Abstract
Rationale: In obese patients, besides absolute fat mass quantity, dysfunctional adipose tissue with fat cell hypertrophy importantly increases metabolic risk including the development of type 2 diabetes. Recent evidence shows that adipocyte expansion both causes and is sustained by disrupted cell metabolism, with reduced mitochondrial function and insulin signaling. The unacylated form of the gastric hormone ghrelin (UnAG) increases skeletal muscle mitochondrial function and insulin signalling in obese rodent models; however, its potential effects on adipose tissue metabolism are currently unknown.
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