ArticleObesity (Silver Spring, Md.)2009
Diet-induced obese mice are leptin insufficient after weight reduction.
Article in Obesity (Silver Spring, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 51 citations in OpenAlex.
- Evaluation of leptin treatment on maintenance of body weight loss in diet-induced obese mice.Diabetes, obesity & metabolism · 2026Article
- Leptin antagonism attenuates hypertension and renal injury in an experimental model of autoimmune disease.Clinical science (London, England : 1979) · 2023Article
- Cafeteria Diet-Induced Obesity Worsens Experimental CKD.Nutrients · 2023Article
- The Effects of a Western Diet vs. a High-Fiber Unprocessed Diet on Health Outcomes in Mice Offspring.Nutrients · 2023Article
- Expansion of the Inguinal Adipose Tissue Depot Correlates With Systemic Insulin Resistance in C57BL/6J Mice.Frontiers in cell and developmental biology · 2022Article
- Intersections in Neuropsychiatric and Metabolic Disorders: Possible Role of TRPA1 Channels.Frontiers in endocrinology · 2021Review
- Sex Differences in Metabolic Recuperation After Weight Loss in High Fat Diet-Induced Obese Mice.Frontiers in endocrinology · 2021Article
- Pathophysiology of NAFLD and NASH in Experimental Models: The Role of Food Intake Regulating Peptides.Frontiers in endocrinology · 2020Review
- Reduced Diet-induced Thermogenesis in Apolipoprotein A-IV Deficient Mice.International journal of molecular sciences · 2019Article
- Neuroendocrine Regulation of Energy Metabolism Involving Different Types of Adipose Tissues.International journal of molecular sciences · 2019Review
- Global Transcriptome Analysis of Brown Adipose Tissue of Diet-Induced Obese Mice.International journal of molecular sciences · 2018Article
- Mice fed fish oil diet and upregulation of brown adipose tissue thermogenic markers.European journal of nutrition · 2016Article
- The effects on weight loss and gene expression in adipose and hepatic tissues of very-low carbohydrate and low-fat isoenergetic diets in diet-induced obese mice.Nutrition & metabolism · 2016Article
- Bardoxolone Methyl Prevents Mesenteric Fat Deposition and Inflammation in High-Fat Diet Mice.TheScientificWorldJournal · 2015Article
- Hypothalamic gliosis associated with high-fat diet feeding is reversible in mice: a combined immunohistochemical and magnetic resonance imaging study.Endocrinology · 2014Article
- Endospanin 1 silencing in the hypothalamic arcuate nucleus contributes to sustained weight loss of high fat diet obese mice.Gene therapy · 2014Article
- Large, binge-type meals of high fat diet change feeding behaviour and entrain food anticipatory activity in mice.Appetite · 2014Article
- Biological mechanisms that promote weight regain following weight loss in obese humans.Physiology & behavior · 2013Review
- Increased adipose tissue hypoxia and capacity for angiogenesis and inflammation in young diet-sensitive C57 mice compared with diet-resistant FVB mice.International journal of obesity (2005) · 2013Article
- Leptin resistance is a secondary consequence of the obesity in ciliopathy mutant mice.Proceedings of the National Academy of Sciences of the United States of America · 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
8 authors at 5 institutions in 3 countries.
Funding
Abstract
Behavioral therapies aimed at reducing excess body fat result in limited fat loss after dieting. To understand the causes for maintenance of adiposity, high-fat (HF) diet-induced obese (DIO) mice were switched to a low-fat chow diet, and the effects of chow on histological and molecular alterations of adipose tissue and metabolic parameters were examined. DIO mice reduced and stabilized their body weights after being switched to chow (HF-chow), but retained a greater amount of adiposity than chow-fed mice. Reduction in adipocyte volume, not number, caused a decrease in fat mass. HF-chow mice showed normalized circulating insulin and leptin levels, improved glucose tolerance, and reduced inflammatory status in white adipose tissue (WAT). Circulating leptin levels corrected for fat mass were lower in HF-chow mice. Leptin administration was used to test whether reduced leptin level of HF-chow mice inhibited further fat loss. Leptin treatment led to an additional reduction in adiposity. Finally, HF-HF mice had lower mRNA levels of beta(3) adrenergic receptor (beta(3)-AR) in epididymal WAT (EWAT) compared to chow-fed mice, and diet change led to an increase in the WAT beta(3)-AR mRNA levels that were similar to the levels of chow-fed mice, suggesting an elevation in sympathetic activation of WAT during diet switch relative to HF-HF mice leading to the reduced leptin level and proinflammatory cytokine content. In summary, HF-chow mice were resistant to further fat loss due to leptin insufficiency. Diet alteration from HF to low fat improved metabolic state of DIO mice, although their adiposity was defended at a higher level.
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.