Assessment – Nutrition-Focused Physical Exam to Detect Macronutrient Deficiencies
Jennifer Doley, Mary J. Marian in Adult Malnutrition, 2023
Muscle atrophy is defined as a reduction in muscle mass, which can be a partial or significant loss.16 Muscle atrophy occurs when the body loses protein at an excessive rate while protein synthesis is diminished and where catabolism exceeds synthesis. Muscle loss is commonly observed in disease-related malnutrition, particularly in diseases such as cancer, chronic obstructive pulmonary disease, heart failure, chronic renal failure, gastrointestinal disorders, and severe burns. Muscle atrophy can also occur due to reduced physical activity, immobility, poor nutritional intake, increased energy and protein needs, and decreased nutrient utilization or absorption. Muscle weakness and atrophy may also develop during the course of hospitalization in the intensive care unit (ICU) and is termed “intensive care unit acquired weakness”.17,18 One study has shown that when patients are admitted and treated in the ICU for 7–10 days, the incidence of ICU-induced muscle weakness increases by 24–55%.18
Clinical Aspects
Marc H. De Baets, Hans J.G.H. Oosterhuis in Myasthenia Gravis, 2019
Localized muscle atrophy is detectable in 5 to 10% of the patients.8,31-33, The incidence is still higher if patients with permanent, nearly complete ophthalmoplegia are considered, who show considerable histological abnormalities at autopsy.32,34,35 Permanent localized muscle weakness, e.g., of the m. levator palpebrae, the facial, and throat muscles of which histological examination is uncommonly done, may occur without visible atrophy. Remarkably few details about the distribution of atrophy were found in literature, 33,36 although a probably highly specific pattern of atrophy of the tongue (triple furrowed tongue, see Figure 18) is sometimes mentioned.37
Bone Regeneration Effect of Cassia occidentalis Linn. Extract and Its Isolated Compounds
Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay in Phytochemistry of Plants of Genus Cassia, 2021
Self-nano emulsifying drug delivery system (SEDDS) is an efficient mode for improving the bioavailability of poorly absorbed compounds often present in phytoextracts. A lipid-based SEDDS of CBE was found to enhance the bioavailabilities of apigenin, isovitexin, THF, luteolin and emodin along with the increase in the skeletal effect. However, CBE at 100 mg/kg dose increased osteogenic effect, the SEDDS formulated CBE achieved the same effect at 50 mg/kg (Pal et al., 2020). The study also found that MP treatment significantly suppressed osteocyte markers including dentin matrix acidic phosphoprotein 1 (DMP-1) and matrix extracellular phosphoglycoprotein (MEPE), and SEDDS formulated CBE maintained their expression (Pal et al., 2020). Muscle atrophy is another signature of GC treatment and we found that SEDDS-formulated CBE significantly improved muscle structure and prevented muscle atrophy. Reports also showed that SEDDS-formulated CBE did not alter the anti-inflammatory effect of MP (Pal et al., 2020). These studies established CO extract and its related formulation as an effective pharmacotherapy for the treatment of GC-induced osteo-sarcopenia.
Nicotinamide protects against skeletal muscle atrophy in streptozotocin-induced diabetic mice
Published in Archives of Physiology and Biochemistry, 2019
Shizhe Guo, Qingyan Chen, Yaying Sun, Jiwu Chen
Muscle atrophy is defined as a decline in muscle mass and subsequently leads to muscle weakness (Guadagnin et al., 2018). Based on the histologic analysis, the average CSA declined in DM group compared with the NC group, indicating the loss of muscle mass induced by diabetes. Besides, the maximum grip strength of diabetic mice was significantly weakened four weeks after the onset of diabetes when compared to NC group. Along with the duration of diabetes, the strength was increasingly weakened. After NAM treatment for four weeks, the grip strength of diabetic mice was reinforced while the strength of the NC group was not affected by NAM. NAM protects against deterioration of muscle function. To sum up, NAM could obviously prevent muscle mass loss and muscle strength attenuation, making it potential precautionary treatment for muscle atrophy in diabetes.
Role of acute exacerbations in skeletal muscle impairment in COPD
Published in Expert Review of Respiratory Medicine, 2021
Harry R. Gosker, Ramon C. Langen, Sami O. Simons
Inactivity, muscle disuse and unloading are well-documented triggers of muscle atrophy. These have been modeled in animals and humans by limb immobilization or suspension, or by enforcing sustained bed rest, which is followed by significant muscle atrophy and reduced muscular strength. Both decreased protein synthesis and increased proteolysis have been reported in skeletal muscle during disuse atrophy, although these changes are only apparent during progressive loss of muscle mass [124,125]. Activation of the ALP as well as UPS have been implicated in inactivity-induced proteolysis [125,126]. Besides MuRF1 and Atrogin-1, which are also transcriptionally activated in response to the other triggers of atrophy discussed here, Nedd4 is an E3 Ub-ligase specifically activated in inactivity-induced muscle atrophy [127]. FOXO and NF-κB, including non-canonical NF-κB signaling, have been implicated in the transcriptional regulation of proteolysis during disuse atrophy [20]. Inactivity also has a profound impact on myonuclear turnover, as it induces apoptosis and affects satellite cell proliferation and muscle regeneration [128,129]. Muscle disuse is a potent trigger of OXPHEN loss [130]. Extensive alterations in mitochondrial biogenesis and mitophagy occur rapidly in response to inactivity, underpinning these OXPHEN decreases [126]. Interestingly, overexpression of PGC-1α prevents disuse-induced muscle OXPHEN [131,132], implying this exercise-responsive master regulator of mitochondrial health as an integrative switch between muscle OXPHEN and mass during muscle adaptive responses to altered activity levels.
Is SARS-CoV-2 vaccination safe and effective for elderly individuals with neurodegenerative diseases?
Published in Expert Review of Vaccines, 2021
Yan Shi, Minna Guo, Wenjing Yang, Shijiang Liu, Bin Zhu, Ling Yang, Chun Yang, Cunming Liu
ALS is a chronic neurodegenerative disease. The primary manifestations are progressive skeletal muscle weakness and muscle atrophy. Studies have found that adjuvants in the vaccine may have a deleterious effect on the occurrence and development of ALS [84]. Adjuvants are nonspecific immune enhancers that can improve the body’s immune response to vaccines. Aluminum hydroxide is currently a commonly used adjuvant in vaccines. However, aluminum is potentially harmful to the CNS and may be associated with neurodegenerative diseases [85]. Mice injected with aluminum hydroxide can induce motor dysfunction and loss of motor neurons, which is similar to ALS [86]. Interestingly, the incidence of ALS among Gulf War veterans may be related to the anthrax vaccine containing aluminum hydroxide, which increases the incidence of ALS and causes a younger onset age [84,87]. It is worth noting that most inactivated vaccines using aluminum hydroxide as an adjuvant, including the CoronaVac developed by Sinovac and the vaccine jointly developed by Sinopharm and Wuhan Institute of Biological Products, are currently under development [39,88]. The impact of the vaccines containing these adjuvants on ALS patients is still unclear, and further evaluation is greatly needed.
Related Knowledge Centers
- Ageing
- Malnutrition
- Muscular Dystrophy
- Myopathy
- Nervous System
- Spinal Cord Injury
- Skeletal Muscle
- Cachexia
- Sedentary Lifestyle
- Sarcopenia