Lipases in Cachexia

Arner, Peter

doi:10.1126/science.1209418

Cited by 33 publications

(51 citation statements)

References 11 publications

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“…This aspect was not evident in the WSC patients. AT atrophy induced by cachexia has been consistently demonstrated in both patients7, 33 and animal models 9, 34. In CC, longitudinal investigation has suggested that fat loss is not only due to loss of adipocyte volume (lipolysis)29, 34, 35 but also may be attributed to a decrease in lipid accretion in these cells,36 both resulting in a smaller cell 37.…”

Section: Discussionmentioning

confidence: 99%

Cachexia-associated adipose tissue morphological rearrangement in gastrointestinal cancer patients

Batista

Henriques

Neves

et al. 2015

Journal of Cachexia, Sarcopenia and Muscle

106

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Background and aimsCachexia is a syndrome characterized by marked involuntary loss of body weight. Recently, adipose tissue (AT) wasting has been shown to occur before the appearance of other classical cachexia markers. We investigated the composition and rearrangement of the extracellular matrix, adipocyte morphology and inflammation in the subcutaneous AT (scAT) pad of gastrointestinal cancer patients.MethodsSurgical biopsies for scAT were obtained from gastrointestinal cancer patients, who were signed up into the following groups: cancer cachexia (CC, n = 11), weight‐stable cancer (WSC, n = 9) and weight‐stable control (non‐cancer) (control, n = 7). The stable weight groups were considered as those with no important weight change during the last year and body mass index <25 kg/m2. Subcutaneous AT fibrosis was quantified and characterized by quantitative PCR, histological analysis and immunohistochemistry.ResultsThe degree of fibrosis and the distribution and collagen types (I and III) were different in WSC and CC patients. CC patients showed more pronounced fibrosis in comparison with WSC. Infiltrating macrophages surrounding adipocytes and CD3 Ly were found in the fibrotic areas of scAT. Subcutaneous AT fibrotic areas demonstrated increased monocyte chemotactic protein 1 (MCP‐1) and Cluster of Differentiation (CD)68 gene expression in cancer patients.ConclusionsOur data indicate architectural modification consisting of fibrosis and inflammatory cell infiltration in scAT as induced by cachexia in gastrointestinal cancer patients. The latter was characterized by the presence of macrophages and lymphocytes, more evident in the fibrotic areas. In addition, increased MCP‐1 and CD68 gene expression in scAT from cancer patients may indicate an important role of these markers in the early phases of cancer.

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Section: Discussionmentioning

confidence: 99%

Cachexia-associated adipose tissue morphological rearrangement in gastrointestinal cancer patients

Batista

Henriques

Neves

et al. 2015

Journal of Cachexia, Sarcopenia and Muscle

106

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“…Cancer cachexia induces wasting of fat mass that accounts for a large part of the dramatic weight loss observed both in humans (Fouladiun et al 2005, Agustsson et al 2007, Dahlman et al 2010) and in animals (Machado et al 2004, Bing et al 2006, Asp et al 2010, and lipid metabolism is markedly altered (Seelaender et al 1996, Tisdale 2009, Arner 2011. Walker 256-induced cachexia was efficient at eliciting loss of body weight in terms of both absolute and relative weight (percentage of total body mass) of the fat depots, with consequent abnormalities in plasma biochemical profile.…”

Section: Discussionmentioning

confidence: 99%

“…During the development of cancer cachexia, a well-characterised loss of both adipose tissue and skeletal muscle occurs (Dahlman et al 2010, Arner 2011. It has been proposed that the former often precedes and is more rapid than the latter (Fouladiun et al 2005).…”

Section: Introductionmentioning

confidence: 99%

“…It has been proposed that the former often precedes and is more rapid than the latter (Fouladiun et al 2005). Several factors culminate in loss of adipose tissue, such as 1) increased lipid mobilisation due to enhanced adipocyte lipolysis (Agustsson et al 2007, Ryden et al 2008, Arner 2011, 2) reduced lipogenesis due to decreased lipoprotein lipase activity (Tisdale 2009) and 3) impairment of fat cell turnover, which results in a disruption in the formation and development of adipose tissue (Arner & Spalding 2010). This knowledge should lead to a deeper understanding of the disease and development of appropriate interventions that might be more effective in preventing or delaying the onset of this syndrome.…”

Section: Introductionmentioning

confidence: 99%

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Heterogeneous time-dependent response of adipose tissue during the development of cancer cachexia

Batista¹,

Neves²,

Peres³

et al. 2012

Journal of Endocrinology

100

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Cancer cachexia induces loss of fat mass that accounts for a large part of the dramatic weight loss observed both in humans and in animal models; however, the literature does not provide consistent information regarding the set point of weight loss and how the different visceral adipose tissue depots contribute to this symptom. To evaluate that, 8-week-old male Wistar rats were subcutaneously inoculated with 1 ml (2!10 7 ) of tumour cells (Walker 256). Samples of different visceral white adipose tissue (WAT) depots were collected at days 0, 4, 7 and 14 and stored at K80 8C (seven to ten animals/each day per group). Mesenteric and retroperitoneal depot mass was decreased to the greatest extent on day 14 compared with day 0. Gene and protein expression of PPARg2 (PPARG) fell significantly following tumour implantation in all three adipose tissue depots while C/EBPa (CEBPA) and SREBP-1c (SREBF1) expression decreased over time only in epididymal and retroperitoneal depots. Decreased adipogenic gene expression and morphological disruption of visceral WAT are further supported by the dramatic reduction in mRNA and protein levels of perilipin. Classical markers of inflammation and macrophage infiltration (f4/80, CD68 and MIF-1a) in WAT were significantly increased in the later stage of cachexia (although showing a incremental pattern along the course of cachexia) and presented a depot-specific regulation. These results indicate that impairment in the lipid-storing function of adipose tissue occurs at different times and that the mesenteric adipose tissue is more resistant to the 'fat-reducing effect' than the other visceral depots during cancer cachexia progression.

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“…There is strong interaction between lipolysis and muscle wasting [66][67][68]. This may also be relevant in heart disease [69].…”

Section: Search Strategymentioning

confidence: 99%

Highlights of the mechanistic and therapeutic cachexia and sarcopenia research 2010 to 2012 and their relevance for cardiology

Anker

Haehling

Springer

et al. 2013

International Journal of Cardiology

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Lipases in Cachexia

Abstract: Enzymes expressed in adipose tissue are involved in the loss of fat mass that occurs in a cancer-associated wasting disorder.

Cited by 33 publications

References 11 publications

Cachexia-associated adipose tissue morphological rearrangement in gastrointestinal cancer patients

Cachexia-associated adipose tissue morphological rearrangement in gastrointestinal cancer patients

Heterogeneous time-dependent response of adipose tissue during the development of cancer cachexia

Highlights of the mechanistic and therapeutic cachexia and sarcopenia research 2010 to 2012 and their relevance for cardiology

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