Obesity

Adipose tissue is important in maintaining metabolic homeostasis, and its dysfunction can lead to obesity and type II diabetes. Increased adipose tissue can result in elevated ER stress induced by free fatty acid
(FFA)-mediated reactive oxygen species (ROS) generation and up-regulation of inflammatory cytokines. Several studies now report the improved function of adipose tissue with exposure to TUDCA, in part by reducing ER stress, maintaining adipocyte autophagy, stabilizing the UPR and inhibiting adipogenesis. Obesity can also lead to deficits in myocardial function.
In one study, ob/ob obese mice were found to exhibit cardiac hypertrophy, compromised contraction of cardiomyocytes, and hypertension in comparison to normal controls. Treatment of ob/ob mice with TUDCA led to a decrease in cardiac hypertrophy, decreased hypertension, and a normalization of cardiac contractility. Moreover, TUDCA-treated ob/ob mice exhibited normalization of sarco(endo)plasmic reticulum Ca(2+)-
ATPase (SERCA) expression and activity