Several agents and pathways regulate lipolysis in adipocytes

Chaves, Valéria Ernestânia; Frasson, Danúbia; Kawashita, Nair Honda

doi:10.1016/j.biochi.2011.05.018

Cited by 95 publications

(73 citation statements)

References 125 publications

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“…Increased cAMP levels could be the consequence of increased adenylyl cyclase activity or reduced cAMP degradation (mainly mediated by PDE3B action). It is wellestablished that the stimulation of G s -coupled receptors induces the activation of adenylyl cyclase, leading to increased intracellular cAMP levels and subsequent activation of PKA and phosphorylation and translocation of HSL to fat droplets ( 23,24 ). Here, we demonstrate that CT-1 increased the levels of G s ␣ without affecting Gi, the inhibitory protein of adenylyl cyclase.…”

Section: In Vivo Effects Of Rct-1 Treatment On Hsl Perilipin Atgl mentioning

confidence: 52%

Cardiotrophin-1 stimulates lipolysis through the regulation of main adipose tissue lipases

López-Yoldi

Fernández‐Galilea

Laiglesia

et al. 2014

Journal of Lipid Research

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This article is available online at http://www.jlr.org effects by interacting with the glycoprotein 130 (gp130)/ leukemia inhibitory factor receptor heterodimer ( 1 ). Adipose tissue has been identifi ed as a source of CT-1 ( 2 ), and this cytokine is capable of activating major signaling pathways involved in metabolic control in adipocytes ( 3 ). Moreover, it has been reported that CT-1 levels are raised in obesity and metabolic syndrome ( 2 ), suggesting that CT-1 could be a new marker for obesity and related diseases. A recent study by our group has revealed that CT-1 is a key regulator of energy homeostasis, as well as of glucose and lipid metabolism ( 4 ). Thus, chronic recombinant CT-1 (rCT-1) treatment reduced body weight and corrected insulin resistance in ob/ob and high-fat-fed obese mice by reducing food intake and enhancing energy expenditure. Moreover, rCT-1 induced dramatic white adipose tissue remodeling characterized by the upregulation of genes implicated in the control of fatty acid oxidation, mitochondrial biogenesis, and lipolysis. In this context, it has been reported that adipocytes from rCT-1-treated mice exhibited an increased lipolytic response to isoproterenol, while adipocytes from old obese CT-1 -null mice responded poorly to isoproterenol, suggesting that CT-1 might play a role in the regulation of lipolysis ( 4 ). However, the mechanism underlying the lipolytic action of CT-1 still remains unknown.During lipolysis, intracellular triacylglycerol (TAG) is hydrolyzed through the consecutive action of three major lipases: adipose triglyceride lipase (ATGL/desnutrin), Abbreviations: AdPLA , adipocyte phospholipase A2; AICAR, aminoimidazole carboxamide ribonucleotide; ATGL, adipose triglyceride lipase (desnutrin); CGI-58, comparative gene identifi cation-58; cGMP, cyclic guanosine monophosphate; CT-1, cardiotrophin-1; DAG, diacylglycerol; Gi, inhibitory guanine nucleotide binding protein; gp130, glycoprotein 130; Gs, stimulatory guanine nucleotide binding protein; G0S2, G0/G1 switch gene 2; HPTLC, high-performance TLC; HSL, hormone sensitive lipase; IL, interleukin; MAG, monoacylglycerol; PDE3B, phosphodiesterase 3B; PK, protein kinase; rCT-1, recombinant cardiotrophin-1; TAG, triacylglycerol. 1 M. Bustos and M. J. Moreno-Aliaga contributed equally to the work.

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Section: In Vivo Effects Of Rct-1 Treatment On Hsl Perilipin Atgl mentioning

confidence: 52%

Cardiotrophin-1 stimulates lipolysis through the regulation of main adipose tissue lipases

López-Yoldi

Fernández‐Galilea

Laiglesia

et al. 2014

Journal of Lipid Research

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“…Akt also regulates several lipogenic enzymes, including the activation of the acetyl-CoA carboxylase (Berggreen et al 2009), the ratelimiting enzyme of FA synthesis. Given that Akt is a chief element of INS signaling (Caruso & Sheridan 2011), it is through Akt that INS exerts its lipogenic and antilipolytic actions (Albalat et al 2005, Chaves et al 2011). The present findings suggest that by reducing the activation of Akt, GH shifts the balance of the antilipolysis/lipogenesislipolysis antagonism toward lipolysis by suppressing antilipolytic/lipogenic processes.…”

Section: Figurementioning

confidence: 99%

“…By contrast, insulin (INS) is lipogenic in mammals and fish as well as directly antilipolytic (via dephosphorylation of HSL) (Harmon et al 1993, Albalat et al 2007, Chaves et al 2011. The effects of GH define on lipid metabolism are complex, and short-term INS-like (antilipolytic) and long-term anti-INS-like (lipolytic) effects have been reported in mammals (Carrel & Allen 2000, Chaves et al 2011. INS-like effects can be observed in adipose tissue not exposed to GH previously (i.e.…”

