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Muscle and Bone Impairment in Infantile Nephropathic Cystinosis: New Concepts.
Haffner, D, Leifheit-Nestler, M, Alioli, C, Bacchetta, J
Cells. 2022;(1)
Abstract
Cystinosis Metabolic Bone Disease (CMBD) has emerged during the last decade as a well-recognized, long-term complication in patients suffering from infantile nephropathic cystinosis (INC), resulting in significant morbidity and impaired quality of life in teenagers and adults with INC. Its underlying pathophysiology is complex and multifactorial, associating complementary, albeit distinct entities, in addition to ordinary mineral and bone disorders observed in other types of chronic kidney disease. Amongst these long-term consequences are renal Fanconi syndrome, hypophosphatemic rickets, malnutrition, hormonal abnormalities, muscular impairment, and intrinsic cellular bone defects in bone cells, due to CTNS mutations. Recent research data in the field have demonstrated abnormal mineral regulation, intrinsic bone defects, cysteamine toxicity, muscle wasting and, likely interleukin-1-driven inflammation in the setting of CMBD. Here we summarize these new pathophysiological deregulations and discuss the crucial interplay between bone and muscle in INC. In future, vitamin D and/or biotherapies targeting the IL1β pathway may improve muscle wasting and subsequently CMBD, but this remains to be proven.
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Muscle-bone axis in children with chronic kidney disease: current knowledge and future perspectives.
Karava, V, Dotis, J, Christoforidis, A, Kondou, A, Printza, N
Pediatric nephrology (Berlin, Germany). 2021;(12):3813-3827
Abstract
Bone and muscle tissue are developed hand-in-hand during childhood and adolescence and interact through mechanical loads and biochemical pathways forming the musculoskeletal system. Chronic kidney disease (CKD) is widely considered as both a bone and muscle-weakening disease, eventually leading to frailty phenotype, with detrimental effects on overall morbidity. CKD also interferes in the biomechanical communication between two tissues. Pathogenetic mechanisms including systemic inflammation, anorexia, physical inactivity, vitamin D deficiency and secondary hyperparathyroidism, metabolic acidosis, impaired growth hormone/insulin growth factor 1 axis, insulin resistance, and activation of renin-angiotensin system are incriminated for longitudinal uncoordinated loss of bone mineral content, bone strength, muscle mass, and muscle strength, leading to mechanical impairment of the functional muscle-bone unit. At the same time, CKD may also interfere in the biochemical crosstalk between the two organs, through inhibiting or stimulating the expression of certain osteokines and myokines. This review focuses on presenting current knowledge, according to in vitro, in vivo, and clinical studies, concerning the pathogenetic pathways involved in the muscle-bone axis, and suggests approaches aimed at preventing bone loss and muscle wasting in the pediatric population. Novel therapeutic targets for preserving musculoskeletal health in the context of CKD are also discussed.
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Adverse effects of androgen deprivation therapy in patients with prostate cancer: Focus on muscle and bone health.
Bargiota, A, Oeconomou, A, Zachos, I, Samarinas, M, L Pisters, L, Tzortzis, V
Journal of B.U.ON. : official journal of the Balkan Union of Oncology. 2020;(3):1286-1294
Abstract
Androgen deprivation therapy (ADT) is the most effective systemic treatment for prostate cancer and can be succeeded either surgically or pharmaceutically. Both approaches lead to hypogonadism with a large variety of adverse events, including obesity, metabolic syndrome, osteoporosis, sarcopenia, diabetes mellitus, cardiovascular disease, gynecomastia and sexual dysfunction. In addition, undesirable effects on muscle and bone health may have a significant impact not only on the quality of life but also on life expectancy. Currently, supervised exercise seems to be the only intervention that could prevent the adverse effects of the ADT and improve quality of life. Lifestyle modification, supplementation of calcium, vitamin D and when indicated antiosteoporotic treatments improve bone health. However, patients receiving ADT must be well informed about the potential benefits as well as the risks of the treatment.
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4.
Histidine Metabolism and Function.
