Tal Pecht

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CONTEXT Adipose tissue macrophages (ATMs) are thought to engulf the remains of dead adipocytes in obesity, potentially resulting in increased intracellular neutral lipid content. Lipid-laden macrophages (foam cells [FCs]) have been described in atherosclerotic lesions and have been proposed to contribute to vascular pathophysiology, which is enhanced in(More)
While obesity is clearly accepted as a major risk factor for cardio-metabolic morbidity, it is also apparent that some obese patients largely escape this association, forming a unique obese subphenotype(s). Current approaches to define such subphenotypes include clinical biomarkers that largely reflect already manifested comorbidities, such as markers of(More)
BACKGROUND Visceral adipose tissue foam cells are increased in human obesity, and were implicated in adipose dysfunction and increased cardio-metabolic risk. In the circulation, non-classical monocytes (NCM) are elevated in obesity and associate with atherosclerosis and type 2 diabetes. We hypothesized that circulating NCM correlate and/or are functionally(More)
Adipose tissue inflammation and dysfunction are considered central in the pathogenesis of obesity-related dysmetabolism, but their role in the rapid metabolic recovery upon obesity reversal is less well defined. We hypothesized that changes in adipose tissue endocrine and paracrine mechanisms may support the rapid improvement of obesity-induced impairment(More)
There is growing interest in understanding how dysregulated autophagy may contribute to pathogenesis of disease. Most frequently, disease states are associated with diminished autophagy, mostly attributed to genetic variation in autophagy genes and/or to dysfunctional posttranscriptional mechanisms. In human adipose tissue (AT), in obesity, expression of(More)
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