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Myosteatosisis strongly associated with NASH in
humans and in preclinical NAFLD models
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EASL 2020 Aug 27-29
Maxime Nachit1,2, Greetje Vande Velde2,3, Wilhelmus J. Kwanten4, Jean-Paul Thissen5, Maxime De Rudder1, Olivier Schakman6, Caroline Bouzin7, Bart Op De Beeck8, Luc Van Gaal9, Yves Horsmans10, Sven Francque4* and Isabelle A.Leclercq1*
1 Laboratoryof Hepato-Gastroenterology, Institut de Recherche Experimentale et Clinique,
UCLouvain, Brussels, Belgium
2 Department of Imaging and Pathology, KU Leuven, Leuven, Belgium
3 Molecular Small Animal Imaging Center (MoSAIC), KU Leuven, Belgium
4 Department of Gastroenterology and Hepatology, Antwerp University Hospital, Antwerp, Belgium
5 Pole of Endocrinology, Diabetes and Nutrition, Institute of Experimental and Clinical Research,
UCLouvain, Brussels, Belgium.
6 Institute of Neuroscience, Universite catholique de Louvain, Brussels, Belgium
7 IREC Imaging Platform, Universite catholique de Louvain, Brussels, Belgium
8 Department of Radiology, Antwerp University Hospital, Antwerp, Belgium.
9 Department of Endocrinology, Diabetology and Metabolism, Antwerp University Hospital, Belgium
10 Service D'Hepato-Gastro-Enterologie, Cliniques Universitaires Saint-Luc, Brussels, Belgium
see presentation below following this insert immediately below explaining myosteatosis which i defined here as fat infiltration in skeletal muscle, something we see in HIV+.
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Abstract
Purpose of review: To summarize the epidemiology of myosteatosis and its association with diabetes.
Recent findings: The role of myosteatosis (fat infiltration in skeletal muscle) in diabetes has received considerable attention. There is reasonably consistent evidence that myosteatosis contributes to glucose and insulin abnormalities and diabetes, possibly even independent of overall obesity. Novel hypotheses that link myosteatosis with insulin resistance and type 2 diabetes have also recently been proposed. These hypotheses suggest that impaired secretion of adipokines, modulation of nutritive blood flow to skeletal muscle, or both may be of importance for the development of myosteatosis. Recent longitudinal data also suggest that myosteatosis increases with aging, regardless of changes in body weight.
Summary: Further studies are needed to identify the specific physiological mechanisms that influence myosteatosis, and the mechanisms that link this fat depot with insulin resistance. Longitudinal studies are also needed to evaluate the remodeling of skeletal muscle fat with aging, across a wider age spectrum, and across different populations, especially those at high risk of developing diabetes. There is also a need to evaluate whether myosteatosis influences the incidence of type 2 diabetes independent of overall adiposity. A better understanding of the factors that regulate myosteatosis may lead to the development of novel therapies that influence a more metabolically 'healthy' skeletal muscle. https://pubmed.ncbi.nlm.nih.gov/20179586/
Muscle mass and strength are critical components for maintaining physical function, here Dr Vera C Mazurak from the University of Alberta explains why.
Muscle mass and strength are critical for maintaining physical function, mobility and vitality. Sarcopenia was first coined to represent the loss of muscle that normally occurs during the aging process. Loss of muscle as a result of disease can be referred to as myopenia, keeping in mind that many older individuals may have lost muscle due to co-morbidities (chronic disease), recent hospitalisation, or medications. Regardless of the cause, or how it is defined, individuals with severe muscle wasting have difficulty performing daily tasks.
Disability, poor functional capacity and shorter survival contribute to high costs as a result of reduced quality of life, increased caregiver burden and health service utilisation. It has been revealed that low muscle mass is prevalent in every body size. Function of muscle is dependent in part on muscle quality. Muscle tissue normally contains only small amounts of fat not intended for long-term lipid storage, but rather as a short term energy source for skeletal muscle contraction. Myosteatosis, characterised by excess deposition of fat into muscle, is considered to be a pathological phenomenon. The more fat a muscle contains, the less dense it becomes, and low density muscle is poor quality muscle. Low muscle density has been described in conditions of aging, detraining, various types of muscle atrophy, insulin resistance, Type 2 diabetes and most recently, cancer. Both low muscle mass and myosteatosis have been identified to increase the risk of poor function and death in a variety of patient populations.
The causes of myopenia and myosteatosis are multifactorial and may share common pathways for development. The complexity of relationships between various tissues is emerging. There is communication (cross-talk) between tissues through the release of mediators from one organ system to another in response to physiological stimuli. Involvement of other tissues to alter amount and quality of muscle adds several orders of complexity to the problems of myosteatosis and myopenia. Many underlying factors contribute to a decline in muscle health, including catabolic humoral mediators (i.e. pro-inflammatory cytokines), anabolic failure (i.e. insulin insensitivity) and activation of proteolytic systems.
Finding a treatment for low muscle mass is on the agenda of many pharmaceutical companies. To date, there are no approved drugs to reverse muscle loss, however several phase 2 and 3 trials are in progress investigating promising potential treatments for muscle loss that occurs during aging and disease.
The ability to modify muscle wasting and intramuscular fat accumulation has a broad scope of application to aging, diabetes, obesity and various forms of muscle atrophy, which share these common features. While treatment for these conditions remains limited, a number of mechanisms may contribute to the ability various drugs and nutrients to alter body composition, however, a more complete understanding of the features of the muscle characterised by wasting and fat infiltration is required. https://www.openaccessgovernment.org/defining-myopenia-myosteatosis/12040/
Although earlier studies investigated changes in skeletal muscle mass to define sarcopenia, recent evidence suggests that fat accumulation within the muscle might be responsible for functional impairment and negative pathophysiological responses even in patients with quantitatively normal or nearly normal muscle mass.15
Myosteatosis is believed to occur when lipids intake exceeds the disposal capacity of the adipose tissue and muscle, functioning as a form of ectopic fat storage in overweight subjects.19, 40 While myosteatosis is also seen in normal weight or underweight patients,41 it is reasonable to assume that the skeletal muscle does not only act as a plain ectopic storage of energy surplus, and as such mechanisms other than excessive fat intake may play an important role in the development of pathological muscle fat deposition.19 In our study, myosteatosis was moderately but significantly associated with the severity of the underlying liver disease (labMELD, Child-Pugh Score, albumin, and platelet count), highlighting the importance of a complex and poorly understood liver-to-muscle cross-talk over a simple nutritional theory.19
https://onlinelibrary.wiley.com/doi/full/10.1111/ajt.15577
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from NASH wrap up by William Alazawi MD UK
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