scholarly journals The Role of Autophagy Modulated by Exercise in Cancer Cachexia

Life ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 781
Author(s):  
Julia Windi Gunadi ◽  
Ariyani Sudhamma Welliangan ◽  
Ray Sebastian Soetadji ◽  
Diana Krisanti Jasaputra ◽  
Ronny Lesmana
Keyword(s):  
Muscle Atrophy ◽  
Muscle Function ◽  
Cancer Cachexia ◽  
Physiological Role ◽  
Energy Utilization ◽  
Patients With Cancer ◽  
Different Types ◽  
Exercise Type ◽  
Type Of Exercise

Cancer cachexia is a syndrome experienced by many patients with cancer. Exercise can act as an autophagy modulator, and thus holds the potential to be used to treat cancer cachexia. Autophagy imbalance plays an important role in cancer cachexia, and is correlated to skeletal and cardiac muscle atrophy and energy-wasting in the liver. The molecular mechanism of autophagy modulation in different types of exercise has not yet been clearly defined. This review aims to elaborate on the role of exercise in modulating autophagy in cancer cachexia. We evaluated nine studies in the literature and found a potential correlation between the type of exercise and autophagy modulation. Combined exercise or aerobic exercise alone seems more beneficial than resistance exercise alone in cancer cachexia. Looking ahead, determining the physiological role of autophagy modulated by exercise will support the development of a new medical approach for treating cancer cachexia. In addition, the harmonization of the exercise type, intensity, and duration might play a key role in optimizing the autophagy levels to preserve muscle function and regulate energy utilization in the liver.

Leucine-rich Diet Improved Muscle Function in Cachectic Walker 256 Tumor-bearing Wistar Rats

2021 ◽  
Author(s):  
Laís Viana ◽  
Gabriela Chiocchetti ◽  
Lucas Oroy ◽  
Willians Vieira ◽  
Carla Salgado ◽  
...  
Keyword(s):  
Protein Degradation ◽  
Muscle Atrophy ◽  
Muscle Function ◽  
Cancer Cachexia ◽  
Muscle Protein ◽  
Tumor Bearing ◽  
Muscle Protein Degradation ◽  
Walker 256 ◽  
Walker 256 Tumor

Abstract Background: Skeletal muscle atrophy occurs in several pathological conditions such as cancer, a condition termed cancer cachexia. This condition is associated with an increase in morbidity and poor treatment response, decreasing quality of life, and increased mortality in cancer patients. A leucine-rich diet could be used as a coadjutant therapy preventing muscle atrophy in cancer cachexia hosts. Besides muscle atrophy, muscle function loss is even more important to the patient’s quality of life. Therefore, this study aimed to evaluate the effects of leucine-rich diet on muscle function activity of cachectic Walker 256 tumor-bearing rats and to correlate such effects with molecular pathways of muscle atrophy. Methods: Adult Wistar rats were randomly distributed into four experimental groups. Two groups were fed with a control diet: Control (C) and Walker 256 tumor-bearing (W), and two other groups were fed with a leucine-rich diet: Leucine Control (L) and Leucine Walker 256 tumor-bearing (LW). The functional analysis (walking, behavior, and strength tests) was measured and before and after tumor inoculation. Cachexia parameters such as body weight loss, muscle and fat mass, pro-inflammatory cytokine profile, and molecular and morphological aspects of skeletal muscle were also performed. Results: Walker 256 tumor growth led to muscle function decline, cachexia manifestation symptoms, muscle fiber cross-section area reduction, associated with the altered morphological pattern and classical muscle protein degradation pathway activation, with up-regulation of FoXO1, MuRF1, and 20S proteins. On the other hand, a leucine-rich diet improved muscle strength while reducing the decline of walking and behavior, partially improving the cachexia manifestations and preventing muscle atrophy and protein degradation in Walker 256 tumor-bearing rats. Conclusions: A leucine-rich diet diminished muscle protein degradation and enhanced oxidative pathways, leading to better muscle functional performance.

