Strategy to Counteract Oxidative Stress in Animal Models of Diabetes Mellitus.International journal of molecular sciences · 2021Review
- Intact vagal gut-brain signalling prevents hyperphagia and excessive weight gain in response to high-fat high-sugar diet.Acta physiologica (Oxford, England) · 2021Article
- Experimental models of metabolic and alcoholic fatty liver disease.World journal of gastroenterology · 2021Review
- Animal Models of Diabetes-Associated Renal Injury.Journal of diabetes research · 2020Review
- Hyperinsulinemia Can Cause Kidney Disease in the IGT Stage of OLETF Rats via the INS/IRS-1/PI3-K/Akt Signaling Pathway.Journal of diabetes research · 2019Article
- Rat Models of Metabolic Syndrome.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Animal models of obesity and diabetes mellitus.Nature reviews. Endocrinology · 2018Review
- Using Animal Models to Determine the Role of Gustatory Neural Input in the Control of Ingestive Behavior and the Maintenance of Body Weight.Chemosensory perception · 2015Article
- Article
- Involvement of prolactin-releasing peptide in the activation of oxytocin neurones in response to food intake.Journal of neuroendocrinology · 2013Article
- Cocaine- and amphetamine-regulated transcript (CART) peptide immunoreactivity in feeding- and reward-related brain areas of young OLETF rats.Journal of chemical neuroanatomy · 2013Article
- Cardiovascular changes in animal models of metabolic syndrome.Journal of diabetes research · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Cholecystokinin (CCK) is a brain gut peptide that plays an important role in satiety. CCK inhibits food intake by reducing meal size. CCK's satiety actions are mediating through its interaction with CCK1 receptors. Otsuka Long Evans Tokushima Fatty (OLETF) rats are a CCK1 receptor knockout model that allows the study of multiple CCK functions. OLETF rats are hyperphagic with the hyperphagia expressed as a significant increase in the size of meals. OLETF rat obesity is secondary to the hyperphagia and has been proposed to derive from two regulatory deficits. One is secondary to the loss of a feedback satiety signal. The other results from increased dorsomedial hypothalamic NPY expression. Recent studies have examined developmental aspects of altered feeding, body weight and orexigenic signaling in OLETF rats. OLETF rats demonstrate increases in meal size in independent ingestion tests as early as two days of age. OLETF pups are also more efficient in suckling situations. Consistent with such developmental differences, examinations of patterns of hypothalamic gene expression in OLETF pups indicate significant increases in DMH NPY expression as early as postnatal day 15. Access to a running wheel and the resulting exercise have age dependent effects on OLETF food intake and obesity. With running wheel access shortly after weaning, food intake decreases to the levels of LETO controls. When running wheel access is discontinued, food intake temporarily increases resulting in an intermediate phenotype and the absence of diabetes. Together these data demonstrate roles for peripheral CCK and CCK in feeding and body weight control and support the use of the OLETF rat as a model for examining obesity development and for investigating how interventions at critical developmental time points can alter genetic influences on food intake and body weight.
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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.