In Vitro Studies Investigating the Effect of Subcutaneous Phosphatidylcholine Injections in the 3T3-L1 Adipocyte Model: Lipolysis or Lipid Dissolution?

Klein, S.; Schreml, Stephan; Nerlich, Michael; Prantl, Lukas

doi:10.1097/prs.0b013e3181adce61

Cited by 44 publications

(46 citation statements)

References 11 publications

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“…These findings suggest that deoxycholate is the primary active ingredient which plays a pivotal role in reduction of adipose tissue. A recent study using an in vitro model demonstrated DOC ability to reduce cell viability as in commercial formulas, not affecting the enzymatic lipolytic pathway (15). Isolated DOC ability to cause adipocyte lysis similar to commercial mixtures has been reported by an observational study on lipomas, showing that a volume reduction was possible using DOC injection alone; in addition, an acute inflammatory response, focal necrosis and haemorrhagic histology could be observed in this area (16).…”

mentioning

confidence: 84%

Effects of Phosphatidylcholine and Sodium Deoxycholate on Human Primary Adipocytes and Fresh Human Adipose Tissue

Palumbo

Melchiorre

et al. 2010

Int J Immunopathol Pharmacol

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Recent studies introduced the novel concept of chemical lipolysis where phosphatidylcholine (PC), an active component of commercial preparations, plays a pivotal role. Other studies suggested that sodium deoxycholate (DOC), an excipient contained in medical preparations, could be the real active component performing an adipocytolytic action. We investigated the effects of PC and DOC on human primary adipocyte cultures and on human fresh adipose tissue. Human adipocytes isolated by Rodbell's method, were cultured onto type I collagen-coated glass coverslips, placed into 24-well tissue culture plates. Cells were incubated with or without DOC (5–7–9%), PC (5%) or DOC/PC mixture and observed under phase contrast microscope. After incubation, cells were stained with Oil Red-O and with acridine orange/ethidium bromide to observe necrotic cells with phase contrast microscope and fluorescent microscope, respectively. Histological specimens from adipose tissue biopsies were observed with phase contrast microscopy and with scanning electron microscopy. To investigate the lipid pattern variability in the different experimental conditions, culture medium obtained from the different treatments was subjected to lipid extraction and subsequently to thin layer chromatography (TLC). Microscopic observation of adipocytes showed that DOC treatment led to a detrimental morphological effect in a dose-dependent manner. PC treatment did not significantly affect adipocyte viability. On the contrary, results from experiments aimed to analyze the effects of PC/DOC combined treatment suggested a PC protective role against the DOC harmful effects on adipocytes. Results indicated that clinical effects, observed in local treatment with pharmaceutical preparation, could be due only to DOC, a detergent inducing nonspecific lysis of cell membranes following adipocyte necrosis. On the other hand, PC could likely be incorporated in the lipid bilayer, thus strongly reducing the disruptive DOC effects.

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mentioning

confidence: 84%

Effects of Phosphatidylcholine and Sodium Deoxycholate on Human Primary Adipocytes and Fresh Human Adipose Tissue

Palumbo

Melchiorre

et al. 2010

Int J Immunopathol Pharmacol

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“…These results suggest that a PPC formulation without SD is sufficient to decompose fat cells. However, Klein et al [22] reported that neither isolated PPC nor deoxycholate induced lipolytic pathways. This discrepancy may reflect differences in the experimental conditions and/or the composition of the PPC formulations.…”

