Cover Story Current Issue

In 1975, Arion and colleagues discovered that hepatocytes release glucose into the bloodstream in response to hypoglycaemia using the glucose-6-phosphatase (G6Pase) system. This system is in the endoplasmic reticulum (ER) and is composed of two functionally linked proteins, a G6P transporter subunit (G6PT) and a catalytic subunit called G6P phosphatase (G6Pase). The G6PT subunit promotes the storage of G6P inside the ER, while G6Pase, which has its catalytic domain in the reticular lumen, hydrolyses G6P to yield free glucose + phosphate. The free glucose stored in the reticular lumen can be transported to the cytosol and from there to the extracellular space in hypoglycaemic conditions by a direct mechanism that has not yet been established, but eventually by glucose transporters (GLUTs).

 

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Current Issue

Leveraging GPCR signaling in thermogenic fat to counteract metabolic diseases

Olivia Sveidahl Johansen, Tao Ma, Zachary Gerhart-Hines

Background

Thermogenic brown and beige adipocytes are recognized for their unique capacity to consume extraordinary levels of metabolites and lipids from the blood to fuel heat-producing catabolic processes [[1][2][3][4][5][6][7]]. In humans, the functions of thermogenic adipocytes are associated with cardiometabolic protection and improved glycemic control [[8][9][10][11][12][13]]. Consequently, engaging these macronutrient-consuming and energy-dissipating activities has gained attention as a promising therapeutic strategy for counteracting metabolic diseases, such as obesity and diabetes.

Scope of review

In this review, we highlight new advances in our understanding of the physiological role of G protein-coupled receptors (GPCRs) in controlling thermogenic adipocyte biology. We further extend our discussion to the opportunities and challenges posed by pharmacologically targeting different elements of GPCR signaling in these highly specialized fat cells.

Major conclusions

GPCRs represent appealing candidates through which to harness adipose thermogenesis. Yet safely and effectively targeting these druggable receptors on brown and beige adipocytes has thus far proven challenging. Therefore, continued interrogation across the GPCR landscape is necessary for future leaps within the field of thermogenic fat biology to unlock the therapeutic potential of adipocyte catabolism.

Articles in Press

Leveraging GPCR signaling in thermogenic fat to counteract metabolic diseases

Olivia Sveidahl Johansen, Tao Ma, Zachary Gerhart-Hines

Background

Thermogenic brown and beige adipocytes are recognized for their unique capacity to consume extraordinary levels of metabolites and lipids from the blood to fuel heat-producing catabolic processes [[1][2][3][4][5][6][7]]. In humans, the functions of thermogenic adipocytes are associated with cardiometabolic protection and improved glycemic control [[8][9][10][11][12][13]]. Consequently, engaging these macronutrient-consuming and energy-dissipating activities has gained attention as a promising therapeutic strategy for counteracting metabolic diseases, such as obesity and diabetes.

Scope of review

In this review, we highlight new advances in our understanding of the physiological role of G protein-coupled receptors (GPCRs) in controlling thermogenic adipocyte biology. We further extend our discussion to the opportunities and challenges posed by pharmacologically targeting different elements of GPCR signaling in these highly specialized fat cells.

Major conclusions

GPCRs represent appealing candidates through which to harness adipose thermogenesis. Yet safely and effectively targeting these druggable receptors on brown and beige adipocytes has thus far proven challenging. Therefore, continued interrogation across the GPCR landscape is necessary for future leaps within the field of thermogenic fat biology to unlock the therapeutic potential of adipocyte catabolism.

2021 impact factor: 8.568

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