Vesicular storage, vesicle trafficking, and secretion of leptin and resistin: the similarities, differences, and interplays

Ye, Feng; Than, Aung; Zhao, Yanying; Goh, Kian Hong.; Chen, Peng

doi:10.1677/joe-10-0090

Cited by 38 publications

(36 citation statements)

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“…The demonstration that manipulation of the transmembrane Cl Ϫ flux causes membrane depolarization has important clinical implications with regard to both the control of the Cadependent functions of white fat adipocytes: lipogenesis (29), lipolysis (17,50), and adipokine secretion such as that of leptin (51). Evidence in support of this idea arises from studies on the use of tamoxifen to treat breast cancer.…”

Section: Resultsmentioning

confidence: 99%

“…Although such manipulations may indeed increase intracellular Ca 2ϩ (29), this effect may not necessarily arise via depolarization of the plasma membrane and voltage-gated Ca 2ϩ influx; an increase in intracellular Ca 2ϩ can also arise through osmotic shrinkage, reverse-mode Na ϩ -Ca 2ϩ exchange, or necrosis. The possible inappropriate use of high extracellular K ϩ to elevate intracellular Ca 2ϩ is especially pertinent when interpreting previous studies that have employed this methodology to investigate the role of intracellular Ca 2ϩ signaling in the physiological functions of white fat adipocytes: insulin-stimulated glucose uptake and lipogenesis (29), ␤-adrenoceptor-mediated lipolysis (17,50), and secretion of various adipokines such as leptin, adiponectin, and resistin (51), especially pertinent events given the clinical importance of understanding the function and physiology of white fat adipocytes in diabesity.…”

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confidence: 99%

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Etiology of the membrane potential of rat white fat adipocytes

Bentley

Pulbutr

Chan

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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The plasma membrane potential (Vm) is key to many physiological processes; however, its ionic etiology in white fat adipocytes is poorly characterized. To address this question, we employed the perforated patch current clamp and cell-attached patch clamp methods in isolated primary white fat adipocytes and their cellular model 3T3-L1. The resting Vm of primary and 3T3-L1 adipocytes were Ϫ32.1 Ϯ 1.2 mV (n ϭ 95) and Ϫ28.8 Ϯ 1.2 mV (n ϭ 87), respectively. Vm was independent of cell size and fat content. Elevation of extracellular K ϩ to 50 mM by equimolar substitution of bath Na ϩ did not affect Vm, whereas substitution of bath Na ϩ with the membrane-impermeant cation N-methyl-D-glucamine ϩ -hyperpolarized Vm by 16 mV, data indicative of a nonselective cation permeability. Substitution of 133 mM extracellular Cl Ϫ with gluconate-depolarized Vm by 25 mV, whereas Cl Ϫ substitution with I Ϫ caused a Ϫ9 mV hyperpolarization. Isoprenaline (10 M), but not insulin (100 nM), significantly depolarized Vm. Single-channel ion activity was voltage independent; currents were indicative for Cl Ϫ with an inward slope conductance of 16 Ϯ 1.3 pS (n ϭ 11) and a reversal potential close to the Cl Ϫ equilibrium potential, Ϫ29 Ϯ 1.6 mV. Although the reduction of extracellular Cl Ϫ elevated the intracellular Ca 2ϩ of adipocytes, this was not as large as that produced by elevation of extracellular K ϩ . In conclusion, the Vm of white fat adipocytes is well described by the Goldman-HodgkinKatz equation with a predominant permeability to Cl Ϫ , where its biophysical and single-channel properties suggest a volume-sensitive anion channel identity. Consequently, changes in serum Cl Ϫ homeostasis or the adipocyte's permeability to this anion via drugs will affect its Vm, intracellular Ca 2ϩ , and ultimately its function and its role in metabolic control. adipocyte; white fat; 3T3-L1 cells; chloride; membrane potential THE PLASMA MEMBRANE POTENTIAL (Vm) is a fundamental biological property for the survival and function of virtually every eukarocytic cell. In excitable tissues of animalia, such as the heart, muscles, and nerves, excursions in Vm in the form of action potentials represent the fastest known biological means of intraorganism communication. The action potential often acts to mediate intracellular signaling; for example, an associated influx of extracellular Ca 2ϩ controls functions as diverse as contraction to secretion. In nonexcitable tissues, subtle changes in Vm are involved in the control of the transmembrane and transcellular fluxes of many solutes. Moreover, the membrane potential per se also has an important role to play in basic cell homoeostasis: the regulation of intracellular ionic composition and the maintenance of osmotic equilibrium. A thorough understanding of the etiology of Vm permits us to accurately control it experimentally, a process that allows us to investigate associated physiological and pathological sequelae.

