Abstract
Presence of thermogenically active adipose tissue in adult humans has been inversely associated with obesity and type 2 diabetes. While it had been shown that insulin is crucial for the development of classical brown fat, its role in development and function of inducible brown-in-white (brite) adipose tissue is less clear. Here we show that insulin deficiency impaired differentiation of brite adipocytes. However, adrenergic stimulation almost fully induced the thermogenic program under these settings. Although brite differentiation of adipocytes as well as browning of white adipose tissue entailed substantially elevated glucose uptake by adipose tissue, the capacity of insulin to stimulate glucose uptake surprisingly was not higher in the brite state. Notably, in line with the insulin-independent stimulation of glucose uptake, our data revealed that brite recruitment results in induction of solute carrier family 2 (GLUT-1) expression in adipocytes and inguinal WAT. These results for the first time demonstrate that insulin signaling is neither essential for brite recruitment, nor is it improved in cells or tissues upon browning.
Highlights
According to estimations of the WHO, nowadays more than 10% of the world’s adult population is obese
The previous observation that insulin signaling is crucial for proper brown adipocyte differentiation and adipose tissue development [25,35], prompted us to screen for insulin-dependent gene expression patterns in white and brite adipocytes during differentiation
There was little impact of insulin on the gene expression levels of both white and brite adipocytes in the correlation heat map, indicating that insulin has no further effects on global gene expression in the initial phase of adipogenic differentiation (Fig. 1A)
Summary
According to estimations of the WHO, nowadays more than 10% of the world’s adult population is obese. Obesity frequently entails detrimental secondary diseases and represents the fifth leading risk for global deaths [1]. Research on BAT has recently been revived by PET/CT-studies demonstrating presence of metabolically active BAT in discrete areas of adult humans, [3,4,5]. Active BAT has the potential to enhance systemic glucose disposal and improve global insulin sensitivity in human subjects [6,7]. Increasing BAT activity is considered a promising option for innovative weight lowering therapies and amelioration of hyperglycemia and insulin resistance, which are hallmarks of type 2 diabetes and the metabolic syndrome, respectively [8]
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