Caveolin-1: A promising therapeutic target for diverse diseases

2021 ◽  
Vol 14 ◽  
Author(s):  
Shivani Gokani ◽  
Lokesh Kumar Bhatt
Keyword(s):  
Viral Entry ◽  
Therapeutic Target ◽  
Hippocampal Neurons ◽  
Physiological Role ◽  
Clinical Applications ◽  
Caveolin 1 ◽  
Patients With Cancer ◽  
Cellular Events ◽  
Promising Therapeutic Target

: The plasma membrane of eukaryotic cells contains small flask-shaped invaginations known as caveolae that are involved in the regulation of cellular signaling. Caveolin-1 is a 21-24kDa protein localized in the caveolar membrane. Caveolin-1 (Cav-1) has been considered as a master regulator among the various signaling molecules. It has been emerging as a chief protein regulating cellular events associated with homeostasis, caveolae formation, and caveolae trafficking. In addition to the physiological role of cav-1, it has a complex role in the progression of various diseases. Caveolin-1 has been identified as a prognosticator in patients with cancer and has a dual role in tumorigenesis. The expression of Cav-1 in hippocampal neurons and synapses is related to neurodegeneration, cognitive decline, and aging. Despite the ubiquitous association of caveolin-1 in various pathological processes, the mechanisms associated with these events are still unclear. Caveolin-1 has a significant role in various events of the viral cycle, such as viral entry. This review will summarize the role of cav-1 in the development of cancer, neurodegeneration, glaucoma, cardiovascular diseases, and infectious diseases. The therapeutic perspectives involving clinical applications of Caveolin-1 have also been discussed. The understanding of the involvement of caveolin-1 in various diseased states provides insights into how it can be explored as a novel therapeutic target.

scholarly journals Leucine-Rich Diet Improved Muscle Function in Cachectic Walker 256 Tumour-Bearing Wistar Rats

Cells ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 3272
Author(s):  
Laís Rosa Viana ◽  
Gabriela de Matuoka e Chiocchetti ◽  
Lucas Oroy ◽  
Willians Fernando Vieira ◽  
Estela Natacha Brandt Busanello ◽  
...  
Keyword(s):  
Protein Degradation ◽  
Muscle Atrophy ◽  
Muscle Function ◽  
Cancer Cachexia ◽  
Muscle Protein ◽  
Tumour Bearing ◽  
Walker 256 Tumour ◽  
Muscle Protein Degradation ◽  
Walker 256

Skeletal muscle atrophy occurs in several pathological conditions, such as cancer, especially during cancer-induced cachexia. This condition is associated with increased morbidity and poor treatment response, decreased quality of life, and increased mortality in cancer patients. A leucine-rich diet could be used as a coadjutant therapy to prevent muscle atrophy in patients suffering from cancer cachexia. Besides muscle atrophy, muscle function loss is even more important to patient quality of life. Therefore, this study aimed to investigate the potential beneficial effects of leucine supplementation on whole-body functional/movement properties, as well as some markers of muscle breakdown and inflammatory status. Adult Wistar rats were randomly distributed into four experimental groups. Two groups were fed with a control diet (18% protein): Control (C) and Walker 256 tumour-bearing (W), and two other groups were fed with a leucine-rich diet (18% protein + 3% leucine): Leucine Control (L) and Leucine Walker 256 tumour-bearing (LW). A functional analysis (walking, behaviour, and strength tests) was performed before and after tumour inoculation. Cachexia parameters such as body weight loss, muscle and fat mass, pro-inflammatory cytokine profile, and molecular and morphological aspects of skeletal muscle were also determined. As expected, Walker 256 tumour growth led to muscle function decline, cachexia manifestation symptoms, muscle fibre cross-section area reduction, and classical muscle protein degradation pathway activation, with upregulation of FoxO1, MuRF-1, and 20S proteins. On the other hand, despite having no effect on the walking test, inflammation status or muscle oxidative capacity, the leucine-rich diet improved muscle strength and behaviour performance, maintained body weight, fat and muscle mass and decreased some protein degradation markers in Walker 256 tumour-bearing rats. Indeed, a leucine-rich diet alone could not completely revert cachexia but could potentially diminish muscle protein degradation, leading to better muscle functional performance in cancer cachexia.

