Adipose tissue remodeling and obesity.

By K. Sun, C. Kusminski, P. Scherer. Journal of Clinical Investigation, 2011

1,757 citations recorded by the source corpus.

Subfields: Cancer Research, Epidemiology, Physiology

View Paper: https://www.semanticscholar.org/paper/2136fd975d5a354a657552c0fc7acefa1a973e5a

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In Cancer Research

Jerrold M. Olefsky

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Citations in the corpus

Adipose Tissue Remodeling: Its Role in Energy Metabolism and Metabolic Disorders (2016, background): “Hypoxia is one of the most potent microenvironmental factors for macrophage recruitment into adipose tissues (185), and recruited macrophages are the predominant producers of pro-angiogenic factors in response to hypoxia (186).”
In vivo identification of bipotential adipocyte progenitors recruited by β3-adrenoceptor activation and high fat feeding (2012, neutral): “The fact that the cellular composition andmetabolic character of adipose tissue is responsive to nutritional and pharmacologic stimuli (Prins and O’Rahilly, 1997) raises the possibility that adipose tissue plasticity might be targeted for therapeutic benefit (Sun et al., 2011).”
Formation of short chain fatty acids by the gut microbiota and their impact on human metabolism (2016, background): “SCFA also inhibit insulin stimulated lipid accumulation in adipocytes via FFAR 2 signaling, resulting in small more responsive adipocytes which is associated with reduced adipose inflammatory infiltrate.(60,61) Acetate also appears to stimulate leptin secretion in adipocytes.”
Fibrosis and Adipose Tissue Dysfunction (2013, background): “Hypoxia is therefore an early determinant for adipose tissue dysfunction (Sun et al., 2011).”
Adipose Tissue Dysfunction as Determinant of Obesity-Associated Metabolic Complications (2019, background): “As mentioned above, adipose tissue responds dynamically to alterations in calories excess through adipocyte hypertrophy and hyperplasia [18,101].”
Inflammatory mechanisms linking obesity and metabolic disease (2017, background): “The expansion of adipose tissue prevents ectopic lipid deposition in other tissues such as liver and muscle, where it has lipotoxic effects (20).”
Obesity and type 2 diabetes mellitus: connections in epidemiology, pathogenesis, and treatments (2023, background): “of insufficient angiogenesis owing to fast and excessive adipose tissue expansion, over-activating the transcription factor hypoxiainducible factor 1a (HIF-1a) that triggers fibrosis, enhances local inflammation and lowers insulin sensitivity (34, 41).”
The role of short-chain fatty acids in immunity, inflammation and metabolism (2020, background): “In insulin-stimulated adipocytes, short-chain fatty acids inhibit lipid accumulation through GPR43 signaling, leading to smaller adipocytes and more sensitive responses, which may be related to fatty inflammatory infiltration (Kimura et al. 2013; Sun, Kusminski, and Scherer 2011).”
Insulin receptor signaling in normal and insulin-resistant states. (2014, background): “Adipose tissue expansion occurs in response to caloric overload, and is associated with an increase in immune cell infiltration and a subsequent proinflammatory response (Sun et al. 2011).”
Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes (2020, background): “Current evidence reveals that hypoxia develops as AT expands because of a relative under perfusion of the enlarged AT or increased oxygen utilization (Gealekman et al., 2011; Sun et al., 2011; Trayhurn, 2013; Lee et al., 2014).”