Objective: Investigate the nature of the relationship between chronic hepatitis B virus (HBV) infection and metabolic syndrome among nondiabetic adults. Methods: This was a cross-sectional analysis of 17,030 nondiabetic adults (7437 males and 9593 females; mean age, 36.0 6 3.9 years) in northern Taiwan from 2008 to 2009. The associations of hepatitis B surface antigen (HBsAg) seropositivity with metabolic syndrome and cardio-metabolic parameters were assessed. A structural equation model was constructed to elucidate the pathways between chronic HBV infection and individual cardiometabolic risk factors. Results: A total of 2982 (17.5%) participants were HBsAg-seropositive. Of the seropositive and seronegative subjects, 15.5 and 16.9% had metabolic syndrome, respectively. The HBsAg-seropositive subjects had a lower odds of having metabolic syndrome compared with the seronegative subjects irrespective of gender and age (OR: 0.76, 95% CI: 0.68-0.85). The inverse associations remained significant after adjusting for body mass index and serum alanine aminotransferase levels. HBsAg seropositivity was inversely associated with hypertriglyceridemia (OR: 0.59, 95% CI: 0.52-0.66), and low serum levels of high-density lipoprotein cholesterol (OR: 0.86, 95% CI: 0.79-0.93) after adjustments. The structural equation model revealed chronic HBV infection had a significant negative effect on dyslipidemia both in males (B 5 20.054) and females (B 5 20.064). Conclusions: The inverse relationship between chronic HBV infection and metabolic syndrome may be attributable to the net beneficial effects on lipid profiles.

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Patients with chronic kidney disease (CKD) often experience a high accumulation of protein-bound uremic toxins (PBUTs), specifically indoxyl sulfate (IS) and p-cresyl sulfate (pCS). In the early stages of CKD, the buildup of PBUTs inhibits bone and muscle function. As CKD progresses, elevated PBUT levels further hinder bone turnover and exacerbate muscle wasting. In the late stage of CKD, hyperparathyroidism worsens PBUT-induced muscle damage but can improve low bone turnover. PBUTs play a significant role in reducing both the quantity and quality of bone by affecting osteoblast and osteoclast lineage. IS, in particular, interferes with osteoblastogenesis by activating aryl hydrocarbon receptor (AhR) signaling, which reduces the expression of Runx2 and impedes osteoblast differentiation. High PBUT levels can also reduce calcitriol production, increase the expression of Wnt antagonists (SOST, DKK1), and decrease klotho expression, all of which contribute to low bone turnover disorders. Furthermore, PBUT accumulation leads to continuous muscle protein breakdown through the excessive production of reactive oxygen species (ROS) and inflammatory cytokines. Interactions between muscles and bones, mediated by various factors released from individual tissues, play a crucial role in the mutual modulation of bone and muscle in CKD. Exercise and nutritional therapy have the potential to yield favorable outcomes. Understanding the underlying mechanisms of bone and muscle loss in CKD can aid in developing new therapies for musculoskeletal diseases, particularly those related to bone loss and muscle wasting.