ArticleInternational journal of obesity (2005)2018
A history of obesity leaves an inflammatory fingerprint in liver and adipose tissue.
Article in International journal of obesity (2005), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05591339 (Diabetes Diagnosis, Management, Prevention and Education in Guinea-Bissau), which is not on this map. Cited by 42 papers.
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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.
Diabetes Diagnosis, Management, Prevention and Education in Guinea-Bissau
Who cites it
42 citing papers in PubMed, 80 citations in OpenAlex.
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- GPR146 in adipose tissue drives adipose-liver crosstalk and promotes hepatic steatosis in mice.Nature communications · 2026Article
- Obesity Alters the microRNA Expression Profile Related to Metabolic Disorders in Peripheral Blood Mononuclear Cells: Preliminary Results.Current issues in molecular biology · 2025Article
- Transcripts with high distal heritability mediate genetic effects on complex metabolic traits.Nature communications · 2025Article
- Review
- Converted Macrophage Polarization and Expression of COL6α3-Early Predictors of Remodeling Processes in Adipose Tissue of Male Children.Biomedicines · 2025Article
- Celastrol Improves Preference for a Fatty Acid, and Taste Bud and Systemic Inflammation in Diet-Induced Obese Mice.Nutrients · 2025Article
- Weight cycling exacerbates glucose intolerance and hepatic triglyceride storage in mice with a history of chronic high fat diet exposure.Journal of translational medicine · 2025Article
- The role of immune cells-mediated memory in weight cycling, glucose disorders and insulin resistance.Frontiers in immunology · 2025Review
- Dynamic Roles and Expanding Diversity of Adipose Tissue Macrophages in Obesity.Journal of obesity & metabolic syndrome · 2024Review
- T cells in obesity-associated inflammation: The devil is in the details.Immunological reviews · 2024Review
- Evaluation of a Standard Dietary Regimen Combined with Heat-InactivatedFoods (Basel, Switzerland) · 2024Article
- The Effect of Diet Composition on the Post-operative Outcomes of Roux-en-Y Gastric Bypass in Mice.Obesity surgery · 2024Article
- The psychological legacy of past obesity and early mortality: evidence from two longitudinal studies.BMC medicine · 2023Article
- Identification of adipose tissue transcriptomic memory of anorexia nervosa.Molecular medicine (Cambridge, Mass.) · 2023Article
- Leptin Increases: Physiological Roles in the Control of Sympathetic Nerve Activity, Energy Balance, and the Hypothalamic-Pituitary-Thyroid Axis.International journal of molecular sciences · 2023Review
- Intrauterine food restriction impairs the lipogenesis process in the mesenteric adipocytes from low-birth-weight rats into adulthood.Frontiers in endocrinology · 2023Article
- Adipocytes control food intake and weight regain via Vacuolar-type HNature communications · 2022Article
- Altered macronutrient composition and genetics influence the complex transcriptional network associated with adiposity in the Collaborative Cross.Genes & nutrition · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectivesDieting is a popular yet often ineffective way to lower body weight, as the majority of people regain most of their pre-dieting weights in a relatively short time. The underlying molecular mechanisms driving weight regain and the increased risk for metabolic disease are still incompletely understood. Here we investigate the molecular alterations inherited from a history of obesity.
methodsIn our model, male high-fat diet (HFD)-fed obese C57BL/6J mice were switched to a low caloric chow diet, resulting in a decline of body weight to that of lean mice. We measured body composition, as well as metrics of glucose, insulin and lipid homeostasis. This was accompanied by histological and gene expression analysis of adipose tissue and liver to assess adipose tissue inflammation and hepatosteatosis. Moreover, acute hypothalamic response to (re-) exposure to HFD was assessed by qPCR. RESULTS &
conclusionsWithin 7 weeks after diet switch, most obesity-associated phenotypes, such as body mass, glucose intolerance and blood metabolite levels were reversed. However, hepatic inflammation, hepatic steatosis as well as hypertrophy and inflammation of perigonadal, but not subcutaneous, adipocytes persisted in formerly obese mice. Transcriptional profiling of liver and perigonadal fat revealed an upregulation of pathways associated with immune function and cellularity. Thus, we show that weight reduction leaves signs of inflammation in liver and perigonadal fat, indicating that persisting proinflammatory signals in liver and adipose tissue could contribute to an increased risk of formerly obese subjects to develop the metabolic syndrome upon recurring weight gain.
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