scholarly journals Potential Biomarkers of Fat Loss as a Feature of Cancer Cachexia

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Maryam Ebadi ◽  
Vera C. Mazurak
Keyword(s):  
Adipose Tissue ◽  
Plasma Levels ◽  
Cancer Cachexia ◽  
Prognostic Biomarker ◽  
Prognostic Biomarkers ◽  
Plasma Biomarker ◽  
Fat Loss ◽  
Early Detection And Prevention ◽  
Potential Biomarkers

Fat loss is associated with shorter survival and reduced quality of life in cancer patients. Effective intervention for fat loss in cachexia requires identification of the condition using prognostic biomarkers for early detection and prevention of further depletion. No biomarkers of fat mass alterations have been defined for application to the neoplastic state. Several inflammatory cytokines have been implicated in mediating fat loss associated with cachexia; however, plasma levels may not relate to adipose atrophy. Zinc-α2-glycoprotein may be a local catabolic mediator within adipose tissue rather than serving as a plasma biomarker of fat loss. Plasma glycerol and leptin associate with adipose tissue atrophy and mass, respectively; however, no study has evaluated their potential as a prognostic biomarker of cachexia-associated fat loss. This review confirms the need for further studies to identify valid prognostic biomarkers to identify loss of fat based on changes in plasma levels of biomarkers.

SUN-P077: Adipose-Tissue Derived Factors as Potential Biomarkers of Cancer Cachexia

2017 ◽  
Vol 36 ◽  
pp. S82
Author(s):  
A. Saray ◽  
V. Papovic ◽  
S. Glavas ◽  
I. Rasic
Keyword(s):  
Adipose Tissue ◽  
Cancer Cachexia ◽  
Potential Biomarkers

scholarly journals Macrophages protect against loss of adipose tissue during cancer cachexia

2018 ◽  
Author(s):  
Merve Erdem ◽  
Diana Möckel ◽  
Sandra Jumpertz ◽  
Cathleen John ◽  
Athanassios Fragoulis ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Mouse Model ◽  
Immune Cells ◽  
Visceral Fat ◽  
Clinical Studies ◽  
Cancer Cachexia ◽  
Myeloid Cell ◽  
Fat Loss ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

AbstractCancer cachexia represents a central obstacle in medical oncology as it is associated with poor therapy response and reduced overall survival. Systemic inflammation is considered to be a key driver of cancer cachexia, however, clinical studies with anti-inflammatory drugs failed to show a robust cachexia-inhibiting effect. To address this contradiction, we investigated the functional importance of innate immune cells for hepatocellular carcinoma (HCC)-associated cachexia. To this end, we used a transgenic HCC mouse model intercrossed with mice harboring a defect in myeloid cell-mediated inflammation. We identified robust cachexia in the HCC mouse model as evidenced by a marked loss of visceral fat and lean mass. Computed tomography-based analyses demonstrated that a subgroup of human HCC patients displays reduced visceral fat mass, complementing the murine data. While the myeloid cell-mediated inflammation defect resulted in reduced expression of pro-inflammatory cytokines in the serum of HCC-bearing mice, this unexpectedly did not translate into diminished, but rather enhanced cachexia-associated fat loss. Defective myeloid cell-mediated inflammation was associated with decreased macrophage abundance in visceral adipose tissue, suggesting a role for local macrophages in the regulation of cancer-induced fat loss. Taken together, myeloid cell-mediated inflammation displays a rather unexpected beneficial function in a murine HCC model. These results demonstrate that immune cells are capable of protecting the host against cancer-induced tissue wasting, adding a further layer of complexity to the pathogenesis of cachexia and providing a potential explanation for the contradictory results of clinical studies with anti-inflammatory drugs.

scholarly journals New insights into adipose tissue atrophy in cancer cachexia

2009 ◽  
Vol 68 (4) ◽  
pp. 385-392 ◽  
Author(s):  
Chen Bing ◽  
Paul Trayhurn
Keyword(s):  
Adipose Tissue ◽  
Cancer Cachexia ◽  
Molecular Mechanisms ◽  
Tissue Expansion ◽  
Experimental Models ◽  
Malignant Tumours ◽  
Morphological Examination ◽  
Fat Loss ◽  
Key Factor