Brosnan, ME, Brosnan, JT
The Journal of nutrition. 2020;(Suppl 1):2570S-2575S
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Abstract
Histidine is a dietary essential amino acid because it cannot be synthesized in humans. The WHO/FAO requirement for adults for histidine is 10 mg · kg body weight-1 · d-1. Histidine is required for synthesis of proteins. It plays particularly important roles in the active site of enzymes, such as serine proteases (e.g., trypsin) where it is a member of the catalytic triad. Excess histidine may be converted to trans-urocanate by histidine ammonia lyase (histidase) in liver and skin. UV light in skin converts the trans form to cis-urocanate which plays an important protective role in skin. Liver is capable of complete catabolism of histidine by a pathway which requires folic acid for the last step, in which glutamate formiminotransferase converts the intermediate N-formiminoglutamate to glutamate, 5,10 methenyl-tetrahydrofolate, and ammonia. Inborn errors have been recognized in all of the catabolic enzymes of histidine. Histidine is required as a precursor of carnosine in human muscle and parts of the brain where carnosine appears to play an important role as a buffer and antioxidant. It is synthesized in the tissue by carnosine synthase from histidine and β-alanine, at the expense of ATP hydrolysis. Histidine can be decarboxylated to histamine by histidine decarboxylase. This reaction occurs in the enterochromaffin-like cells of the stomach, in the mast cells of the immune system, and in various regions of the brain where histamine may serve as a neurotransmitter.
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Targeting reactive oxygen species (ROS) to combat the age-related loss of muscle mass and function.
Thoma, A, Akter-Miah, T, Reade, RL, Lightfoot, AP
Biogerontology. 2020;(4):475-484
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Abstract
The loss of muscle mass and function with age, termed sarcopenia, is an inevitable process, which has a significant impact on quality of life. During ageing we observe a progressive loss of total muscle fibres and a reduction in cross-sectional area of the remaining fibres, resulting in a significant reduction in force output. The mechanisms which underpin sarcopenia are complex and poorly understood, ranging from inflammation, dysregulation of protein metabolism and denervation. However, there is significant evidence to demonstrate that modified ROS generation, redox dis-homeostasis and mitochondrial dysfunction may have an important role to play. Based on this, significant interest and research has interrogated potential ROS-targeted therapies, ranging from nutritional-based interventions such as vitamin E/C, polyphenols (resveratrol) and targeted pharmacological compounds, using molecules such as SS-31 and MitoQ. In this review we evaluate these approaches to target aberrant age-related ROS generation and the impact on muscle mass and function.
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The effect of diet and exercise on lipid droplet dynamics in human muscle tissue.
Daemen, S, van Polanen, N, Hesselink, MKC
The Journal of experimental biology. 2018;(Pt Suppl 1)
Abstract
The majority of fat in the human body is stored as triacylglycerols in white adipose tissue. In the obese state, adipose tissue mass expands and excess lipids are stored in non-adipose tissues, such as skeletal muscle. Lipids are stored in skeletal muscle in the form of small lipid droplets. Although originally viewed as dull organelles that simply store lipids as a consequence of lipid overflow from adipose tissue, lipid droplets are now recognized as key components in the cell that exert a variety of relevant functions in multiple tissues (including muscle). Here, we review the effect of diet and exercise interventions on myocellular lipid droplets and their putative role in insulin sensitivity from a human perspective. We also provide an overview of lipid droplet biology and identify gaps for future research.
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Potential link between excess added sugar intake and ectopic fat: a systematic review of randomized controlled trials.
Ma, J, Karlsen, MC, Chung, M, Jacques, PF, Saltzman, E, Smith, CE, Fox, CS, McKeown, NM
Nutrition reviews. 2016;(1):18-32
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Abstract
CONTEXT The effect of added sugar intake on ectopic fat accumulation is a subject of debate. OBJECTIVE A systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted to examine the potential effect of added sugar intake on ectopic fat depots. DATA SOURCES MEDLINE, CAB Abstracts, CAB Global Health, and EBM (Evidence-Based Medicine) Reviews - Cochrane Central Register of Controlled Trials databases were searched for studies published from 1973 to September 2014. DATA EXTRACTION RCTs with a minimum of 6 days' duration of added sugar exposure in the intervention group were selected. The dosage of added sugar intake as a percentage of total energy was extracted or calculated. Means and standard deviations of pre- and post-test measurements or changes in ectopic fat depots were collected. DATA SYNTHESIS Fourteen RCTs were included. Most of the studies had a medium to high risk of bias. Meta-analysis showed that, compared with eucaloric controls, subjects who consumed added sugar under hypercaloric conditions likely increased ectopic fat, particularly in the liver (pooled standardized mean difference = 0.9 [95%CI, 0.6-1.2], n = 6) and muscles (pooled SMD = 0.6 [95%CI, 0.2-1.0], n = 4). No significant difference was observed in liver fat, visceral adipose tissue, or muscle fat when isocaloric intakes of different sources of added sugars were compared. CONCLUSIONS Data from a limited number of RCTs suggest that excess added sugar intake under hypercaloric diet conditions likely increases ectopic fat depots, particularly in the liver and in muscle fat. There are insufficient data to compare the effect of different sources of added sugars on ectopic fat deposition or to compare intake of added sugar with intakes of other macronutrients. Future well-designed RCTs with sufficient power and duration are needed to address the role of sugars on ectopic fat deposition.
