The health benefits of dietary fiber are widely recognized, but its impact on muscle health remains unclear. Therefore, this study aimed to elucidate the relationship between dietary fiber intake and muscle strength through a cross-sectional analysis of data from the Korea National Health and Examination Survey (KNHANES). Data from a single 24-h dietary recall and handgrip strength tests of 10,883 younger adults aged 19 to 64 years and 3,961 older adults aged ≥ 65 years were analyzed. Low muscle strength was defined as handgrip strength < 28 kg for men and < 18 kg for women. Multivariable linear and logistic regression analyses were conducted to determine the association of dietary fiber intake with muscle strength. Approximately 43% of Korean adults met the recommended intake of dietary fiber, and those with higher dietary fiber consumption also had higher total energy and protein intake. After adjusting for confounding variables, dietary fiber intake was found to be positively associated with maximal handgrip strength in younger women aged 19 to 64 years (β = 0.015; standard error [SE] = 0.006) and older men aged ≥ 65 years (β = 0.035; SE = 0.014). For older women aged ≥ 65 years, those in the lowest quartile of dietary fiber intake had a higher risk of low muscle strength than those in the highest quartile after adjustment of confounders (odds ratio 1.709; 95% confidence interval 1.130–2.585). These results suggest that adequate dietary fiber intake may reduce the risk of sarcopenia in older Korean women.
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Iron plays a role in energy metabolism as a component of vital enzymes and electron transport chains (ETCs) for adenosine triphosphate (ATP) synthesis. The tricarboxylic acid (TCA) cycle and oxidative phosphorylation are crucial in generating ATP in mitochondria. At the mitochondria matrix, heme and iron-sulfur clusters are synthesized. Iron-sulfur cluster is a part of the aconitase in the TCA cycle and a functional or structural component of electron transfer proteins. Heme is the prosthetic group for cytochrome c, a principal component of the respiratory ETC. Regarding fat metabolism, iron regulates mitochondrial fat oxidation and affects the thermogenesis of brown adipose tissue (BAT). Thermogenesis is a process that increases energy expenditure, and BAT is a tissue that generates heat via mitochondrial fuel oxidation. Iron deficiency may impair mitochondrial fuel oxidation by inhibiting iron-containing molecules, leading to decreased energy expenditure. Although it is expected that impaired mitochondrial fuel oxidation may be restored by iron supplementation, its underlying mechanisms have not been clearly identified. Therefore, this review summarizes the current evidence on how iron regulates energy metabolism considering the TCA cycle, oxidative phosphorylation, and thermogenesis. Additionally, we relate iron-mediated metabolic regulation to obesity and obesity-related complications.
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