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Adipose Tissue

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Alan R. Saltiel – One of the best experts on this subject based on the ideXlab platform.

  • Adapting to obesity with Adipose Tissue inflammation
    Nature Reviews Endocrinology, 2017
    Co-Authors: Shannon M. Reilly, Alan R. Saltiel

    Abstract:

    Adipocytes have an important role in sensing and managing energy status Adipose Tissue responds to overnutrition by mounting an immune response; however, the initial inflammatory trigger in Adipose Tissue is unknown Inflammation induces insulin resistance through a variety of molecular mechanisms The maladaptive responses that occur in long-term obesity are a result of chronic inflammation, particularly catecholamine resistance Inflammatory pathways are intriguing therapeutic targets for metabolic disease; however, the clinical efficacy of drugs targeting these pathways has been disappointing Adipose Tissue inflammation is an adaptive response to overnutrition in the early stages of obesity, but later becomes maladaptive. Here, Reilly and Saltiel review the cellular and molecular mechanisms of obesity-induced inflammation in Adipose Tissue and discuss potential therapeutic approaches. Adipose Tissue not only has an important role in the storage of excess nutrients but also senses nutrient status and regulates energy mobilization. An overall positive energy balance is associated with overnutrition and leads to excessive accumulation of fat in adipocytes. These cells respond by initiating an inflammatory response that, although maladaptive in the long run, might initially be a physiological response to the stresses obesity places on Adipose Tissue. In this Review, we characterize Adipose Tissue inflammation and review the current knowledge of what triggers obesity-associated inflammation in Adipose Tissue. We examine the connection between Adipose Tissue inflammation and the development of insulin resistance and catecholamine resistance and discuss the ensuing state of metabolic inflexibility. Finally, we review the current and potential new anti-inflammatory treatments for obesity-associated metabolic disease.

  • adapting to obesity with Adipose Tissue inflammation
    Nature Reviews Endocrinology, 2017
    Co-Authors: Shannon M. Reilly, Alan R. Saltiel

    Abstract:

    Adipose Tissue not only has an important role in the storage of excess nutrients but also senses nutrient status and regulates energy mobilization. An overall positive energy balance is associated with overnutrition and leads to excessive accumulation of fat in adipocytes. These cells respond by initiating an inflammatory response that, although maladaptive in the long run, might initially be a physiological response to the stresses obesity places on Adipose Tissue. In this Review, we characterize Adipose Tissue inflammation and review the current knowledge of what triggers obesity-associated inflammation in Adipose Tissue. We examine the connection between Adipose Tissue inflammation and the development of insulin resistance and catecholamine resistance and discuss the ensuing state of metabolic inflexibility. Finally, we review the current and potential new anti-inflammatory treatments for obesity-associated metabolic disease.

Rinke Stienstra – One of the best experts on this subject based on the ideXlab platform.

  • Adipose Tissue macrophages: going off track during obesity
    Diabetologia, 2016
    Co-Authors: Lily Boutens, Rinke Stienstra

    Abstract:

    Inflammation originating from the Adipose Tissue is considered to be one of the main driving forces for the development of insulin resistance and type 2 diabetes in obese individuals. Although a plethora of different immune cells shapes Adipose Tissue inflammation, this review is specifically focused on the contribution of macrophages that reside in Adipose Tissue in lean and obese conditions. Both conventional and Tissue-specific functions of Adipose Tissue macrophages (ATMs) in lean and obese Adipose Tissue are discussed and linked with metabolic and inflammatory changes that occur during the development of obesity. Furthermore, we will address various circulating and Adipose Tissue-derived triggers that may be involved in shaping the ATM phenotype and underlie ATM function in lean and obese conditions. Finally, we will highlight how these changes affect Adipose Tissue inflammation and may be targeted for therapeutic interventions to improve insulin sensitivity in obese individuals. Highlights • Macrophages play a significant role in regulating Adipose Tissue functioning during health and disease • In addition to conventional functions such as clearing cellular debris and participating in Tissue immune surveillance, lipid buffering is an important function of ATMs • Obesity-induced inflammation, characterised by an elevated number of proinflammatory macrophages in Adipose Tissue, has been suggested to contribute to systemic insulin resistance • Their origin, as well as a combination of peripheral changes and Adipose Tissue-derived stressors, probably contribute to ATM dysfunction and inflammatory traits during obesity • Identification of transcriptional differences between ATMs from lean vs obese Adipose Tissue at several key points during the development of obesity and insulin resistance may reveal upstream triggers, regulatory factors and intracellular pathways that shape ATM function • Targeting metabolic capacity rather than the inflammatory phenotype of ATMs may hold potential to restore ATM function and Adipose Tissue homeostasis in obese individuals