Section: Introductionmentioning

confidence: 99%

PKC and ERK mediate GH-stimulated lipolysis

Bergan

Kittilson

Sheridan

2013

Journal of Molecular Endocrinology

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GH regulates several physiological processes in vertebrates, including the promotion of growth, an anabolic process, and the mobilization of stored lipids, a catabolic process. In this study, we used hepatocytes isolated from rainbow trout (Oncorhynchus mykiss) as a model to examine the mechanism of GH action on lipolysis. GH stimulated lipolysis as measured by increased glycerol release in both a time-and a concentration-related manner. The promotion of lipolysis was accompanied by GH-stimulated phosphorylation of the lipolytic enzyme hormone-sensitive lipase (HSL). GH-stimulated lipolysis was also manifested by an increased expression of the two HSL-encoding mRNAs, HSL1 and HSL2. The signaling pathways that underlie GH-stimulated lipolysis were also studied. GH resulted in the activation of phospholipase C (PLC)/protein kinase C (PKC) and the MEK/ERK pathway, whereas JAK-STAT and the PI3K-Akt pathway were deactivated. The blockade of PLC/PKC and the MEK/ERK pathway inhibited GH-stimulated lipolysis and GH-stimulated phosphorylation of HSL as well as GH-stimulated HSL mRNA expression, whereas the blockade of JAK-STAT or the PI3K-Akt pathway had no effect on the activation of lipolysis or the expression of HSL stimulated by GH. These results indicate that GH promotes lipolysis by activating HSL and by enhancing the de novo expression of HSL mRNAs via the activation of PKC and ERK. These findings also suggest molecular mechanisms for activating the lipid catabolic actions of GH while simultaneously deactivating anabolic processes such as antilipolysis and the growth-promoting actions of GH.

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“…NEFAs taken up by fatty acid translocase (CD36) or fatty acid transport protein (FATP1) in adipose tissue are either transported into the mitochondria by carnitine palmitoyl transferase I (CPTI) to be oxidized, or are reesterified with glyceride-glycerol and stored as triglycerides for later use (Reshef et al, 2003;Gertow et al, 2004;Doh et al, 2005;Schwenk et al, 2010). As they are responsive to changes in circulating hormones as well as to changes in nutritional state, intracellular lipases such as hormone-sensitive lipase (HSL) or adipose triglyceride lipase (ATGL) can be activated to readily make NEFA available when an organism's energetic demands increase (Chaves et al, 2011;Reshef et al, 2003;Bertile and Raclot, 2011), such as with fasting. Hormones such as apelin and insulin can inhibit lipolysis by preventing lipase activation within adipocytes.…”

Section: Introductionmentioning

confidence: 99%

Decreased expression of adipose CD36 and FATP1 are associated with increased plasma non-esterified fatty acids during prolonged fasting in northern elephant seal pups (Mirounga angustirostris)

Viscarra

Vázquez‐Medina

Rodríguez

et al. 2012

Journal of Experimental Biology

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SUMMARYThe northern elephant seal pup (Mirounga angustirostris) undergoes a 2-3month post-weaning fast, during which it depends primarily on the oxidation of fatty acids to meet its energetic demands. The concentration of non-esterified fatty acids (NEFAs) increases and is associated with the development of insulin resistance in late-fasted pups. Furthermore, plasma NEFA concentrations respond differentially to an intravenous glucose tolerance test (ivGTT) depending on fasting duration, suggesting that the effects of glucose on lipid metabolism are altered. However, elucidation of the lipolytic mechanisms including lipase activity during prolonged fasting in mammals is scarce. To assess the impact of fasting and glucose on the regulation of lipid metabolism, adipose tissue and plasma samples were collected before and after ivGTTs performed on early (2weeks, N5) and late (6-8weeks; N8) fasted pups. Glucose administration increased plasma triglycerides and NEFA concentrations in late-fasted seals, but not plasma glycerol. Fasting decreased basal adipose lipase activity by 50%. Fasting also increased plasma lipase activity twofold and decreased the expressions of CD36, FAS, FATP1 and PEPCK-C by 22-43% in adipose tissue. Plasma acylcarnitine profiling indicated that late-fasted seals display higher incomplete LCFA -oxidation. Results suggest that long-term fasting induces shifts in the regulation of lipolysis and lipid metabolism associated with the onset of insulin resistance in northern elephant seal pups. Delineation of the mechanisms responsible for this shift in regulation during fasting can contribute to a more thorough understanding of the changes in lipid metabolism associated with dyslipidemia and insulin resistance in mammals.

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Several agents and pathways regulate lipolysis in adipocytes

Cited by 95 publications

References 125 publications

Cardiotrophin-1 stimulates lipolysis through the regulation of main adipose tissue lipases

Cardiotrophin-1 stimulates lipolysis through the regulation of main adipose tissue lipases

PKC and ERK mediate GH-stimulated lipolysis

Decreased expression of adipose CD36 and FATP1 are associated with increased plasma non-esterified fatty acids during prolonged fasting in northern elephant seal pups (Mirounga angustirostris)

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