Key result
Chronic Urotensin-II improves glucose tolerance and reduces adipose tissue weight in obese mice.
Why the study?
Conflicting findings exist regarding the effects of urotensin-II on blood glucose, prompting investigation into its effects on glucose metabolism in high-fat diet-fed mice.
Does chronic Urotensin-II administration improve glucose tolerance in high-fat diet-fed mice?
Does chronic Urotensin-II administration improve glucose tolerance in high-fat diet-fed mice?
p-value: p=<0.05
Chronic Urotensin-II administration improves glucose tolerance and reduces adiposity in a mouse model of diet-induced obesity, suggesting a potential metabolic regulatory role.
Does not support clinical use in metabolic disease; leaves open a potential regulatory role for urotensin-II pending human translation.
Urotensin-II (U-II) is an endogenous peptide agonist of a G protein-coupled receptor— urotensin receptor. There are many conflicting findings about the effects of U-II on blood glucose. This study aims to explore the effects of U-II on glucose metabolism in high-fat diet-fed mice. Male C57BL/6J mice were fed a 45% high-fat diet or chow diet and were administered U-II intraperitoneally for in vivo study. skeletal muscle C2C12 cells were used to determine the effects of U-II on glucose and fatty acid usage as well as mitochondrial respiratory function. In this study, we found that chronic U-II administration (more than seven days) ameliorated glucose tolerance in high-fat diet-fed mice. In addition, chronic U-II administration reduced weight gain and adipose tissue weights, including that of visceral, subcutaneous and brown fat, but without a significant change in blood lipid levels. These were accompanied by increased mRNA expression of the mitochondrial thermogenesis gene Ucp3 in skeletal muscle. Furthermore, in vitro treatment with U-II directly enhanced glucose and free fatty acid consumption with increased aerobic respiration in C2C12 cells. Taken together, chronic U-II stimulation leads to improvement on glucose tolerance in high-fat diet-fed mice and this effect maybe closely related with the reduction in adipose tissue weights and enhancement on energy substrates usage in skeletal muscle.
No takes yet. Share an insight, caveat, or question.
Chen et al. (2019) studied High-fat diet-induced obesity and glucose intolerance (n=105). Urotensin-II vs. Normal saline was evaluated on Glucose tolerance (IPGTT AUC) (p=<0.05). Chronic Urotensin-II administration for 21 days significantly improved whole-body glucose tolerance and reduced adipose tissue weight in high-fat diet-induced obese mice.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: