Lipolysis Response to Endoplasmic Reticulum Stress in Adipose Cells

Deng, Jingna; Liu, Shangxin; Zou, Liangqiang; Xu, Chong; Geng, Bin; Gao, Xu

doi:10.1074/jbc.m111.299115

Cited by 111 publications

(102 citation statements)

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“…In this context, our data show that incubation with the JNK inhibitor SP600125 (2 h) stimulates the phosphorylation of HSL at Ser 563 and Ser 660 as well as phospho-PKA substrate/perilipin ratio, supporting the idea that JNK inhibition leads to increased lipolysis. However, our current data and previous studies show that the amount of glycerol released into the media is not modifi ed or even reduced by longer-term incubation with SP600125 ( 41,50 ), suggesting that the effects of JNK inhibition on lipolysis might be time dependent. Our results demonstrated that LA induced a time-dependent inhibition of JNK phosphorylation, which might suggest the Supplemental Material can be found at: ( 13,61 ).…”

mentioning

confidence: 41%

Effects of lipoic acid on lipolysis in 3T3-L1 adipocytes

Fernández‐Galilea

Pérez-Matute

Prieto-Hontoria

et al. 2012

Journal of Lipid Research

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This article is available online at http://www.jlr.org properties. In fact, LA is able to directly scavenge reactive oxygen species (ROS) and regenerate endogenous antioxidants, such as glutathione and vitamins E and C ( 1, 2 ). Moreover, several studies have described potential beneficial effects of LA on obesity and its associated comorbidities, such as insulin resistance, type 2 diabetes, or fatty liver diseases. Thus, in rodents LA has been shown to cause profound weight loss by reducing food intake and enhancing energy expenditure ( 3 ) as well as by inducing a reduction on intestinal sugar absorption ( 4 ). More recently, two clinical trials in humans reported that LA caused signifi cant reductions of body weight, body mass index, blood pressure, and abdominal circumference in obese subjects ( 5, 6 ). LA also improved insulin sensitivity and plasma lipid profi le possibly through amelioration of oxidative stress and chronic infl ammatory status in obese patients with impaired glucose tolerance ( 7 ). Previous studies have provided strong evidence that LA is able to deeply affect adipose tissue development and function by the inhibition of adipogenesis ( 8 ), the regulation of the secretion of several adipokines such as leptin ( 9 ) and apelin ( 10 ), and by the promotion of mitochondrial biogenesis ( 11 ).In this context, previous studies suggested that LA seems to stimulate the lipolytic response in an in vitro model of broiler chicken adipocytes ( 12 ). However, the molecular mechanisms that mediate these effects remain unclear. Lipolysis is a complex process that is highly regulated and Lipoic acid (LA), or 1,2-dithiolane-3-pentaenoic acid, is a naturally occurring compound that contains two thiol groups with diverse benefi cial effects on health. The biological effects of LA were primarily associated with its antioxidant This work was supported, in part,

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mentioning

confidence: 41%

Effects of lipoic acid on lipolysis in 3T3-L1 adipocytes

Fernández‐Galilea

Pérez-Matute

Prieto-Hontoria

et al. 2012

Journal of Lipid Research

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“…as obesity and diabetes, where increased lipolysis occurs in parallel to activation of PKA and HSL phosphorylation at Ser563, Ser660 (31). Based on our observations, HSL and its upstream modulators PKA and MAPK were all suppressed under severe and acute traumatic stress conditions, yet we still observed augmented lipolysis and even more severe …”