  • Adipose Tissue macrophages
    Diabetologia, 2016
    Co-Authors: Lily Boutens, Rinke Stienstra

    Abstract:

    Inflammation originating from the Adipose Tissue is considered to be one of the main driving forces for the development of insulin resistance and type 2 diabetes in obese individuals. Although a plethora of different immune cells shapes Adipose Tissue inflammation, this review is specifically focused on the contribution of macrophages that reside in Adipose Tissue in lean and obese conditions. Both conventional and Tissue-specific functions of Adipose Tissue macrophages (ATMs) in lean and obese Adipose Tissue are discussed and linked with metabolic and inflammatory changes that occur during the development of obesity. Furthermore, we will address various circulating and Adipose Tissue-derived triggers that may be involved in shaping the ATM phenotype and underlie ATM function in lean and obese conditions. Finally, we will highlight how these changes affect Adipose Tissue inflammation and may be targeted for therapeutic interventions to improve insulin sensitivity in obese individuals.(Table presented.)

Esben Søndergaard – One of the best experts on this subject based on the ideXlab platform.

  • Quantification of Adipose Tissue insulin sensitivity.
    Journal of Investigative Medicine, 2016
    Co-Authors: Esben Søndergaard, Michael D. Jensen

    Abstract:

    In metabolically healthy humans, Adipose Tissue is exquisitely sensitive to insulin. Similar to muscle and liver, Adipose Tissue lipolysis is insulin resistant in adults with central obesity and type 2 diabetes. Perhaps uniquely, however, insulin resistance in Adipose Tissue may directly contribute to development of insulin resistance in muscle and liver because of the increased delivery of free fatty acids to those Tissues. It has been hypothesized that insulin Adipose Tissue resistance may precede other metabolic defects in obesity and type 2 diabetes. Therefore, precise and reproducible quantification of Adipose Tissue insulin sensitivity, in vivo, in humans, is an important measure. Unfortunately, no consensus exists on how to determine Adipose Tissue insulin sensitivity. We review the methods available to quantitate Adipose Tissue insulin sensitivity and will discuss their strengths and weaknesses.

  • Chronic adrenergic stimulation induces brown Adipose Tissue differentiation in visceral Adipose Tissue.
    Diabetic Medicine, 2015
    Co-Authors: Esben Søndergaard, Lars C. Gormsen, Mette Høgh Christensen, Steen B. Pedersen, P Christiansen, Søren Nielsen, P. L. Poulsen, Niels Jessen

    Abstract:

    Background

    Recruitment of brown Adipose Tissue is a promising strategy to treat obesity and Type 2 diabetes, but the physiological effects of a large amount of metabolically active brown Adipose Tissue in humans are unknown.

    Case report

    In the present paper, we report a case of massive brown Adipose Tissue infiltration of the visceral Adipose Tissue depot in a person with Type 2 diabetes with a catecholamine-secreting paraganglioma. The patient was evaluated with [18F]-fludeoxyglucose positron emission tomography/computed tomography on three occasions: pre-therapy, during α-blockade and postoperatively. During surgery, biopsies of visceral and subcutaneous Adipose Tissue were obtained and evaluated for brown Adipose Tissue. At diagnosis, brown Adipose Tissue glucose uptake, assessed by [18F]-fludeoxyglucose-positron emission tomography, was massively increased. [18F]-fludeoxyglucose uptake was confined to known locations for brown Adipose Tissue, with additional uptake in the visceral Adipose Tissue. As a result of increased thermogenesis, resting energy expenditure was doubled. After surgical removal of the tumour, antidiabetic medicine was no longer needed, despite an 8.2-kg weight gain.

    Conclusion

    These results show that human visceral Adipose Tissue holds an unprecedented potential for brown adipogenic differentiation; however, a detrimental effect on glucose metabolism persisted despite massive brown Adipose Tissue activity, with a doubling of resting energy expenditure.