Section: Discussionmentioning

confidence: 99%

Phosphatidylcholine Causes Lipolysis and Apoptosis in Adipocytes through the Tumor Necrosis Factor Alpha-Dependent Pathway

et al. 2017

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A phosphatidylcholine (PPC) formulation has been used to treat cellulite; however, its underlying mechanism of action remains unclear. In this study, we demonstrated that PPC induces lipolysis and apoptosis in adipocytes, and evaluated a possible tumor necrosis factor alpha (TNFα)-dependent pathway, whereby PPC exerts these effects. For in vitro study, fully differentiated 3T3-L1 cells, mouse adipocytes were treated with various concentrations of PPC and cell apoptosis and lipolysis were assayed. For in vivo experiments, mice fed on a high-fat diet for 8 weeks were injected twice to abdominal subcutaneous fat tissues of either vehicle or PPC. We found that PPC induced lipolysis and apoptosis dose-dependently in fully differentiated 3T3-L1 cells. In addition, PPC augmented both expression and release of TNFα in a dose-dependent fashion. Induction of TNFα by PPC was associated with the stimulation of nuclear factor kappa B (NFκB)-mediated transcriptional activity. Small interfering RNA (siRNA)-mediated suppression of NFκB abrogated the effect of PPC on TNFα secretion. Suppression of TNFα with specific siRNA abrogated the effects of PPC on lipolysis and apoptosis. Through in vivo experiments, we demonstrated that PPC injection not only stimulated the local lipolysis and apoptosis, resulting in weight loss, but also induced TNFα mRNA expression and neutrophil infiltration. Furthermore, PPC injection prevented lipogenesis and suppressed the mRNA expression of adipokines (such as adiponectin and leptin), due to the down-sizing of adipocytes. In conclusion, we suggest that PPC induces lipolysis and apoptosis in adipocytes through TNFα-dependent pathways.

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“…However, direct evidence is lacking. Bile acid deoxycholate has no pro-lipolytic activity in 3T3L-1 adipocytes (Klein et al, 2009). Therefore, further studies are needed to decipher the pro-lipolytic effects of bile acids.…”

Section: Bile Acidsmentioning

confidence: 99%

Non-adrenergic control of lipolysis and thermogenesis in adipose tissues

Braun

Oeckl

Westermeier

et al. 2018

Journal of Experimental Biology

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The enormous plasticity of adipose tissues, to rapidly adapt to altered physiological states of energy demand, is under neuronal and endocrine control. In energy balance, lipolysis of triacylglycerols and re-esterification of free fatty acids are opposing processes operating in parallel at identical rates, thus allowing a more dynamic transition from anabolism to catabolism, and vice versa. In response to alterations in the state of energy balance, one of the two processes predominates, enabling the efficient mobilization or storage of energy in a negative or positive energy balance, respectively. The release of noradrenaline from the sympathetic nervous system activates lipolysis in a depot-specific manner by initiating the canonical adrenergic receptor-G s -protein-adenylyl cyclase-cyclic adenosine monophosphate-protein kinase A pathway, targeting proteins of the lipolytic machinery associated with the interface of the lipid droplets. In brown and brite adipocytes, lipolysis stimulated by this signaling pathway is a prerequisite for the activation of non-shivering thermogenesis. Free fatty acids released by lipolysis are direct activators of uncoupling protein 1-mediated leak respiration. Thus, pro-and anti-lipolytic mediators are bona fide modulators of thermogenesis in brown and brite adipocytes. In this Review, we discuss adrenergic and non-adrenergic mechanisms controlling lipolysis and thermogenesis and provide a comprehensive overview of pro-and anti-lipolytic mediators.

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In Vitro Studies Investigating the Effect of Subcutaneous Phosphatidylcholine Injections in the 3T3-L1 Adipocyte Model: Lipolysis or Lipid Dissolution?

Abstract: These results suggest that no enzymatic lipolytic pathway is induced. The decrease in volume after Lipostabil injections is likely attributable to the detergent effect of deoxycholate.

Cited by 44 publications

References 11 publications

Effects of Phosphatidylcholine and Sodium Deoxycholate on Human Primary Adipocytes and Fresh Human Adipose Tissue

Effects of Phosphatidylcholine and Sodium Deoxycholate on Human Primary Adipocytes and Fresh Human Adipose Tissue

Phosphatidylcholine Causes Lipolysis and Apoptosis in Adipocytes through the Tumor Necrosis Factor Alpha-Dependent Pathway

Non-adrenergic control of lipolysis and thermogenesis in adipose tissues

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