Profound loss of adipose and other tissues is a hallmark of cancer cachexia, a debilitating condition associated with increased morbidity and mortality. Fat loss cannot be attributable to reduced appetite alone as it precedes the onset of anorexia and is much more severe in experimental models of cachexia than in food restriction. Morphological examination has shown marked remodelling of adipose tissue in cancer cachexia. It is characterised by the tissue containing shrunken adipocytes with a major reduction in cell size and increased fibrosis in the tissue matrix. The ultrastructure of ‘slimmed’ adipocytes has revealed severe delipidation and modifications in cell membrane conformation. Although the molecular mechanisms remain to be established, evidence suggests that altered adipocyte metabolism may lead to adipose atrophy in cancer cachexia. Increased lipolysis appears to be a key factor underlying fat loss, while inhibition of adipocyte development and lipid deposition may also contribute. Both tumour and host-derived factors are implicated in adipose atrophy. Zinc-α2-glycoprotein (ZAG), which is overexpressed by certain malignant tumours, has been identified as a novel adipokine. ZAG transcripts and protein expression in adipose tissue are up regulated in cancer cachexia but reduced with adipose tissue expansion in obesity. Studies in vitro demonstrate that recombinant ZAG stimulates lipolysis. ZAG may therefore act locally, as well as systemically, to promote lipid mobilisation in cancer cachexia. Further elucidation of ZAG function in adipose tissue may lead to novel targets for preventing adipose atrophy in malignancy.

The dual nature of obesity in metabolic programming: quantity versus quality of adipose tissue

2020 ◽  
Vol 134 (18) ◽  
pp. 2447-2451
Author(s):  
Anissa Viveiros ◽  
Gavin Y. Oudit
Keyword(s):  
Adipose Tissue ◽  
Environmental Factors ◽  
Maternal Obesity ◽  
Metabolic Programming ◽  
Dual Nature ◽  
Prevalence Of Obesity ◽  
Adipose Tissue Volume ◽  
Males And Females ◽  
Metabolically Healthy

Abstract The global prevalence of obesity has been rising at an alarming rate, accompanied by an increase in both childhood and maternal obesity. The concept of metabolic programming is highly topical, and in this context, describes a predisposition of offspring of obese mothers to the development of obesity independent of environmental factors. Research published in this issue of Clinical Science conducted by Litzenburger and colleagues (Clin. Sci. (Lond.) (2020) 134, 921–939) have identified sex-dependent differences in metabolic programming and identify putative signaling pathways involved in the differential phenotype of adipose tissue between males and females. Delineating the distinction between metabolically healthy and unhealthy obesity is a topic of emerging interest, and the precise nature of adipocytes are key to pathogenesis, independent of adipose tissue volume.

Cumulus Cell Genes as Potential Biomarkers for the Diagnosis of the Quality of Oocytes and Embryos

2017 ◽  
Vol 8 (1) ◽  
pp. 91-98
Author(s):  
Olena A. Shepel ◽  
Tetyana Yu. Voznesenska ◽  
Taras V. Blashkiv ◽  
Roman I. Yanchii
Keyword(s):  
Cumulus Cell ◽  
Potential Biomarkers

scholarly journals Cardio- and Neurometabolic Adipobiology: Consequences and Implications for Therapy

2021 ◽  
Vol 22 (8) ◽  
pp. 4137
Author(s):  
Jan Frohlich ◽  
George N. Chaldakov ◽  
Manlio Vinciguerra
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Nerve Growth Factor ◽  
Human Life ◽  
Signaling Proteins ◽  
New Developments ◽  
Cardiometabolic Diseases ◽  
The Past ◽  
Neurotrophin 3

