ArticleNature medicine2011
A role for central nervous system PPAR-γ in the regulation of energy balance.
Article in Nature medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 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.
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Who cites it
118 citing papers in PubMed, 212 citations in OpenAlex.
- PPAR-γ agonism as a modulator of mood: proof-of-concept for pioglitazone in bipolar depression.CNS drugs · 2014Trial
- A randomized, double blind, placebo-controlled trial of pioglitazone in combination with riluzole in amyotrophic lateral sclerosis.PloS one · 2012Trial
- The signaling pathway of PPAR-γ and its protective role in various diseases.Caspian journal of internal medicine · 2026Review
- Phospholipase D: emerging therapeutic targets in signaling, metabolism, and immune-oncology.Cell communication and signaling : CCS · 2025Review
- Advancement of artificial intelligence based treatment strategy in type 2 diabetes: A critical update.Journal of pharmaceutical analysis · 2025Review
- Mechanisms of Macrophage Polarization Regulated by Oridonin: A Review.Journal of inflammation research · 2025Review
- The role of PPARγ in cancer cachexia: friend or foe?Frontiers in endocrinology · 2025Review
- Tanycytic transcytosis inhibition disrupts energy balance, glucose homeostasis and cognitive function in male mice.Molecular metabolism · 2024Article
- New advances in drug development for metabolic dysfunction-associated diseases and alcohol-associated liver disease.Cell & bioscience · 2024Review
- Maternal circadian rhythm disruption affects neonatal inflammation via metabolic reprograming of myeloid cells.Nature metabolism · 2024Article
- Article
- Integrating Metabolomics and Network Pharmacology to Explore the Mechanism of Xiao-Yao-San in the Treatment of Inflammatory Response in CUMS Mice.Pharmaceuticals (Basel, Switzerland) · 2023Article
- An Update on the Molecular and Cellular Basis of Pharmacotherapy in Type 2 Diabetes Mellitus.International journal of molecular sciences · 2023Review
- Resveratrol alleviates oxidative stress induced by oxidized soybean oil and improves gut function via changing gut microbiota in weaned piglets.Journal of animal science and biotechnology · 2023Article
- Development of PPARγ Agonists for the Treatment of Neuroinflammatory and Neurodegenerative Diseases: Leriglitazone as a Promising Candidate.International journal of molecular sciences · 2023Review
- Regulatory T cells differentiation in visceral adipose tissues contributes to insulin resistance by regulating JAZF-1/PPAR-γ pathway.Journal of cellular and molecular medicine · 2023Article
- The Small Molecule PPARγ Agonist GL516 Induces Feeding-Stimulatory Effects in Hypothalamus Cells Hypo-E22 and Isolated Hypothalami.Molecules (Basel, Switzerland) · 2022Article
- Novel Noninvasive Approaches to the Treatment of Obesity: From Pharmacotherapy to Gene Therapy.Endocrine reviews · 2022Review
- Role of the Peroxisome Proliferator Activated Receptors in Hypertension.Circulation research · 2021Review
- Gut microbiota and metabolic marker alteration following dietary isoflavone-photoperiod interaction.Endocrinology, diabetes & metabolism · 2021Article
58 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The peroxisome proliferator-activated receptor-γ (PPAR-γ) is a nuclear receptor that is activated by lipids to induce the expression of genes involved in lipid and glucose metabolism, thereby converting nutritional signals into metabolic consequences. PPAR-γ is the target of the thiazolidinedione (TZD) class of insulin-sensitizing drugs, which have been widely prescribed to treat type 2 diabetes mellitus. A common side effect of treatment with TZDs is weight gain. Here we report a previously unknown role for central nervous system (CNS) PPAR-γ in the regulation of energy balance. We found that both acute and chronic activation of CNS PPAR-γ, by either TZDs or hypothalamic overexpression of a fusion protein consisting of PPAR-γ and the viral transcriptional activator VP16 (VP16-PPAR-γ), led to positive energy balance in rats. Blocking the endogenous activation of CNS PPAR-γ with pharmacological antagonists or reducing its expression with shRNA led to negative energy balance, restored leptin sensitivity in high-fat-diet (HFD)-fed rats and blocked the hyperphagic response to oral TZD treatment. These findings have implications for the widespread clinical use of TZD drugs and for understanding the etiology of diet-induced obesity.
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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.