Thomas Skurk

TL;DR: There seems to be a differential expression of pro- and antiinflammatory factors with increasing adipocyte size resulting in a shift toward dominance of proinflammatory adipokines largely as a result of a dysregulation of hypertrophic, very large cells.

TL;DR: Proinflammatory T-lymphocytes are present in visceral adipose tissue and may contribute to local inflammatory cell activation before the appearance of macrophages, suggesting that these cells could play an important role in the initiation and perpetuation of adipOSE tissue inflammation as well as the development of IR.

TL;DR: The data support a mechanism in which adipocyte lipid storage and removal have different roles in health and pathology, and identify adipocytes lipid turnover as a novel target for prevention and treatment of metabolic disease.

TL;DR: It is shown that physiological challenges increased interindividual variation even in phenotypically similar volunteers, revealing metabotypes not observable in baseline metabolite profiles; volunteer‐specific metabolite concentrations were consistently reflected in various biofluids; and readouts from a systematic model of β‐oxidation showed significant and stronger associations with physiological parameters than absolute metabolite concentration.

TL;DR: Impaired fibrinolysis in obesity is probably also due to an increased expression of PAI-1 in adipose tissue, and an altered function of the endocrine system and an impaired auto-/paracrine function at the fat cell levels may mediate this disturbance of the fibrinoslytic system and thereby increase the risk for cardiovascular disease.