Abstract
Rationale: Adipose tissue is key player in the development of obesity and obesity-related complications. Recent evidence shows that adipocyte size regulation through actin cytoskeleton remodeling is mechanistically interlinked with disrupted cell metabolism, including reduced mitochondrial function and insulin signaling. The unacylated form of the hormone ghrelin (UnAG) is a novel profound metabolic modulator, with whole-body and tissue-specific effects. In rodent models it improves obesity-induced skeletal muscle insulin resistance, however its impact on adipocyte expansion and metabolism is currently unknown.
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