Hormone-sensitive lipase is critical mediators of acute exercise-induced regulation of lipolysis in rat adipocytes

Ogasawara, Jun; Nomura, Sadahiro; Rahman, Nazibur; Sakurai, Takeshi; Kizaki, Takako; Izawa, Tetsuya; Ishida, Hideyuki; Haga, Shukoh; Ohno, Hideki

doi:10.1016/j.bbrc.2010.08.026

Cited by 20 publications

(18 citation statements)

References 23 publications

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“…Functional studies on PNPLA2-and LIPE-deficient mice showed that these two enzymes have synergistic effects and they are responsible for more than 95% of TAG hydrolase activity; only PNPLA2, but not LIPE, is activated by CGI-58 [36]. Homozygous nonsense mutations in PNPLA2 impairing both lipase activity and binding to lipid droplets (LD) or CGI-58 were described in patients with an only slightly more severe phenotype, implying that another enzyme, possibly LIPE, may compensate for the complete loss of PNPLA2 function.…”

Section: Discussionmentioning

confidence: 98%

The phenotypic spectrum of neutral lipid storage myopathy due to mutations in the PNPLA2 gene

et al. 2011

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Neutral lipid storage disease is caused by mutations in the CGI-58 or the PNPLA2 genes. Lipid storage can be detected in various cell types including blood granulocytes. While CGI-58 mutations are associated with Chanarin-Dorfman syndrome, a condition characterized by lipid storage and skin involvement (ichthyosis), mutations in the patatin-like phospholipase domain-containing protein 2 gene (PNPLA2) were reported with skeletal and cardiac muscle disease only. We describe clinical, myopathological, magnetic resonance imaging (MRI), and genetic findings of six patients carrying different recessive PNPLA2 mutations. Pulse-chase labeling of control and patient cells with supplementation of clenbuterol, salmeterol, and dexamethasone was performed in vitro. The patients share a recognizable phenotype with prominent shoulder girdle weakness and mild pelvic girdle and distal muscle weakness, with highly elevated creatine kinase (CK) and cardiomyopathy developing at later stages. Muscle histology invariably reveals massive accumulation of lipid droplets. New muscle or whole-body MRI techniques may assist diagnosis and may become a useful tool to quantify intramuscular lipid storage. Four novel and two previously reported mutations were detected, affecting different parts of the PNPLA2 gene. Activation of hormone-sensitive lipase by beta-adrenergic substances such as clenbuterol appears to bypass the enzymatic block in PNPLA2-deficient patient cells in vitro. PNPLA2 deficiency is a slowly progressive myopathy with onset around the third decade. Cardiac involvement is relatively common at a later stage. Muscle MRI may detect increased lipid in a characteristic distribution, which could be used for monitoring disease progression. Beta-adrenergic agents may be beneficial in improving triacylglycerol breakdown in patients with PNPLA2 mutations.

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Section: Discussionmentioning

confidence: 98%

The phenotypic spectrum of neutral lipid storage myopathy due to mutations in the PNPLA2 gene

et al. 2011

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“…Genetic ablation of ATGL and HSL in mice demonstrates that these proteins are important for maintaining FFA availability during exercise, 78 whereas the exercise-induced increase in plasma FFA is normal in Plin1 À/À mice. 79 ATGL Ser-406 phosphorylation in mice 53 and HSL Ser-563 and Ser-660 phosphorylation in rats 80 and humans 81 are increased during moderate intensity exercise, which corresponds to increased epinephrine and plasma FFA levels. One study, to our knowledge, has examined the protein-protein interactions between some key lipolytic proteins and their intracellular localization during exercise.…”

Section: The Cellular Regulation Of Lipolysis During Acute Exercise Imentioning

confidence: 89%

“…Exercise increases HSL abundance at the lipid droplet and its interaction with PLIN1, while CGI-58 concomitantly dissociates from PLIN1. 80 Thus, the limited in vivo studies support components of the lipolytic model outlined for cells, assuming β-adrenergic stimulation models an "exercise" response.…”

Section: The Cellular Regulation Of Lipolysis During Acute Exercise Imentioning

confidence: 95%

Exercise and the Regulation of Adipose Tissue Metabolism

Tsiloulis

Watt

2015

Progress in Molecular Biology and Translational Science

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“…FA mobilization from WAT is regulated by the activity of hormone-sensitive lipase (HSL), monoglyceride lipase (MGL) and adipose triglyceride lipase (ATGL) [39]. Since exercise promotes lipolysis from adipocytes by activating HSL and ATGL [40, 41], exercise-induced hypotrophy of adipocytes is, at least in part, responsible for the reduction of WAT mass in obese individuals. However, it remains uncertain whether endurance exercise regulates adipogenesis by altering adipogenic gene expression.…”

Section: Introductionmentioning

confidence: 99%

Acute exercise regulates adipogenic gene expression in white adipose tissue

Shen¹,

Zhou²,

Jin³

et al. 2016

Biol Sport

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White adipose tissue expansion is associated with both hypertrophy and hyperplasia of adipocytes. Exercise training results in adipocyte hypotrophy by activating lipolysis, but it is poorly understood whether exercise regulates adipogenesis by altering adipogenic gene expression. The purpose of this study was to evaluate the effect of a single bout of swimming exercise on adipogenic gene expression in white adipose tissue (WAT). Male C57BL/6J mice were divided into two groups: a sedentary control group and a 120-minute swimming exercise group. Immediately after acute exercise, adipogenic gene expression in WAT was analysed by RT-PCR, and tdTomato positive cells in WAT from UCP1-cre-tdTomato mice were observed under a confocal microscope. In epididymal white adipose tissue (eWAT), PPARγ2 and C/EBPα expression at the mRNA level was significantly decreased with high induction of Wnt10b and KLFs (KLF2, KLF3, KLF7, KLF6, KLF9 and KLF15), whereas PPARγ2, not C/EBPα, was decreased with high induction of Wnt6 and KLFs (KLF2, KLF3, KLF7, KLF6 and KLF9) in inguinal white adipose tissue (iWAT) after acute exercise. The expression of C/EBPβ and C/EBPδ was upregulated in both WATs with a high level of PGC-1α expression. Expression level of UCP1 was increased only in adipocytes of eWAT, while beige cell specific gene expression was comparable between groups and tdTomato positive cells were not found in WAT of UCP1-cre-tdTomato reporter mouse immediately after acute exercise. These results suggest that acute exercise suppresses adipogenic gene expression and may regulate thermogenesis by activating C/EBPβ, PGC-1α and UCP1 in WAT.

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Hormone-sensitive lipase is critical mediators of acute exercise-induced regulation of lipolysis in rat adipocytes

Cited by 20 publications

References 23 publications

The phenotypic spectrum of neutral lipid storage myopathy due to mutations in the PNPLA2 gene

The phenotypic spectrum of neutral lipid storage myopathy due to mutations in the PNPLA2 gene

Exercise and the Regulation of Adipose Tissue Metabolism

Acute exercise regulates adipogenic gene expression in white adipose tissue

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