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Etiology of the membrane potential of rat white fat adipocytes

Bentley

Pulbutr

Chan

et al. 2014

American Journal of Physiology-Endocrinology and Metabolism

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“…Adipocytes (fat cells), the major depots for excess energy, are also active endocrine cells producing a variety of secretory factors (adipocytokines) that play critical roles in regulating metabolic homeostasis (10,65,66). Obesity (excess fat accumulation) is closely associated with various metabolic disorders (67).…”

Section: Discussionmentioning

confidence: 99%

Apelin Attenuates Oxidative Stress in Human Adipocytes

Than

Zhang

Leow

et al. 2014

Journal of Biological Chemistry

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107

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Background: Antioxidant effects of apelin on adipocytes are unknown. Results: Apelin not only suppresses production and release of reactive oxygen species, but also relieves oxidative-stress induced cellular dysfunctions in adipocytes. Conclusion: Apelin-APJ signaling acts as the negative autocrine feedbacks against oxidative stress in adipocytes. Significance: Apelin signaling may serve as a potential therapeutic target for metabolic disorders.

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“…We demonstrate that adipocyte lipase activities, specifi cally ATGL and, to a lesser extent, HSL, are involved in the regulated secretion of aP2, and genetic deletion or chemical inhibition of these enzymes dramatically diminishes aP2 secretion from adipocytes. It has been reported in various systems that cAMP signaling positively regulates classical and nonclassical hormone secretion (50)(51)(52)(53). However, induction of hormone secretion has not previously been associated with specifi c lipase activity or free fatty acid availability in adipocytes and has not been linked to aP2 secretion.…”

Section: Downloaded Frommentioning

confidence: 99%

Secretion of fatty acid binding protein aP2 from adipocytes through a nonclassical pathway in response to adipocyte lipase activity

Ertunc

Sikkeland

Fenaroli

et al. 2015

Journal of Lipid Research

128

172

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Journal of Lipid Research Volume 56, 2015 423Adipose tissue is an endocrine organ whose products orchestrate the metabolic functions of various tissues, including brain, pancreas, and liver, to maintain systemic homeostasis. Adipocytes respond to metabolic and immune cues by mobilizing their fat stores through lipolysis and by secreting a variety of hormones and cytokines ( 1, 2 ). Such signals converge on target tissues, for example on liver to regulate glucose production, and on ␤ cells to modulate insulin production. A critical molecule for the integration of adipocyte biology with systemic metabolic regulation is aP2 [fatty acid binding protein (FABP) 4], a lipid binding protein that is upregulated during differentiation of adipocytes and upon macrophage activation ( 3, 4 ). Since its identifi cation, aP2 has been studied primarily for its intracellular functions in lipid metabolism and infl ammation ( 3,4 ). Genetic deletion models demonstrated that this FABP plays a critical role in the pathogenesis of several chronic metabolic diseases, including diabetes, atherosclerosis, and fatty liver. Mice defi cient in aP2 or aP2 and the related protein FABP5/mal1 together have improved adipose and liver function, increased insulin sensitivity, and reduced fatty liver and cardiovascular disease in the context of high-fat diet and genetic mouse models of obesity and atherosclerosis ( 5-12 ). The link between aP2 and metabolic disease is also supported by genetic association studies in multiple populations demonstrating metabolic and cardiovascular benefi ts in individuals carrying a rare haploinsuffi ciency mutation in the aP2 locus, validating the relevance of this pathway in human disease ( 13,14 ).

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Vesicular storage, vesicle trafficking, and secretion of leptin and resistin: the similarities, differences, and interplays

Cited by 38 publications

References 50 publications

Etiology of the membrane potential of rat white fat adipocytes

Etiology of the membrane potential of rat white fat adipocytes

Apelin Attenuates Oxidative Stress in Human Adipocytes

Secretion of fatty acid binding protein aP2 from adipocytes through a nonclassical pathway in response to adipocyte lipase activity

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