Compartmentalization of cAMP Signaling in Adipogenesis, Lipogenesis, and Lipolysis

Rogne, Marie; Taskén, Kjetil

doi:10.1055/s-0034-1389955

Cited by 57 publications

(57 citation statements)

References 61 publications

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“…Conventionally, lipolysis is initiated by β-adrenergic receptor activation of Gαs and adenyl cyclase (Carey, 1998). The resulting rise in cAMP activates protein kinase A (PKA) which then phosphorylates a series of substrates including hormone sensitive lipase (HSL), perilipin (PLIN) and cAMP response element-binding protein (CREB) (Rogne and Taskén, 2014). These changes provide a signature for lipolysis pathway activation in immunoblots from cultured adipocytes.…”

Section: White Adipocyte Opn3 Is Required For Normal Lipolysis Duringmentioning

confidence: 99%

Adaptive thermogenesis in mice requires adipocyte light-sensing via Opsin 3

Nayak

Vemaraju

Zhang

et al. 2019

Preprint

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Almost all life forms can decode light information for adaptive advantage. Examples include the visual system, where photoreceptor signals are interpreted as images, and the circadian system, where light entrains a physiological clock. Here we describe a local, nonvisual light response in mice that employs encephalopsin (OPN3, a 480 nm, blue light responsive opsin) to regulate the function of adipocytes. Germ line null and adipocytespecific conditional null mice show a deficit in thermogenesis that is phenocopied in mice under blue-light deficient conditions. We show that blue light stimulation of adipocytes activates hormone sensitive lipase, the rate limiting enzyme in the lipolysis pathway, and that this is OPN3-dependent. Opn3 adipocyte conditional null mice also use reduced levels of fat mass when fasted and cold exposed further suggesting a lipolysis deficit. These data suggest the hypothesis that in mice, a local, OPN3-dependent light response in adipocytes is a mechanism for regulation of energy homeostasis.

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Section: White Adipocyte Opn3 Is Required For Normal Lipolysis Duringmentioning

confidence: 99%

Adaptive thermogenesis in mice requires adipocyte light-sensing via Opsin 3

Nayak

Vemaraju

Zhang

et al. 2019

Preprint

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“…Consequently, the release of incretins and insulin is induced in enteroendocrine cells and pancreatic β cells, respectively . The cAMP signaling pathway is very important in the regulation of adipogenesis and lipolysis in white adipose tissue and lipid metabolism in liver . The cAMP‐dependent Protein Kinase A (PKA) activation directly phosphorylates serine residues of liver X‐receptor (LXR)‐α and subsequently inhibits LXRα‐induced SREBP‐1c expression in both primary hepatocytes and liver tissues .…”

Section: Pharmacological Applications Of Gpr119 Ligandsmentioning

confidence: 99%

Therapeutic application of GPR119 ligands in metabolic disorders

Yang

Kim

Choi

et al. 2017

Diabetes Obesity Metabolism

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GPR119 belongs to the G protein-coupled receptor family and exhibits dual modes of action upon ligand-dependent activation: pancreatic secretion of insulin in a glucose-dependent manner and intestinal secretion of incretins. Hence, GPR119 has emerged as a promising target for treating type 2 diabetes mellitus without causing hypoglycaemia. However, despite continuous efforts by many major pharmaceutical companies, no synthetic GPR119 ligand has been approved as a new class of anti-diabetic agents thus far, nor has any passed beyond phase II clinical studies. Herein, we summarize recent advances in research concerning the physiological/pharmacological effects of GPR119 and its synthetic ligands on the regulation of energy metabolism, and we speculate on future applications of GPR119 ligands for the treatment of metabolic diseases, focusing on non-alcoholic fatty liver disease.

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“…In addition to Drp1, PKA can also phosphorylate mitofusin 2 (Mfn2) [63] and bind to optic atrophy 1 (OPA1) [64, 65]. Both Mfn2 and OPA1 are involved in mitochondrial fusion [9].…”

Section: Camp Signaling In the Outer-mitochondrial Compartment (Fig 2)mentioning

confidence: 99%

Mitochondrial cAMP signaling

Zhang

et al. 2016

Cell. Mol. Life Sci.

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Cyclic adenosine 3, 5′-monophosphate (cAMP) is a ubiquitous second messenger regulating many biological processes, such as cell migration, differentiation, proliferation and apoptosis. cAMP signaling functions not only on the plasma membrane, but also in the nucleus and in organelles such as mitochondria. Mitochondrial cAMP signaling is an indispensable part of the cytoplasm-mitochondrion crosstalk that maintains mitochondrial homeostasis, regulates mitochondrial dynamics, and modulates cellular stress responses and other signaling pathways. Recently, the compartmentalization of mitochondrial cAMP signaling has attracted great attentions. This new input should be carefully taken into account when we interpret the findings of mitochondrial cAMP signaling. In this review, we summarize previous and recent progress in our understanding of mitochondrial cAMP signaling, including the components of the signaling cascade, and the function and regulation of this signaling pathway in different mitochondrial compartments.

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Compartmentalization of cAMP Signaling in Adipogenesis, Lipogenesis, and Lipolysis

Cited by 57 publications

References 61 publications

Adaptive thermogenesis in mice requires adipocyte light-sensing via Opsin 3

Adaptive thermogenesis in mice requires adipocyte light-sensing via Opsin 3

Therapeutic application of GPR119 ligands in metabolic disorders

Mitochondrial cAMP signaling

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