A mediating role of visceral adipose tissue on the association of health behaviours and metabolic inflammation in menopause: a population-based cross-sectional study

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Fat distribution changes with advancing menopause, which predisposes to metabolic inflammation. However, it remains unclear, how health behaviours, including sleeping, eating and physical activity, or their combinations contribute to metabolic inflammation caused by visceral adipose tissue (VAT). The aim of the present study was to examine whether health behaviours are associated with metabolic inflammation and whether VAT mediates these associations in menopausal women. This cross-sectional study consisted of a sample of middle-aged women (n = 124). Health behaviours were assessed by self-report questionnaire with measures of sleeping, eating (Eating Disorder Examination Questionnaire, EDE-Q), and physical activity behaviours. Metabolic inflammation was measured using GlycA, a composite biomarker of inflammation, and bioimpedance device was used to assess VAT. Structural equation modelling was used to examine the direct and indirect associations of health behaviours with inflammation, as well as the moderation effect of health behaviours on VAT and metabolic inflammation. VAT was directly associated with inflammation. Two indirect pathways were found: eating and physical activity behaviours were both inversely associated with inflammation through VAT, whereas sleeping behaviour was not. Physical activity moderated the association between VAT and metabolic inflammation. The association was stronger in those who were physically less active. Furthermore, eating behaviour and physical activity had an interaction on VAT. Physical activity was negatively associated with VAT among women with normal eating behaviour, but the association was less clear among women with features of disordered eating behaviour. It is possible to impede the menopausal shift to adverse visceral adiposity through increased physical activity and further decrease the risk of metabolic inflammation in menopausal women. The present study offers potential hypotheses for future longitudinal research.