ArticleInternational journal of obesity (2005)2021
Non-hematopoietic IL-4Rα expression contributes to fructose-driven obesity and metabolic sequelae.
Article in International journal of obesity (2005), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 6 citations in OpenAlex.
- Fructose impairs brown adipogenesis by promoting thyroid hormone resistance in differentiated brown adipocytes.Biology open · 2026Article
- Helminth infection induces RELMα-dependent adipose tissue transcriptional reprogramming and protection against diet-induced obesity.bioRxiv : the preprint server for biology · 2026Article
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- Population-enriched innate immune variants may identify candidate gene targets at the intersection of cancer and cardio-metabolic disease.Frontiers in endocrinology · 2023Review
- System biology approaches identified novel biomarkers and their signaling pathways involved in renal cell carcinoma with different human diseases.Bioscience reports · 2022Article
- Article
- A luminescence-based protocol for assessing fructose metabolism via quantification of ketohexokinase enzymatic activity in mouse or human hepatocytes.STAR protocols · 2021Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveThe risks of excess sugar intake in addition to high-fat diet consumption on immunopathogenesis of obesity-associated metabolic diseases are poorly defined. Interleukin-4 (IL-4) and IL-13 signaling via IL-4Rα regulates adipose tissue lipolysis, insulin sensitivity, and liver fibrosis in obesity. However, the contribution of IL-4Rα to sugar rich diet-driven obesity and metabolic sequelae remains unknown.
methodsWT, IL-4Rα-deficient (IL-4Rα
resultsWe show that IL-4Rα regulated HF + HC diet-driven weight gain, whole body adiposity, adipose tissue inflammatory gene expression, energy expenditure, locomotor activity, glucose metabolism, hepatic steatosis, hepatic inflammatory gene expression and hepatocellular damage. These effects were potentially, and in part, dependent on non-hematopoietic IL-4Rα expression but were independent of direct STAT6 activation. Mechanistically, hepatic ketohexokinase-A and C expression was dependent on IL-4Rα, as it was reduced in IL-4Rα-deficient mice. KHK activity was also affected by HF + HC dietary challenge. Further, reduced expression/activity of KHK in IL-4Rα mice had a significant effect on fatty acid oxidation and fatty acid synthesis pathways.
conclusionOur findings highlight potential contribution of non-hematopoietic IL-4Rα activation of a non-canonical signaling pathway that regulates the HF + HC diet-driven induction of obesity and severity of obesity-associated sequelae.
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