Inflammation and metabolism: the role of adiposity in sarcopenic obesity

Abstract

Sarcopenic obesity is characterised by the double burden of diminished skeletal muscle mass and the presence of excess adiposity. From a mechanistic perspective, both obesity and sarcopenia are associated with sub-acute, chronic pro-inflammatory states that impede metabolic processes, disrupting adipose and skeletal functionality, which may potentiate disease. Recent evidence suggests that there is an important cross-talk between metabolism and inflammation, which has shifted focus upon metabolic-inflammation as a key emerging biological interaction. Dietary intake, physical activity and nutritional status are important environmental factors that may modulate metabolic-inflammation. This paradigm will be discussed within the context of sarcopenic obesity risk. There is a paucity of data in relation to the nature and the extent to which nutritional status affects metabolic-inflammation in sarcopenic obesity. Research suggests that there may be scope for the modulation of sarcopenic obesity with alterations in diet. The potential impact of increasing protein consumption and reconfiguration of dietary fat composition in human dietary interventions are evaluated. This review will explore emerging data with respect to if and how different dietary components may modulate metabolic-inflammation, particularly with respect to adiposity, within the context of sarcopenic obesity.

Free Fatty Acid Species Differentially Modulate the Inflammatory Gene Response in Primary Human Skeletal Myoblasts

“…Inflammation has been implicated in skeletal muscle wasting in animal studies [ 21 , 22 , 23 ]. The high level of systemic inflammatory proteins was suggested to play a key role in the development of human sarcopenic obesity; however, it has been difficult to clarify which proteins are clinically relevant [ 21 , 22 , 24 ].…”

“…Inflammation has been implicated in skeletal muscle wasting in animal studies [ 21 , 22 , 23 ]. The high level of systemic inflammatory proteins was suggested to play a key role in the development of human sarcopenic obesity; however, it has been difficult to clarify which proteins are clinically relevant [ 21 , 22 , 24 ]. One limitation of clinical studies is the reverse causality mechanism, implying that sarcopenic obesity could be a risk factor for the development of an inflammatory state.…”

Sarcopenic Obesity: An Emerging Public Health Problem

“…This definition was supported by a more recent critical appraisal of the definition and diagnostic criteria of SO based on a systematic review which noted that most existing studies defined SO based on the co-existence of obesity and sarcopenia [ 19 ] ( Table 1 ). SO is a complex geriatric syndrome characterized by an aged-associated reduced muscle mass and dysfunction and excess adiposity [ 11 , 20 ]. Therefore, individuals with SO have a double burden of malnutrition and are at an increased risk of frailty, disability, morbidity, and mortality.…”

“…The etiology and pathogenesis of SO are intertwined and intricate. The core biological factors leading to SO are changes in body composition related to aging, hormonal changes, the interplay between metabolism and inflammation, environmental factors (unhealthy diet and lack of exercise), and chronic diseases [ 5 , 6 , 11 , 44 ]. Aging and obesity cause atrophy of fast type II muscle fibers and a switch to slow type I muscle fibers and neurodegeneration, leading to loss of muscle neurotrophic effects and promotion of intramyocellular lipid (IMCL) deposition.…”

“…The main etiological factors include age-related changes in body composition, sex-specific hormonal changes, chronic low-grade inflammation, insulin resistance, sedentary behavior, and unhealthy diet [ 5 , 10 ]. Inflammation, oxidative stress, and insulin resistance are considered to be the key factors in the development of SO [ 5 , 11 , 12 ]. As the evidence accumulated, optimal diet and exercise strategies are of cardinal importance for preventing and treating SO and to combating the adverse outcomes.…”