Alpha-lipoic acid induces adipose triglyceride lipase expression and decreases intracellular lipid accumulation in HepG2 cells

Kuo, Yung Ting; Lin, Ting; Chen, Wei Lu; Lee, Horng Mo

doi:10.1016/j.ejphar.2012.07.028

Cited by 44 publications

(32 citation statements)

References 38 publications

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“…Another explanation for the beneficial effect of LA in preventing apoptosis in hepatocytes is its capacity for reducing intracellular lipid accumulation [76] also observed under our experimental conditions. In fact, our data show for the first time that LA is able to decrease PA upake by decreasing CD36/FAT levels and lipogenic gene expression, as well as increase fatty acid oxidation in hepatocytes.…”

Section: Discussionmentioning

confidence: 62%

Essential role of Nrf2 in the protective effect of lipoic acid against lipoapoptosis in hepatocytes

Valdecantos

Prieto-Hontoria

Pardo

et al. 2015

Free Radical Biology and Medicine

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Section: Discussionmentioning

confidence: 62%

Essential role of Nrf2 in the protective effect of lipoic acid against lipoapoptosis in hepatocytes

Valdecantos

Prieto-Hontoria

Pardo

et al. 2015

Free Radical Biology and Medicine

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“…As noted above, ATGL is the rate limiting enzyme in the lipolytic cascade and a decrease in expression of ATGL and HSL is associated with insulin-resistance and obesity [159]. FOXO1 binds to the promoter region of ATGL thereby increasing ATGL expression and promoting lipolysis in 3T3L-1 cells, and conversely, its knockdown diminishes both basal and isoproterenol-stimulated lipolysis [47].…”

Section: Possible Non-sns Lipid Mobilization From Watmentioning

confidence: 99%

Neural innervation of white adipose tissue and the control of lipolysis

Bartness

Liu

Shrestha

et al. 2014

Frontiers in Neuroendocrinology

272

263

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White adipose tissue (WAT) is innervated by the sympathetic nervous system (SNS) and its activation is necessary for lipolysis. WAT parasympathetic innervation is not supported. Fully-executed SNS-norepinephrine (NE)-mediated WAT lipolysis is dependent on β-adrenoceptor stimulation ultimately hinging on hormone sensitive lipase and perilipin A phosphorylation. WAT sympathetic drive is appropriately measured by electrophysiological and neurochemical (NE turnover) in non-human animals and this drive is fat pad-specific preventing generalizations among WAT depots and non-WAT organs. Leptin-triggered SNS-mediated lipolysis is weakly supported, whereas insulin or adenosine inhibition of SNS/NE-mediated lipolysis is strongly supported. In addition to lipolysis control, increases or decreases in WAT SNS drive/NE inhibit and stimulate white adipocyte proliferation, respectively. WAT sensory nerves are of spinal-origin and sensitive to local leptin and increases in sympathetic drive, the latter implicating lipolysis. Transsynaptic viral tract tracer use revealed WAT central sympathetic and sensory circuits including SNS-sensory feedback loops that may control lipolysis.

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“…ATGL expression increases during food deprivation in humans, rats, and seals [21, 23, 32] and so is likely responsible for the increased circulating FFA concentration during fasting. AMP-activated protein kinase (AMPk) activity has also been reported to increase with fasting in rats and elephant seals [19, 33, 34], and because its upregulation increases ATGL expression in vitro [35, 36], it is likely responsible for the increased ATGL expression in vivo during prolonged fasting. Though its affinity for TAG molecules is much less than that of ATGL, HSL is capable of hydrolyzing TAG, DAG, and MAG molecules [37].…”

Section: Mechanisms Regulating Substrate Availabilitymentioning

confidence: 99%

Cellular mechanisms regulating fuel metabolism in mammals: Role of adipose tissue and lipids during prolonged food deprivation

Viscarra

Ortiz

2013

Metabolism

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Food deprivation in mammals results in profound changes in fuel metabolism and substrate regulation. Among these changes are decreased reliance on the counter-regulatory dynamics by insulin-glucagon due to reduced glucose utilization, and increased concentrations of lipid substrates in plasma to meet the energetic demands of peripheral tissues. As the primary storage site of lipid substrates, adipose tissue must then be a primary contributor to the regulation of metabolism in food deprived states. Through its regulation of lipolysis, adipose tissue influences the availability of carbohydrate, lipid, and protein substrates. Additionally, lipid substrates can act as ligands to various nuclear receptors (retinoid x receptor (RXR), liver x receptor (LXR), and peroxisome proliferator-activated receptor (PPAR)) and exhibit prominent regulatory capabilities over the expression of genes involved in substrate metabolism within various tissues. Therefore, through its control of lipolysis, adipose tissue also indirectly regulates the utilization of metabolic substrates within peripheral tissues. In this review, these processes are described in greater detail and the extent to which adipose tissue and lipid substrates regulate metabolism in food deprived mammals is explored with comments on future directions to better assess the contribution of adipose tissue to metabolism.

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Alpha-lipoic acid induces adipose triglyceride lipase expression and decreases intracellular lipid accumulation in HepG2 cells

Cited by 44 publications

References 38 publications

Essential role of Nrf2 in the protective effect of lipoic acid against lipoapoptosis in hepatocytes

Essential role of Nrf2 in the protective effect of lipoic acid against lipoapoptosis in hepatocytes

Neural innervation of white adipose tissue and the control of lipolysis

Cellular mechanisms regulating fuel metabolism in mammals: Role of adipose tissue and lipids during prolonged food deprivation

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