Defining the role of dietary intake in determining weight change in patients with cancer cachexia

2018 ◽  
Vol 37 (1) ◽  
pp. 235-241 ◽  
Author(s):  
R. Nasrah ◽  
M. Kanbalian ◽  
C. Van Der Borch ◽  
N. Swinton ◽  
S. Wing ◽  
...  
Keyword(s):  
Dietary Intake ◽  
Weight Change ◽  
Cancer Cachexia ◽  
Patients With Cancer

scholarly journals Neurohypophyseal hormones and skeletal muscle: a tale of two faces

2020 ◽  
Vol 30 (1) ◽  
pp. 53-57
Author(s):  
Alexandra Benoni ◽  
Alessandra Renzini ◽  
Giorgia Cavioli ◽  
Sergio Adamo
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Striated Muscle ◽  
Cardiac Atrophy ◽  
Neurohypophyseal Hormones

The neurohypophyseal hormones vasopressin and oxytocin were invested, in recent years, with novel functions upon striated muscle, regulating its differentiation, trophism, and homeostasis. Recent studies highlight that these hormones not only target skeletal muscle but represent novel myokines. We discuss the possibility of exploiting the muscle hypertrophying activity of oxytocin to revert muscle atrophy, including cancer cachexia muscle wasting. Furthermore, the role of oxytocin in cardiac homeostasis and the possible role of cardiac atrophy as a concause of death in cachectic patients is discussed.

SUBCELLULAR LOCALIZATION OF NEUROTRANSMITTERS AND RELEASING FACTORS IN THE RAT MEDIAN EMINENCE

1970 ◽  
Vol 48 (2) ◽  
pp. 205-213 ◽  
Author(s):  
F. CLEMENTI ◽  
B. CECCARELLI ◽  
E. CERATI ◽  
M. L. DEMONTE ◽  
M. FELICI ◽  
...  
Keyword(s):  
Median Eminence ◽  
Gradient Centrifugation ◽  
Physiological Role ◽  
Sucrose Density Gradient ◽  
Nerve Terminals ◽  
Sucrose Density Gradient Centrifugation ◽  
Different Types ◽  
Releasing Factors ◽  
Electron Microscopical

SUMMARY The neurohaemal part of the median eminence of the rat hypothalamus is characterized by numerous nerve terminals which end near a rich network of fenestrated capillaries. An attempt was made to isolate different types of nerve terminals by means of sucrose density-gradient centrifugation. The subcellular fractions obtained were assayed for dopamine, noradrenaline and 5-hydroxytryptamine. In addition FSH- and GH-releasing activities were determined. A sample of each fraction obtained was taken for electron microscopical observations. Dopamine, noradrenaline, 5-hydroxytryptamine, GH- and FSH-releasing factors were present in higher concentration in the nerve endings. A further fractionation showed that noradrenaline was present in the lightest synaptosomal band, dopamine in the middle one, and 5-hydroxytryptamine in the heaviest. GH-RF and FSH-RF were recovered mainly from the band containing dopamine. The relevance of this localization to the physiological role of the median eminence is discussed.

scholarly journals The mechanism by which noncoding RNAs regulate muscle wasting in cancer cachexia

2021 ◽  
Author(s):  
Xueer Zhou ◽  
Shoushan Hu ◽  
Yunan Zhang ◽  
Guannan Du ◽  
Yi Li
Keyword(s):  
Metabolic Syndrome ◽  
Muscle Atrophy ◽  
Intercellular Communication ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Expression Profiles ◽  
Noncoding Rnas ◽  
Diagnostic Methods ◽  
Novel Therapies ◽  
Patients With Cancer

Abstract Cancer cachexia (CC) is a subject of concern because it is a complex metabolic syndrome that accelerates muscle wasting and affects up to 80% of patients with cancer; however, timely diagnostic methods and effective cures are lacking. Although a considerable number of studies have focused on the mechanism of CC-induced muscle atrophy, few novel therapies have been applied in the last decade. In recent years, noncoding RNAs (ncRNAs) have attracted great attention since many differentially expressed ncRNAs in cancer cachectic muscles have been reported to participate in the inhibition of myogenesis and activation of proteolysis. In addition, extracellular vesicles (EVs), which function as ncRNA carriers in intercellular communication, are closely involved in changing ncRNA expression profiles in muscle and promoting the development of muscle wasting; thus, EV-related ncRNAs may represent potential therapeutic targets. This review comprehensively describes the process of ncRNA transmission through EVs and summarizes the pathways and targets of ncRNAs that lead to CC-induced muscle atrophy.

