ArticleEndocrinology2014
Hypothalamic gliosis associated with high-fat diet feeding is reversible in mice: a combined immunohistochemical and magnetic resonance imaging study.
Article in Endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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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.
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Who cites it
61 citing papers in PubMed, 110 citations in OpenAlex.
- Weight loss aggravates obesity-induced hypothalamic inflammation in mid-aged mice.GeroScience · 2026Article
- Acute anti-obesity treatment with celastrol reduces body weight, cerebral inflammation and metabolic imbalances in mice.Molecular medicine (Cambridge, Mass.) · 2026Article
- Hypothalamic astrocytes: connecting brain and periphery in metabolic control.Reviews in endocrine & metabolic disorders · 2026Review
- Aquaporin-4 inhibition alters cerebral glucose dynamics predominantly in obese animals: an MRI study.Scientific reports · 2025Article
- Update on Hypothalamic Inflammation and Gliosis: Expanding Evidence of Relevance Beyond Obesity.Current obesity reports · 2025Review
- Age and duration of obesity modulate the inflammatory response and expression of neuroprotective factors in mammalian female brain.Aging cell · 2024Article
- Hypothalamic neuronal-glial crosstalk in metabolic disease.npj metabolic health and disease · 2024Review
- Comparison Between Two Divergent Diets, Mediterranean and Western, on Gut Microbiota and Cognitive Function in Young Sprague Dawley Rats.Gut microbes reports · 2024Article
- Microglia in Central Control of Metabolism.Physiology (Bethesda, Md.) · 2024Review
- Pituitary T1 signal intensity at magnetic resonance imaging is reduced in patients with obesity: results from the CHIASM study.International journal of obesity (2005) · 2023Review
- Obesity-associated microglial inflammatory activation paradoxically improves glucose tolerance.Cell metabolism · 2023Article
- Dietary Fat Modulation of Gut Microbiota and Impact on Regulatory Pathways Controlling Food Intake.Nutrients · 2023Review
- The Neurobiology of Eating Behavior in Obesity: Mechanisms and Therapeutic Targets: A Report from the 23rd Annual Harvard Nutrition Obesity Symposium.The American journal of clinical nutrition · 2023Article
- Obesity-Induced Brain Neuroinflammatory and Mitochondrial Changes.Metabolites · 2023Review
- Trends in Gliosis in Obesity, and the Role of Antioxidants as a Therapeutic Alternative.Antioxidants (Basel, Switzerland) · 2022Review
- HypoMap-a unified single-cell gene expression atlas of the murine hypothalamus.Nature metabolism · 2022Article
- Palmitoylethanolamide dampens neuroinflammation and anxiety-like behavior in obese mice.Brain, behavior, and immunity · 2022Article
- Inverse Association Between Hypothalamic N-Acetyl Aspartate/Creatine Ratio and Indices of Body Mass in Adolescents with Obesity.The Journal of nutrition · 2022Article
- Evidence That Hypothalamic Gliosis Is Related to Impaired Glucose Homeostasis in Adults With Obesity.Diabetes care · 2022Article
- Effect of Propionic Acid on Diabetes-Induced Impairment of Unfolded Protein Response Signaling and Astrocyte/Microglia Crosstalk in Rat Ventromedial Nucleus of the Hypothalamus.Neural plasticity · 2022Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Gliosis, the activation of astrocyte and microglial cell populations, is a hallmark of central nervous system injury and is detectable using either immunohistochemistry or in vivo magnetic resonance imaging (MRI). Obesity in rodents and humans is associated with gliosis of the arcuate nucleus, a key hypothalamic region for the regulation of energy homeostasis and adiposity, but whether this response is permanent or reversible is unknown. Here we combine terminal immunohistochemistry analysis with serial, noninvasive MRI to characterize the progression and reversibility of hypothalamic gliosis in high-fat diet (HFD)-fed mice. The effects of HFD feeding for 16 weeks to increase body weight and adiposity relative to chow were nearly normalized after the return to chow feeding for an additional 4 weeks in the diet-reversal group. Mice maintained on the HFD for the full 20-week study period experienced continued weight gain associated with the expected increases of astrocyte and microglial activation in the arcuate nucleus, but these changes were not observed in the diet-reversal group. The proopiomelanocortin neuron number did not differ between groups. Although MRI demonstrated a positive correlation between body weight, adiposity, and the gliosis-associated T2 signal in the mediobasal hypothalamus, it did not detect the reversal of gliosis among the HFD-fed mice after the return to chow diet. We conclude that hypothalamic gliosis associated with 16-week HFD feeding is largely reversible in rodents, consistent with the reversal of the HFD-induced obesity phenotype, and extend published evidence regarding the utility of MRI as a tool for studying obesity-associated hypothalamic gliosis in vivo.
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Registered trials
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