scholarly journals Multifactorial Mechanism of Sarcopenia and Sarcopenic Obesity. Role of Physical Exercise, Microbiota and Myokines

Cells ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 160
Author(s):  
Jan Bilski ◽  
Piotr Pierzchalski ◽  
Marian Szczepanik ◽  
Joanna Bonior ◽  
Jerzy A. Zoladz

Obesity and ageing place a tremendous strain on the global healthcare system. Age-related sarcopenia is characterized by decreased muscular strength, decreased muscle quantity, quality, and decreased functional performance. Sarcopenic obesity (SO) is a condition that combines sarcopenia and obesity and has a substantial influence on the older adults’ health. Because of the complicated pathophysiology, there are disagreements and challenges in identifying and diagnosing SO. Recently, it has become clear that dysbiosis may play a role in the onset and progression of sarcopenia and SO. Skeletal muscle secretes myokines during contraction, which play an important role in controlling muscle growth, function, and metabolic balance. Myokine dysfunction can cause and aggravate obesity, sarcopenia, and SO. The only ways to prevent and slow the progression of sarcopenia, particularly sarcopenic obesity, are physical activity and correct nutritional support. While exercise cannot completely prevent sarcopenia and age-related loss in muscular function, it can certainly delay development and slow down the rate of sarcopenia. The purpose of this review was to discuss potential pathways to muscle deterioration in obese individuals. We also want to present the current understanding of the role of various factors, including microbiota and myokines, in the process of sarcopenia and SO.

2017 ◽  
pp. 1-7
Author(s):  
L.A. CONSITT ◽  
B.C. CLARK

The age-related loss of skeletal muscle (sarcopenia) is a major health concern as it is associated with physical disability, metabolic impairments, and increased mortality. The coexistence of sarcopenia with obesity, termed ‘sarcopenic obesity’, contributes to skeletal muscle insulin resistance and the development of type 2 diabetes, a disease prevalent with advancing age. Despite this knowledge, the mechanisms contributing to sarcopenic obesity remain poorly understood, preventing the development of targeted therapeutics. This article will discuss the clinical and physiological consequences of sarcopenic obesity and propose myostatin as a potential candidate contributing to this condition. A special emphasis will be placed on examining the role of myostatin signaling in impairing both skeletal muscle growth and insulin signaling. In addition, the role of myostatin in regulating muscle-to fat cross talk, further exacerbating metabolic dysfunction in the elderly, will be highlighted. Lastly, we discuss how this knowledge has implications for the design of myostatin-inhibitor clinical trials.


2010 ◽  
Author(s):  
Charlotte Froger ◽  
Badiaa Bouazzaoui ◽  
Laurence Taconnat

2020 ◽  
pp. 55-64
Author(s):  
N. Zarechnov ◽  
A. Kuznetsov ◽  
N. Seliverstova

The article is devoted to the problem of nutrition of patients receiving palliative care. The authors emphasize the importance of nutritional support for this group of patients and describe the experience of enteral and paraenteral nutrition.


2020 ◽  
Vol 17 ◽  
Author(s):  
Christina Karakosta ◽  
Argyrios Tzamalis ◽  
Michalis Aivaliotis ◽  
Ioannis Tsinopoulos

Background/Objective:: The aim of this systematic review is to identify all the available data on human lens proteomics with a critical role to age-related cataract formation in order to elucidate the physiopathology of the aging lens. Materials and Methods:: We searched on Medline and Cochrane databases. The search generated 328 manuscripts. We included nine original proteomic studies that investigated human cataractous lenses. Results:: Deamidation was the major age-related post-translational modification. There was a significant increase in the amount of αA-crystallin D-isoAsp58 present at all ages, while an increase in the extent of Trp oxidation was apparent in cataract lenses when compared to aged normal lenses. During aging, enzymes with oxidized cysteine at critical sites included GAPDH, glutathione synthase, aldehyde dehydrogenase, sorbitol dehydrogenase, and PARK7. Conclusion:: D-isoAsp in αA crystallin could be associated with the development of age-related cataract in human, by contributing to the denaturation of a crystallin, and decreasing its ability to act as a chaperone. Oxidation of Trp may be associated with nuclear cataract formation in human, while the role of oxidant stress in age-related cataract formation is dominant.


Author(s):  
Юлия Черткова ◽  
Yuliya Chertkova ◽  
Марина Егорова ◽  
Marina Yegorova

The paper reflects one of the aspects of the research carried out within the framework of the project “Nature of variability of negative personality traits: a twin study”. The research reviews the adaptive component of negative personal traits. The sample of the study consisted of 136 members of monozygotic twins and 401 only children in their families aged 18-78. Life satisfaction was a generalized metric of psychological adaptation. It is shown that a number of negative personality traits (in particular, narcissism, authoritarianism) positively correlate with life satisfaction. The biased value of various personality traits, which can also indirectly serve as an indicator of adaptability of these psychological properties, was assessed using a semantic differential. The age-related changes in the perfect image of the self, which are associated primarily with some more attractive negative personal traits, as well as the multidirectional desired changes in personality traits in themselves and the twin (more power and conflict in themselves and less of the same in the brother/sister) also indicate that a number of negative personal traits play a positive role in psychological adaptation. It is assumed that these traits can have a compensatory function during stress, and the destructiveness of these traits can have a greater impact on people around than on themselves.


Author(s):  
Elisa M. Trucco ◽  
Gabriel L. Schlomer ◽  
Brian M. Hicks

Approximately 48–66% of the variation in alcohol use disorders is heritable. This chapter provides an overview of the genetic influences that contribute to alcohol use disorder within a developmental perspective. Namely, risk for problematic alcohol use is framed as a function of age-related changes in the relative contribution of genetic and environmental factors and an end state of developmental processes. This chapter discusses the role of development in the association between genes and the environment on risk for alcohol use disorder. Designs used to identify genetic factors relevant to problematic alcohol use are discussed. Studies examining developmental pathways to alcohol use disorder with a focus on endophenotypes and intermediate phenotypes are reviewed. Finally, areas for further investigation are offered.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yaarit Kutsher ◽  
Michal Fisler ◽  
Adi Faigenboim ◽  
Moshe Reuveni

AbstractIt is widely known that during the reproductive stage (flowering), plants do not root well. Most protocols of shoot regeneration in plants utilize juvenile tissue. Adding these two realities together encouraged us to study the role of florigen in shoot regeneration. Mature tobacco tissue that expresses the endogenous tobacco florigen mRNA regenerates poorly, while juvenile tissue that does not express the florigen regenerates shoots well. Inhibition of Nitric Oxide (NO) synthesis reduced shoot regeneration as well as promoted flowering and increased tobacco florigen level. In contrast, the addition of NO (by way of NO donor) to the tissue increased regeneration, delayed flowering, reduced tobacco florigen mRNA. Ectopic expression of florigen genes in tobacco or tomato decreased regeneration capacity significantly. Overexpression pear PcFT2 gene increased regeneration capacity. During regeneration, florigen mRNA was not changed. We conclude that florigen presence in mature tobacco leaves reduces roots and shoots regeneration and is the possible reason for the age-related decrease in regeneration capacity.


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