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Eicosapentaenoic acid in cancer improves body composition and modulates metabolism.
Pappalardo, G, Almeida, A, Ravasco, P
Nutrition (Burbank, Los Angeles County, Calif.). 2015;(4):549-55
Abstract
OBJECTIVES The objective of this review article is to present the most recent intervention studies with EPA on nutritional outcomes in cancer patients, e.g. nutritional status, weight & lean body mass. METHODS For this purpose a PubMed(®) and MedLine(®) search of the published literature up to and including January 2014 that contained the keywords: cancer, sarcopenia, EPA, ω-3 fatty acids, weight, intervention trial, muscle mass was conducted. The collected data was summarized and written in text format and in tables that contained: study design, patient' population, sample size, statistical significance and results of the intervention. The paper will cover malignancy, body composition, intervention with EPA, physiological mechanisms of action of EPA, effect of EPA on weight and body composition, future research. RESULTS In cancer patients deterioration of muscle mass can be present regardless of body weight or Body Mass Index (BMI). Thus, sarcopenia in cancer patients with excessive fat mass (FM), entitled sarcopenic obesity, has gained greater relevance in clinical practice; it can negatively influence patients' functional status, tolerance to treatments & disease prognosis. The search for an effective nutritional intervention that improves body composition (preservation of muscle mass and muscle quality) is of utmost importance for clinicians and patients. The improvement of muscle quality is an even more recent area of interest because it has probable implications in patients' prognosis. Eicosapentaenoic acid (EPA) has been identified as a promising nutrient with the wide clinical benefits. Several mechanisms have been proposed to explain EPA potential benefits on body composition: inhibition of catabolic stimuli by modulating pro-inflammatory cytokines production and enhancing insulin sensitivity that induces protein synthesis; also, EPA may attenuate deterioration of nutritional status resulting from antineoplastic therapies by improving calorie and protein intake as well. CONCLUSIONS Indeed, cancer-related sarcopenia/cachexia is a multifactorial syndrome characterized by inflammation, anorexia, weight loss, and muscle/adipose tissue loss mediated by proinflammatory cytokines, e.g. TNF-α and IL-6, resulting in increased chemotherapy toxicity, costs, morbidity and mortality. With this review we found that EPA can reduce inflammation and has the potential to modulate nutritional status/body composition. In view of the modest survival benefits of chemotherapy/radiotherapy in some cancers, important issues for physicians are to optimize well-being, Quality of Life via nutritional status and adequate body composition. Thus, improvement in nutritional status is a central outcome.
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Relationship between 25-hydoxyvitamin D, muscle strength, and incidence of injury in healthy adults: a systematic review.
Redzic, M, Lewis, RM, Thomas, DT
Nutrition research (New York, N.Y.). 2013;(4):251-8
Abstract
The purpose of this systematic review is to answer the following clinical questions in healthy adults: is vitamin D status related to (1) muscle strength? (2) or incidence of injury? A literature search was performed using Pubmed, SPORTDiscus, and Web of Science to capture relevant articles that have examined these outcomes. Inclusion criteria required studies to address at least one of the 2 questions stated above, enroll healthy human subjects with a mean age of 18 to 65 years of age, and include serum 25-hydoxyvitamin D measures. Study characteristics such as vitamin D status, study design, and study population were documented. Measured assessors and outcomes from all studies were extracted to answer at least one of the two questions. When applicable, data were used to compute effect sizes at a 95% confidence interval for comparisons across studies to answer the 2 questions. The results of these studies indicate a weak to moderate effect of higher 25-hydoxyvitamin D levels on greater muscle strength and reduced incidence of injury. Randomized controlled clinical trials examining these questions are scarce when compared with the popularity of vitamin D testing; therefore, future trials are necessary to advance our understanding and to clarify the effect vitamin D has on extraskeletal outcomes in healthy adults.
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The effects of vitamin D deficiency in athletes.
Angeline, ME, Gee, AO, Shindle, M, Warren, RF, Rodeo, SA
The American journal of sports medicine. 2013;(2):461-4
Abstract
Vitamin D acts to maintain calcium and phosphate homeostasis within the body. It is now estimated that 1 billion people worldwide are vitamin D deficient. This problem is particularly important to athletes of all ages, as vitamin D plays a significant role in bone health, immune function, and physical performance. In the deficient state, the athlete may be at an increased risk for potential problems such as stress fractures, respiratory infections, and muscle injuries. The purpose of this article is to examine vitamin D deficiency and review its relationship to the athlete.