ArticleInternational journal of obesity (2005)2016
Characteristics of adipose tissue macrophages and macrophage-derived insulin-like growth factor-1 in virus-induced obesity.
Article in International journal of obesity (2005), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- What we know and what we need to know about adenovirus 36-induced obesity.International journal of obesity (2005) · 2020Review
- Article
- Targeting viperin improves diet-induced glucose intolerance but not adipose tissue inflammation.Oncotarget · 2017Article
- Growth hormone-releasing hormone is produced by adipocytes and regulates lipolysis through growth hormone receptor.International journal of obesity (2005) · 2017Article
- α-Mangostin ameliorates hepatic steatosis and insulin resistance by inhibition C-C chemokine receptor 2.PloS one · 2017Article
- Traditional Chinese Medicine for Metabolic Syndrome via TCM Pattern Differentiation: Tongue Diagnosis for Predictor.Evidence-based complementary and alternative medicine : eCAM · 2016Article
- Adipose Tissue: Sanctuary for HIV/SIV Persistence and Replication.Trends in microbiology · 2015Article
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4 authors at 1 institution in 1 country.
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Abstract
backgroundVarious pathogens are implicated in the induction of obesity. Previous studies have confirmed that human adenovirus 36 (Ad36) is associated with increased adiposity, improved glycemic control and induction of inflammation. The Ad36-induced inflammation is reflected in the infiltration of macrophages into adipose tissue. However, the characteristics and role of adipose tissue macrophages (ATMs) and macrophage-secreted factors in virus-induced obesity (VIO) are unclear. Although insulin-like growth factor-1 (IGF-1) is involved in obesity metabolism, the contribution of IGF secreted by macrophages in VIO has not been studied.
methodsFour-week-old male mice were studied 1 week and 12 weeks after Ad36 infection for determining the characteristics of ATMs in VIO and diet-induced obesity (DIO). In addition, macrophage-specific IGF-1-deficient (MIKO) mice were used to study the involvement of IGF-1 in VIO.
resultsIn the early stage of VIO (1 week after Ad36 infection), the M1 ATM sub-population increased, which increased the M1/M2 ratio, whereas DIO did not cause this change. In the late stage of VIO (12 weeks after Ad36 infection), the M1/M2 ratio did not change because the M1 and M2 ATM sub-populations increased to a similar extent, despite an increase in adiposity. By contrast, DIO increased the M1/M2 ratio. In addition, VIO in wild-type mice upregulated angiogenesis in adipose tissue and improved glycemic control. However, MIKO mice showed no increase in adiposity, angiogenesis, infiltration of macrophages into adipose tissue, or improvement in glycemic control after Ad36 infection.
conclusionsThese data suggest that IGF-1 secreted by macrophages may contribute to hyperplasia and hypertrophy in adipose tissue by increasing angiogenesis, which helps to maintain the 'adipose tissue robustness'.
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