Leveraging GPCR signaling in thermogenic fat to counteract metabolic diseases

Research output: Contribution to journalReviewpeer-review

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Leveraging GPCR signaling in thermogenic fat to counteract metabolic diseases. / Sveidahl Johansen, Olivia; Ma, Tao; Gerhart-Hines, Zachary.

In: Molecular Metabolism, Vol. 60, 101474, 2022.

Research output: Contribution to journalReviewpeer-review

Harvard

Sveidahl Johansen, O, Ma, T & Gerhart-Hines, Z 2022, 'Leveraging GPCR signaling in thermogenic fat to counteract metabolic diseases', Molecular Metabolism, vol. 60, 101474. https://doi.org/10.1016/j.molmet.2022.101474

APA

Sveidahl Johansen, O., Ma, T., & Gerhart-Hines, Z. (2022). Leveraging GPCR signaling in thermogenic fat to counteract metabolic diseases. Molecular Metabolism, 60, [101474]. https://doi.org/10.1016/j.molmet.2022.101474

Vancouver

Sveidahl Johansen O, Ma T, Gerhart-Hines Z. Leveraging GPCR signaling in thermogenic fat to counteract metabolic diseases. Molecular Metabolism. 2022;60. 101474. https://doi.org/10.1016/j.molmet.2022.101474

Author

Sveidahl Johansen, Olivia ; Ma, Tao ; Gerhart-Hines, Zachary. / Leveraging GPCR signaling in thermogenic fat to counteract metabolic diseases. In: Molecular Metabolism. 2022 ; Vol. 60.

Bibtex

@article{f402043a27594c249b2241e1a829bb74,
title = "Leveraging GPCR signaling in thermogenic fat to counteract metabolic diseases",
abstract = "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 [1–7]. In humans, the functions of thermogenic adipocytes are associated with cardiometabolic protection and improved glycemic control [8–13]. 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.",
keywords = "Brown adipose tissue, Cell signaling, Diabetes, Energy expenditure, G protein-coupled receptor, Obesity",
author = "{Sveidahl Johansen}, Olivia and Tao Ma and Zachary Gerhart-Hines",
note = "Publisher Copyright: {\textcopyright} 2022 The Author(s)",
year = "2022",
doi = "10.1016/j.molmet.2022.101474",
language = "English",
volume = "60",
journal = "Molecular Metabolism",
issn = "2212-8778",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Leveraging GPCR signaling in thermogenic fat to counteract metabolic diseases

AU - Sveidahl Johansen, Olivia

AU - Ma, Tao

AU - Gerhart-Hines, Zachary

N1 - Publisher Copyright: © 2022 The Author(s)

PY - 2022

Y1 - 2022

N2 - 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 [1–7]. In humans, the functions of thermogenic adipocytes are associated with cardiometabolic protection and improved glycemic control [8–13]. 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.

AB - 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 [1–7]. In humans, the functions of thermogenic adipocytes are associated with cardiometabolic protection and improved glycemic control [8–13]. 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.

KW - Brown adipose tissue

KW - Cell signaling

KW - Diabetes

KW - Energy expenditure

KW - G protein-coupled receptor

KW - Obesity

U2 - 10.1016/j.molmet.2022.101474

DO - 10.1016/j.molmet.2022.101474

M3 - Review

C2 - 35339729

AN - SCOPUS:85128545982

VL - 60

JO - Molecular Metabolism

JF - Molecular Metabolism

SN - 2212-8778

M1 - 101474

ER -

ID: 305686546