Dominic Stone
Fatty infiltration of muscle, also known as myosteatosis, is characterised by an abnormal accumulation of adipocytes in non-adipose tissue, resulting in adverse metabolic and mobility impairments. The regulatory mechanism of fat infiltration in skeletal muscle is complex, involving the interplay of genes, regulators, and signalling pathways. Aging, disuse, sex steroid deficiencies, altered leptin signalling, and glucocorticoid treatments are among the factors that contribute to fatty infiltration. This condition is associated with muscle atrophy, chronic inflammation, and a decrease in muscle strength and endurance. In addition, fatty infiltration can lead to irreversible muscle dysfunction, known as fatty degeneration, which further reduces mobility and quality of life.
| Characteristics | Values |
|---|---|
| Definition | Fatty infiltration is characterized by an abnormal accumulation of adipocytes in non-adipose tissue. |
| Other Names | Intramuscular fat, intramyocellular (IMC) lipid, myosteatosis, IMAT, MFI |
| Causes | Aging, disuse, sex steroid deficiency, altered leptin signaling, glucocorticoid treatment, tendon rupture, nerve damage, estrogen deficiency, androgen deprivation therapy |
| Effects | Loss of muscle mass and strength, insulin insensitivity, inflammation, functional deficits, chronic inflammation, muscle atrophy, decreased mobility, reduced life expectancy |
| Prevention/Treatment | CLA, linseed, AdipoRon, resistance exercise |
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What You'll Learn
Aging and frailty
Aging in humans is accompanied by a loss of subcutaneous fat but an accumulation of AC and lipids in non-adipose depots, such as bone marrow, liver, and skeletal muscle. Fatty infiltration of skeletal muscle, also known as myosteatosis, has been recognized as an important component of aging and frailty.
Myosteatosis is associated with inflammation, fibrosis, and impaired contractile capacity of both type I and type II muscle fibers, leading to a dramatic decrease in muscle power. Advancing age is often associated with reduced daily activity, which can contribute to muscle disuse and inactivity, a major regulator of myosteatosis development. The accumulation of intramyocellular (IMC) lipids within muscle fibers is associated with insulin insensitivity, inflammation, and functional deficits in skeletal muscle. This accumulation of IMC lipids leads to muscle weakness and an increased risk of fractures in the elderly.
The impact of aging on skeletal muscle can be assessed through quantitative MR imaging, which has revealed associations with frailty and muscle strength. Studies have shown that physical activity and regular exercise are effective countermeasures against fatty infiltration of muscle with aging. For example, resistance training 3 days a week for adults over 55 years of age decreased thigh intramuscular adipose tissue. Additionally, the resumption of physical activity after periods of inactivity can reverse fatty infiltration in older adults.
Therapeutic strategies to prevent myosteatosis may improve muscle function and reduce fall risk in the elderly. This can potentially impact the incidence of bone fractures, a major cause of morbidity and mortality among the elderly. Understanding the triggers and regulatory mechanisms of fat infiltration in skeletal muscle is vital for improving human health and maintaining skeletal muscle development.
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Estrogen deficiency
Fatty infiltration of the skeletal muscle, also known as myosteatosis, is an important component of aging and frailty. It is characterised by an abnormal accumulation of adipocytes in non-adipose tissue, resulting in cellular activity, metabolism, and functional abnormalities.
Research has shown that ovariectomized rodents and mice exhibit increased lipid content in skeletal muscle due to estrogen deficiency. Similarly, post-menopausal women experience more severe muscular fatty infiltration as a result of decreased estrogen levels. This is supported by studies that collected supraspinatus muscle samples from female patients with or without menopause, which revealed a correlation between decreased estrogen and muscular fat accumulation.
Furthermore, estrogen deficiency is implicated in bone loss and marrow adipose tissue (AC) accumulation in women. Conditions such as disuse, sex steroid deficiency, altered leptin signaling, and glucocorticoid treatment are also found to stimulate the accumulation of ACs and intramyocellular (IMC) lipids in skeletal muscle.
The accumulation of IMC lipids due to estrogen deficiency has been associated with insulin insensitivity, inflammation, and functional deficits in skeletal muscle. This can lead to impaired muscle strength and postural instability. Thus, estrogen deficiency plays a significant role in the development of fatty infiltration in skeletal muscle, particularly in post-menopausal women, affecting muscle function and overall locomotor ability.
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Insulin insensitivity
Insulin resistance is often associated with obesity and type 2 diabetes mellitus (T2DM). In insulin-resistant individuals, the rates of fatty acid (FA) uptake are significantly higher, leading to increased intracellular lipid accumulation in skeletal muscle. This accumulation of lipids, particularly within the myofibers themselves (intramuscular fat or intramyocellular [IMC] lipid), is a key characteristic of fatty infiltration of the muscle. The increased lipid accumulation in skeletal muscle contributes to insulin resistance by impairing normal protein synthesis and inducing pathological changes that affect muscle function.