scholarly journals MMP12 Knockout Prevent Weight and Muscle Loss Induced by Cancer Cachexia

2021 ◽  
Author(s):  
Lingbi Jiang ◽  
Mingming Yang ◽  
Shihui He ◽  
Zhengyang Li ◽  
Haobin Li ◽  
...  
Keyword(s):  
Weight Loss ◽  
Interleukin 6 ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Critical Role ◽  
Muscle Loss ◽  
Glycolipid Metabolism ◽  
Patients With Cancer

AbstractWeight loss and muscle wasting can have devastating impacts on survival and quality of life of patients with cancer cachexia. Here, we have established a hybrid mouse of ApcMin/+ mice and MMP12 knockout mice (ApcMin/+; MMP12-/-) and found that knockout MMP12 can suppress the weight and muscle loss of ApcMin/+ mice. In detail, we found that interleukin 6 was highly upregulated in the serum of cancer patients and MMP12 was increased in muscle of tumor-bearing mice. Interestingly, the interleukin 6 secreted by tumor cells led to MMP12 overexpression in the macrophages, which further resulted in degradation of insulin and insulin-like growth factor 1 and interruption of glycolipid metabolism. Notably, depletion of MMP12 prevented weight loss of ApcMin/+ mice. Our study uncovers the critical role of MMP12 in controlling weight and highlights the great potential of MMP12 in the treatment of cancer cachexia.

scholarly journals Relation between skeletal muscle strength and ubiquitin ligase expression in muscle atrophy models in zebrafish larvae (Danio Rerio)

2020 ◽  
Author(s):  
Jiao Liu ◽  
Elisabeth Le ◽  
Matthias Schwartzkopf ◽  
Anders Arner
Keyword(s):  
Skeletal Muscle ◽  
Food Intake ◽  
Muscle Weakness ◽  
Muscle Atrophy ◽  
Ubiquitin Ligase ◽  
Muscle Function ◽  
Skeletal Muscle Atrophy ◽  
Active Force ◽  
Zebrafish Larvae

Abstract Background Skeletal muscle atrophy is often seen in patients with chronic diseases or muscle disuse. Upregulated expression of ubiquitin ligases such as Muscle Ring Finger 1 (MuRF-1) and Muscle Atrophy F-box (MAFbx) has been shown in different immobilization-induced atrophy models, which is believed to be responsible for the enhanced muscle protein proteolysis and thereafter results in muscle weakness. However, currently used immobilization animal models can include artefacts due to difficulty of food intake and stress. Zebrafish larvae 5-6 days after hatching do not require active movement for food intake, and it is possible to assess the muscle function of their trunk muscle. Therefore, we established two muscle atrophy models using zebrafish larvae and aimed to investigate the role of the MuRFs and MAFbx in relation with muscle function.Methods An actin-myosin interaction blocker (BTS) was used to immobilize zebrafish larvae from 3-6 days after hatching; in another series, dexamethasone was fed to larvae from 3-5 days after hatching. Maximal active force of trunk muscles was examined and the distance between adjacent filaments in sarcomeric structure was measured using small angle x-ray diffraction. MuRF and MAFbx expression was determined using real time PCR. Two-way ANOVA was used to analyze the difference between groups.Results We found a significant up-regulation of MuRF-1 and a lower active force generation in dexamethasone treated larvae. However, although the BTS immobilization induced muscle weakness, it was associated with decreased of MuRF-1 to 3 and MAFbx. After 3 days of immobilization, sarcomere became more compressed compared to the controls.Conclusions Two kinds of muscle atrophy models were successfully established in zebrafish larvae. MuRFs and MAFbx was lowered in BTS treated model whereas MuRF-1 was up-regulated in dexamethasone treated model implicating the complex role of ubiquitin ligase in different muscle atrophy models.

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