Computed Tomography-Derived Myosteatosis and Metabolic Disorders

Abstract

The role of ectopic adipose tissue infiltration into skeletal muscle (i.e., myosteatosis) for metabolic disorders has received considerable and increasing attention in the last 10 years. The purpose of this review was to evaluate and summarize existing studies focusing on computed tomography (CT)-derived measures of myosteatosis and metabolic disorders. There is consistent evidence that CT-derived myosteatosis contributes to dysglycemia, insulin resistance, type 2 diabetes mellitus, and inflammation, and, to some extent, dyslipidemia, independent of general obesity, visceral fat, and other relevant risk factors, suggesting that it may serve as a tool for metabolic risk prediction. Identification of which muscles should be examined, and the standardized CT protocols to be employed, are necessary to enhance the applicability of findings from epidemiologic studies of myosteatosis. Additional and longer longitudinal studies are necessary to confirm a role of myosteatosis in the development of type 2 diabetes mellitus, and examine these associations in a variety of muscles across multiple race/ethnic populations. Given the emerging role of myosteatosis in metabolic health, well-designed intervention studies are needed to investigate relevant lifestyle and pharmaceutical approaches.

Muscle Fat Content Is Strongly Associated With Hyperuricemia: A Cross-Sectional Study in Chinese Adults

“…A longitudinal study suggested that increase in intermuscular adipose was a more consistent marker of aging than sarcopenia ( 23 ). Myosteatosis is also closely related to insulin resistance and has been reported as an independent risk factor of diabetes ( 19 ). It is indicated that the intramyocellular lipids content, which is analyzed by muscle biopsies, was significantly correlate with insulin resistance in T2DM patients, obesity as well as lean subjects ( 17 ).…”

“…A high muscle fat content (often known as myosteatosis) may play a key role in the risk of metabolic abnormalities. Studies have indicated that myosteatosis is associated with insulin resistance, type 2 diabetes mellitus (T2DM), dyslipidemia and cardiometabolic diseases ( 17 , 18 ), and there was also a link between skeletal muscle density and biomarkers of inflammation, such as CRP, IL-6, TNF-α, adiponectin and leptin ( 19 ). Myosteatosis has also been identified as a risk factor for decreased muscle strength, osteoporotic fractures, and reduced physical function ( 20 , 21 ).…”

Advances in muscle health and nutrition: A toolkit for healthcare professionals

“…Computerized tomography scan data show myosteatosis has been associated with low muscle strength, poor preoperative physical fitness, muscle metabolic dysfunction, and mortality in different populations [110,132,133]. Myosteatosis has also been associated with greater risk of prediabetes and type 2 diabetes, increased homeostasis model assessment for insulin resistance (HOMA-IR), as well as circulating levels of glucose, insulin, CRP, and IL-6 [134]. Also importantly, patients with both myosteatosis and low muscle mass may present at greater risk for poorer outcomes, compared to each of these conditions alone [30,135].…”

Ammonia and the Muscle: An Emerging Point of View on Hepatic Encephalopathy

“…It is defined as a muscle mass two standard deviations below the healthy young adult mean [25]. Myosteatosis is a fat infiltration of the skeletal muscle mass with an increased proportion of intramuscular and intermuscular fat that could impact muscle function and lead to a systemic inflammation [26].…”

“…Regarding myosteatosis, the physiopathological association with hyperammonemia and HE is more complex and partially unknown. Myosteatosis seems to derive from a complex mechanism involving the metabolism of fatty acids and glycogen; the pivotal point of this process is mediated by the proinflammatory state that is present and that leads to muscle depletion [26]. Nardelli et al have demonstrated the association between myosteatosis and HE, hypothezing that fat infiltration, by reducing the fat-free mass, may contribute to the reduction of leads to partial loss of function of glutamate synthetase, expressed in the muscle cell.…”