Physical inactivity and a lack of exercise can contribute to insulin resistance. Exercise enhances the body's sensitivity to insulin and helps build muscle that can absorb blood glucose. Additionally, exercise can decrease lipid accumulation in muscle cells and increase their capacity for lipid oxidation, thereby preventing insulin resistance. Certain dietary choices, such as a diet high in processed foods, carbohydrates, and saturated fats, have also been linked to insulin resistance.
There are other factors that can influence insulin sensitivity. Certain medications, such as steroids, blood pressure medications, and HIV treatments, can contribute to insulin resistance. Hormonal disorders, such as Cushing's syndrome and acromegaly, can also affect how the body uses insulin. Furthermore, certain inherited genetic disorders, such as Type A insulin resistance syndrome, Donohue syndrome, and myotonic dystrophy, are rare but known causes of insulin resistance.
The accumulation of lipid intermediates, including diacylglycerols, ceramides, and long-chain fatty acyl coenzyme A molecules, is believed to play a role in attenuating the insulin signal, leading to impaired glucose transport. Inflammation in skeletal muscle, particularly in obesity, can also contribute to insulin resistance. Obese individuals may experience increased secretion of pro-inflammatory molecules and cytokines, such as TNF-α, which can induce muscle inflammation and negatively affect myocyte metabolism, ultimately contributing to insulin resistance.
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Chronic inflammation
Fatty infiltration of the skeletal muscle, also known as myosteatosis, is associated with chronic inflammation. This condition is characterized by an abnormal accumulation of adipocytes in non-adipose tissue, leading to lipotoxicity and various metabolic abnormalities.
The presence of chronic inflammation in fatty infiltration is linked to insulin resistance and dyslipidemia, particularly in older individuals and those with metabolic disorders such as obesity and diabetes. The decrease in muscle strength coincides with an increase in fatty infiltration, indicating a decline in muscle quality. This loss of muscle strength is attributed to the accumulation of lipids within myofibers, known as intramuscular fat or intramyocellular lipid.
Additionally, the accumulation of sphingolipid ceramide has been found to have a detrimental effect on skeletal muscle function. Lipotoxicity, a result of fatty infiltration, impairs mitochondrial function, increases ROS release, and contributes to persistent low-level chronic inflammation. This chronic inflammation further disrupts fibrin homeostasis and negatively impacts skeletal muscle generation, apoptosis, and damage repair.
The effects of chronic inflammation on fatty infiltration extend beyond muscle metabolism. It induces a series of pathological changes that impair skeletal muscle function and contribute to conditions such as osteoporosis and sarcopenia. The loss of muscle mass and strength associated with fatty infiltration highlights the importance of understanding and addressing this condition, especially in the aging population.
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Genes and regulators
Several genes and signalling pathways are involved in regulating fat infiltration. These include cAMP-PKA, hedgehog, Wnt/β-catenin, AMPK, MAPK, miRNAs, and lncRNAs. The Wnt/β-catenin pathway, for example, is a key regulator of adipogenesis, and its inhibition can block adipogenesis and limit steatosis.
The adipogenic marker genes Pparγ and C/ebpα are significantly upregulated in obese individuals, indicating a link between obesity and fat deposition in skeletal muscle. Estrogen deficiency in women also increases lipid content in skeletal muscle and the expression of adipogenic genes.
Additionally, the PAX7 gene, an important marker gene for MuSCs, regulates the myogenic differentiation genes Myod and Myf5. The absence of both Myod and Myf5 results in the failure of muscle growth initiation. Fatty infiltration impacts the damage repair process of muscle fibres, particularly MuSCs, leading to atrophy and a decrease in their number.
The regulatory mechanisms of fat infiltration in skeletal muscle are complex and involve the interplay of various genes and signalling pathways. While some aspects are understood, further research is needed to fully comprehend the regulatory processes.
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Frequently asked questions
Fatty infiltration of muscle is characterised by an abnormal accumulation of adipocytes in non-adipose tissue. This can lead to adverse metabolic and mobility impairments.
Fatty infiltration of muscle can be caused by several factors, including ageing, tendon rupture, nerve damage, and insulin insensitivity.
Ageing is associated with a loss of subcutaneous fat and an accumulation of lipids in non-adipose tissues, such as skeletal muscle.
Insulin is an anabolic factor for skeletal muscle. Accumulation of muscle ACs and IMC lipid decreases insulin sensitivity, impairing normal protein synthesis and leading to fatty infiltration.
Nerve injuries can cause muscle atrophy and fatty infiltration, leading to chronic inflammation and decreased expression of adipokines such as adiponectin, which has anti-inflammatory and anti-apoptotic effects.