Section: Discussionmentioning

confidence: 64%

Alternative Mechanism for White Adipose Tissue Lipolysis after Thermal Injury

Patsouris

Sadri

et al. 2015

Mol Med

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Extensively burned patients often suffer from sepsis, a complication that enhances postburn hypermetabolism and contributes to increased incidence of multiple organ failure, morbidity and mortality. Despite the clinical importance of burn sepsis, the molecular and cellular mechanisms of such infection-related metabolic derangements and organ dysfunction are still largely unknown. We recently found that upon endoplasmic reticulum (ER) stress, the white adipose tissue (WAT) interacts with the liver via inflammatory and metabolic signals leading to profound hepatic alterations, including hepatocyte apoptosis and hepatic fatty infiltration. We therefore hypothesized that burn plus infection causes an increase in lipolysis of WAT after major burn, partially through induction of ER stress, contributing to hyperlipidemia and profound hepatic lipid infiltration. We used a two-hit rat model of 60% total body surface area scald burn, followed by intraperitoneal (IP) injection of Pseudomonas Aeruginosa-derived lipopolysaccharide (LPS) 3 d postburn. One day later, animals were euthanized and liver and epididymal WAT (EWAT) samples were collected for gene expression, protein analysis and histological study of inflammasome activation, ER stress, apoptosis and lipid metabolism. Our results showed that burn plus LPS profoundly increased lipolysis in WAT associated with significantly increased hepatic lipid infiltration. Burn plus LPS augmented ER stress by upregulating CHOP and activating ATF6, inducing NLRP3 inflammasome activation and leading to increased apoptosis and lipolysis in WAT with a distinct enzymatic mechanism related to inhibition of AMPK signaling. In conclusion, burn sepsis causes profound alterations in WAT and liver that are associated with changes in organ function and structure.

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“…Additionally, ER stress has been shown to induce an intracellular inflammatory cascade and insulin resistance in adipocytes [15] . Our work and other previous studies have shown that ER stress can trigger lipolysis in cultured adipocytes [9,16] . This information suggests that ER stress may be one key pathway leading to metabolic disease states.…”

Section: Introductionmentioning

confidence: 75%

“…The activation of protein kinase A (PKA) and mitogenactivated protein kinase (MAPK) [16] has been shown to be involved in the activation of lipolysis signaling, and we therefore evaluated the activity of these kinases in the tissue samples. As shown in Figure 3D1 and 3D2, the phosphorylation of PKA and MAPK was significantly increased, indicating that these kinases were activated in CKD.…”

Section: Enhanced Lipolysis In White Adipose Tissue In Rrm Ratsmentioning

confidence: 99%

The effect of inhibition of endoplasmic reticulum stress on lipolysis in white adipose tissue in a rat model of chronic kidney disease

et al. 2014

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Aim: Lipolysis in fat tissue plays an important role in the development of metabolic disturbances, a characteristic feature of chronic kidney disease (CKD). In the present study, we tested the hypothesis that the inhibition of endoplasmic reticulum (ER) stress could alleviate lipolysis in white adipose tissue in a rat model of CKD. Methods: A rat model of CKD was established by a method of reduced renal mass (RRM). Lipolysis was measured as the release of glycerol in ex vivo fat pads and cultured primary adipocytes. The activity of lipases and markers of ER stress were measured by Western blotting and immunoprecipitation. Results: Our data showed that lipolysis in visceral white adipose tissue was increased in RRM rats compared with control rats. In addition, increased phosphorylation of hormone-sensitive lipase (HSL) and binding of adipose triglyceride lipase (ATGL) to comparative gene identification-58 (CGI-58) protein were observed in the RRM rats. The phosphorylation of ER stress markers, including IRE1α, PERK, and eukaryotic initiation factor (eIF) 2α, and the expression of ER stress marker 78 kDa glucose-regulated protein (GRP78) were significantly increased in RRM rats. Treatment with an inhibitor of ER stress partially but significantly alleviated lipolysis, and this alleviation was accompanied by reduced binding of ATGL to CGI-58. Conclusion: Our results showed that enhanced lipolysis and ER stress occurred in visceral white adipose tissue in a rat model of CKD. Moreover, inhibition of ER stress significantly alleviated lipolysis. These findings suggest that ER stress is a potential therapeutic target for the metabolic disturbances associated with CKD.

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Lipolysis Response to Endoplasmic Reticulum Stress in Adipose Cells

Cited by 111 publications

References 50 publications

Effects of lipoic acid on lipolysis in 3T3-L1 adipocytes

Effects of lipoic acid on lipolysis in 3T3-L1 adipocytes

Alternative Mechanism for White Adipose Tissue Lipolysis after Thermal Injury

The effect of inhibition of endoplasmic reticulum stress on lipolysis in white adipose tissue in a rat model of chronic kidney disease

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