Publications by authors named "Sander L Wijers"

Alterations in musculoskeletal health with advanced age contribute to sarcopenia and decline in bone mineral density (BMD) and bone strength. This decline may be modifiable via dietary supplementation. To test the hypothesis that a specific oral nutritional supplement can result in improvements in measures of bone health.

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Brown and beige adipocytes combust nutrients for thermogenesis and through their metabolic activity decrease pro-atherogenic remnant lipoproteins in hyperlipidemic mice. However, whether the activation of thermogenic adipocytes affects the metabolism and anti-atherogenic properties of high-density lipoproteins (HDL) is unknown. Here, we report a reduction in atherosclerosis in response to pharmacological stimulation of thermogenesis linked to increased HDL levels in APOE*3-Leiden.

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Background & Aim: Sarcopenia, the age-related decrease in muscle mass, strength, and function, is a main cause of reduced mobility, increased falls, fractures and nursing home admissions. Cross-sectional and prospective studies indicate that sarcopenia may be influenced in part by reversible factors like nutritional intake. The aim of this study was to compare functional and nutritional status, body composition, and quality of life of older adults between age and sex-matched older adults with and without sarcopenia.

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Background: Age-related losses of muscle mass, strength, and function (sarcopenia) pose significant threats to physical performance, independence, and quality of life. Nutritional supplementation could positively influence aspects of sarcopenia and thereby prevent mobility disability.

Objective: To test the hypothesis that a specific oral nutritional supplement can result in improvements in measures of sarcopenia.

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Context: Recently, brown adipose tissue (BAT) gained interest as a possible target for cold-induced thermogenesis, and therefore a target for treatment of obesity in adult humans. However, mitochondrial uncoupling takes place not only in BAT but also in skeletal muscle tissue. Both tissues may be involved in cold-induced thermogenesis, which is presumably regulated by the sympathetic nervous system.

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On entering a cold environment, people react by increasing insulation and energy expenditure (EE). However, large interindividual differences exist in the relative contribution of each mechanism. Short-term studies revealed that obese subjects increase EE (i.

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Adaptive thermogenesis, the increase in energy expenditure in response to diet or cold exposure, shows large interindividual differences. The objective of this study was to investigate the proteins in human muscle tissue that relate to this variation. Therefore, we studied correlations between changes in expressions of proteins and increases in energy expenditure.

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Background: Mild cold exposure and overfeeding are known to elevate energy expenditure in mammals, including humans. This process is called adaptive thermogenesis. In small animals, adaptive thermogenesis is mainly caused by mitochondrial uncoupling in brown adipose tissue and regulated via the sympathetic nervous system.

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Context: Adaptive thermogenesis is defined as the increase in energy expenditure in response to overfeeding or cold. Large interindividual differences in adaptive thermogenesis have been described.

Objective: Because there are indications for a common underlying mechanism, we studied in humans whether the increase in thermogenesis during short-term overfeeding (3 d) is related to mild cold-induced thermogenesis.

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