Heart failure with preserved ejection fraction in older adults
Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich in Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Haykowsky and colleagues further extended their results by using dual-energy X-ray absorptiometry and found that percent body fat and percent leg fat were significantly increased, whereas percent body lean and leg lean mass were significantly reduced, and the slope of the relation of peak VO2 with percent leg lean mass was markedly reduced in the older HFpEF patients versus a healthy control group (94). These data suggest that poor “quality” of skeletal muscle may contribute to the reduced peak VO2 found in older HFpEF patients. These investigators later assessed thigh muscle composition using phase-contrast MRI, which showed abnormal fat infiltration into the thigh skeletal muscle, associated with reduced peak exercise VO2 in HFpEF (95). Indeed, Bhella et al. (92), using phosphate-31 magnetic resonance spectroscopy during and after performing static leg lifts, showed impaired skeletal muscle oxidative metabolism in patients with HFpEF. Thus, a number of potential intramuscular fat-mediated structural and biochemical alterations may decrease oxygen transport to and/or utilization by the active muscles.
Exercise in Older Adults with Diabetes
Medha N. Munshi, Lewis A. Lipsitz in Geriatric Diabetes, 2007
Accompanying the loss in muscle mass, strength, and power with aging is a decrease in basal metabolic rate and whole body fat oxidation (21), in addition to reduced energy expenditure and physical activity (22,23). These metabolic changes may help to explain the concurrent increase in body weight and fat mass with advancing age; even without a change in body weight, it appears that the amount of fat mass still increases with age (6). In both men and women, weight and fat mass increases progressively from around the age of 20 up until 60 to 65 years, with a gradual decline thereafter (3,24). However, perhaps more important are the changes in body fat distribution. Much of the age-related increase in fat mass is due to abdominal (visceral) fat accumulation, whereas subcutaneous fat in the arms and legs tends to decrease (25). This progressive increase in visceral and truncal fat has been strongly linked to an increased risk of CVD and type 2 diabetes (26,27). Recent data also indicate that there is an age-related increase in intramuscular fat, which is a marker of muscle lipid content (28). This increased fat infiltration within muscle has been shown to be associated with skeletal muscle insulin resistance independent of total or abdominal adiposity (29), and higher values have been observed in adults with type 2 diabetes (30). These findings indicate that the quality of muscle may also be an important determinant of disease risk in older adults.
Stroke
John M. Saxton in Exercise and Chronic Disease, 2011
Bilateral mid-thigh computer tomography (CT) scans can be used to illustrate the severe atrophy caused by chronic hemiparesis (Figure 4.2) (Ryan et al. 2002). There is extreme gross muscular atrophy in the paretic leg mid-thigh CT scans, showing 20 per cent lower muscle area compared to the non-paretic thigh. In addition, intramuscular area fat is 25 per cent greater in the paretic thigh compared to the non-paretic thigh (Ryan et al. 2002). Elevated intramuscular fat is linked to insulin resistance and its complications (Frontera et al. 1997). These body composition abnormalities may impact upon whole body metabolic health and function.
High Visceral Fat is Associated with a Worse Survival after Liver Resection for Intrahepatic Cholangiocarcinoma
Published in Nutrition and Cancer, 2022
Laurence Lacaze, Damien Bergeat, Chloé Rousseau, Laurent Sulpice, David Val-Laillet, Ronan Thibault, Karim Boudjema
Body composition parameters were measured at L3 level on abdominal CT scans performed with the most recent scanner available (median: 26.5 day before surgery, maximum 151 day). This was made in a semi-automated way using the ImageJ® software (National Institutes of Health, Bethesda, Maryland, USA).20 The density threshold was set between −29 and +150 Hounsfield Units (HU)20 for muscle, and between −190 and −30 HU for fat.21 Measurements were performed by a single observer (LL). Two measurements were made on two successive slices of CT scan at the level of L3 and the average of the two areas was considered for analysis. Abdominal skeletal muscle area (SMA) was measured as the sum of psoas muscle, external and internal oblique muscles, transverse muscle and paravertebral muscles areas. Skeletal muscle index (SMI) (cm2/m2) was calculated as SMA/height (m)2. Intramuscular fat was measured in the same area and distinguished from the muscle by its difference of density. Visceral fat area (VFA), subcutaneous fat area (SCFA), and intramuscular fat area (IMFA) were also measured. Total fat area was calculated as the sum of VFA, SCFA and IMFA. The respective fat indexes (cm2/m2) (visceral (VFI), subcutaneous (SCFI), intramuscular (IMFI), total fat) were calculated as normalized by height, as for a SMI calculation.
Neurogenic obesity and systemic inflammation following spinal cord injury: A review
Published in The Journal of Spinal Cord Medicine, 2018
Gary J. Farkas, David R. Gater
TNFα was the first discovered adipokine implicated in the link between obesity, type 2 diabetes mellitus, insulin resistance, and inflammation.45,47 This adipokine may be the initial trigger in systemic inflammation and may subsequently prolong the inflammatory state by further triggering its release from adipose tissue.48 This proinflammatory adipokine is thought to promote insulin resistance through the upregulation of suppressor of cytokine signaling-3 (SOCS3). This inhibits the phosphorylation of the insulin receptor substrate 1 (IRS-1) and subsequently the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (PKB, Akt) signaling cascade in muscle and adipose tissue (Figure 1).3,49,50 In addition, TNFα downregulates GLUT4 gene transcription and translocation in both tissues.51 TNFα is also thought to be able to induce insulin resistance by negatively influencing both the differentiation and lipid metabolism of adipocytes through the activation of NF-κB and extracellular signaling regulated kinase, as well as reducing the secretion of anti-inflammatory adipokines. This leads to an increased lipolytic state with the infiltration of NEFA into skeletal muscle (Figure 1).52 Intramuscular fat is therefore increased, as noted in SCI.2,27
Gender difference in the relationship between lipid accumulation product index and pulse pressure in nondiabetic Korean adults: The Korean National Health and Nutrition Examination Survey 2013–2014
Published in Clinical and Experimental Hypertension, 2022
Hyun Ho Sung, Mi Young Gi, Ju Ae Cha, Hye Eun Cho, Ae Eun Moon, Hyun Yoon
Visceral or intra-abdominal fat surrounds internal organs inside the peritoneal cavity, in contrast to subcutaneous fat, which is found underneath the skin, and intramuscular fat, which is found interspersed in skeletal muscle (1). An increase in visceral fat is associated with an increased risk of cancer, cardiovascular disease (CVD), and all-cause mortality (2). The lipid accumulation product (LAP) is a gender-specific index based on waist circumference (WC) and triglycerides (TGs) and reflects the physiological changes related to intra-abdominal lipid over-accumulation (3). LAP has been suggested as an effective marker of lipid accumulation in ectopic sites, such as the skeletal system and liver (4). Previous studies have revealed that LAP is a better predictor of increased risk of CVD events and all-cause morbidity and mortality compared to body mass index (BMI) or WC (3,5,6).
Related Knowledge Centers
- Diglyceride
- Lipodystrophy
- Metabolite
- Obesity
- Type 2 Diabetes
- Insulin Resistance
- Skeletal Muscle
- Mitochondrion
- HIV
- HIV/AIDS