ArticleInternational journal of obesity (2005)2021
GHS-R suppression in adipose tissues protects against obesity and insulin resistance by regulating adipose angiogenesis and fibrosis.
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 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Meta-inflammation through the lens of macrophage programming and nutrient-sensing ghrelin signaling.Immunometabolism (Cobham, Surrey) · 2026Review
- Naringenin Decreases Retroperitoneal Adiposity and Improves Metabolic Parameters in a Rat Model of Western Diet-Induced Obesity.Metabolites · 2025Article
- Genetic or pharmacological GHSR blockade has sexually dimorphic effects in rodents on a high-fat diet.Communications biology · 2024Article
- Article
- Innate immunity in peripheral tissues is differentially impaired under normal and endotoxic conditions in aging.Frontiers in immunology · 2024Article
- Growth hormone/insulin-like growth factor I axis in health and disease states: an update on the role of intra-portal insulin.Frontiers in endocrinology · 2024Review
- Genetic or pharmacological GHSR blockade has sexually dimorphic effects in rodents on a high-fat diet.Research square · 2023Article
- Article
- Novel Role of Ghrelin Receptor in Gut Dysbiosis and Experimental Colitis in Aging.International journal of molecular sciences · 2022Article
- Regulation of adipose tissue lipolysis by ghrelin is impaired with high-fat diet feeding and is not restored with exercise.Adipocyte · 2021Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
BACKGROUND/
objectivesGhrelin is an orexigenic hormone that increases food intake, adiposity, and insulin resistance through its receptor Growth Hormone Secretagogue Receptor (GHS-R). We previously showed that ghrelin/GHS-R signaling has important roles in regulation of energy homeostasis, and global deletion of GHS-R reduces obesity and improves insulin sensitivity by increasing thermogenesis. However, it is unknown whether GHS-R regulates thermogenic activation in adipose tissues directly.
methodsWe generated a novel adipose tissue-specific GHS-R deletion mouse model and characterized the mice under regular diet (RD) and high-fat diet (HFD) feeding. Body composition was measured by Echo MRI. Metabolic profiling was determined by indirect calorimetry. Response to environmental stress was assessed using a TH-8 temperature monitoring system. Insulin sensitivity was evaluated by glucose and insulin tolerance tests. Tissue histology was analyzed by hematoxylin/eosin and immunofluorescent staining. Expression of genes involved in thermogenesis, angiogenesis and fibrosis in adipose tissues were analyzed by real-time PCR.
resultsUnder RD feeding, adipose tissue-specific GHS-R deletion had little or no impact on metabolic parameters. However, under HFD feeding, adipose tissue-specific GHS-R deletion attenuated diet-induced obesity and insulin resistance, showing elevated physical activity and heat production. In addition, adipose tissue-specific GHS-R deletion increased expression of master adipose transcription regulator of peroxisome proliferator-activated receptor (PPAR) γ1 and adipokines of adiponectin and fibroblast growth factor (FGF) 21; and differentially modulated angiogenesis and fibrosis evident in both gene expression and histological analysis.
conclusionsThese results show that GHS-R has cell-autonomous effects in adipocytes, and suppression of GHS-R in adipose tissues protects against diet-induced obesity and insulin resistance by modulating adipose angiogenesis and fibrosis. These findings suggest adipose GHS-R may constitute a novel therapeutic target for treatment of obesity and metabolic syndrome.
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