Studies over the past 30 years have revealed that adipose tissue is the major endocrine and paracrine organ of the human body. Arguably, adiopobiology has taken its reasonable place in studying obesity and related cardiometabolic diseases (CMDs), including Alzheimer’s disease (AD), which is viewed herein as a neurometabolic disorder. The pathogenesis and therapy of these diseases are multiplex at basic, clinical and translational levels. Our present goal is to describe new developments in cardiometabolic and neurometabolic adipobiology. Accordingly, we focus on adipose- and/or skeletal muscle-derived signaling proteins (adipsin, adiponectin, nerve growth factor, brain-derived neuroptrophic factor, neurotrophin-3, irisin, sirtuins, Klotho, neprilysin, follistatin-like protein-1, meteorin-like (metrnl), as well as growth differentiation factor 11) as examples of metabotrophic factors (MTFs) implicated in the pathogenesis and therapy of obesity and related CMDs. We argue that these pathologies are MTF-deficient diseases. In 1993 the “vascular hypothesis of AD” was published and in the present review we propose the “vasculometabolic hypothesis of AD.” We discuss how MTFs could bridge CMDs and neurodegenerative diseases, such as AD. Greater insights on how to manage the MTF network would provide benefits to the quality of human life.

scholarly journals Extracellular vesicles-released parathyroid hormone-related protein from Lewis lung carcinoma induces lipolysis and adipose tissue browning in cancer cachexia

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wenjun Hu ◽  
Hairong Xiong ◽  
Zeyuan Ru ◽  
Yan Zhao ◽  
Yali Zhou ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Parathyroid Hormone ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Cancer Cachexia ◽  
Lewis Lung ◽  
Related Protein ◽  
Parathyroid Hormone Related Protein ◽  
Tissue Browning

AbstractCancer cachexia is a metabolic disorder characterized by skeletal muscle wasting and white adipose tissue browning. Specific functions of several hormones, growth factors, and cytokines derived from tumors can trigger cachexia. Moreover, adipose tissue lipolysis might explain weight loss that occurs owing to cachexia. Extracellular vesicles (EVs) are involved in intercellular communication. However, whether EVs participate in lipolysis induced by cancer cachexia has not been thoroughly investigated. Using Lewis lung carcinoma (LLC) cell culture, we tested whether LLC cell-derived EVs can induce lipolysis in 3T3-L1 adipocytes. EVs derived from LLC cells were isolated and characterized biochemically and biophysically. Western blotting and glycerol assay were used to study lipolysis. LLC cell-derived EVs induced lipolysis in vivo and vitro. EVs fused directly with target 3T3-L1 adipocytes and transferred parathyroid hormone-related protein (PTHrP), activating the PKA signaling pathway in 3T3-L1 adipocytes. Blocking PTHrP activity in LLC-EVs using a neutralizing antibody and by knocking down PTHR expression prevented lipolysis in adipocytes. Inhibiting the PKA signaling pathway also prevents the lipolytic effects of EVs. In vivo, suppression of LLC-EVs release by knocking down Rab27A alleviated white adipose tissue browning and lipolysis. Our data showed that LLC cell-derived EVs induced adipocyte lipolysis via the extracellular PTHrP-mediated PKA pathway. Our data demonstrate that LLC-EVs induce lipolysis in vitro and vivo by delivering PTHrP, which interacts with PTHR. The lipolytic effect of LLC-EVs was abrogated by PTHR knockdown and treatment with a neutralizing anti-PTHrP antibody. Together, these data show that LLC-EV-induced lipolysis is mediated by extracellular PTHrP. These findings suggest a novel mechanism of lipid droplet loss and identify a potential therapeutic strategy for cancer cachexia.

Influence of dietary fatty acids on adipose tissue composition and subsequent eating quality of finishing pigs

1996 ◽  
Vol 1996 ◽  
pp. 155-155
Author(s):  
M S Redshaw ◽  
J Wiseman ◽  
D J A Cole ◽  
J D Wood ◽  
M Enser ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Profile ◽  
Sensory Quality ◽  
Dietary Fatty Acids ◽  
Eating Quality ◽  
Finishing Pigs ◽  
Tissue Composition

It is well established that the fatty acid combustion of adipose issue in pigs (non-ruminants) may be manipulated by changes in the fatty acid profile of the diets. The objective of this program of work was to quantify the responses of adipose depots of finishing pigs to changes in the level and profile of dietary fatty acids and to relate these changes to the sensory quality of meat as determined by taste panel.

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