Brante P. Sampey

TL;DR: The CAF provided a robust model of human metabolic syndrome compared to traditional lard‐based HFD, creating a phenotype of exaggerated obesity with glucose intolerance and inflammation, and displayed remarkable inflammation in white fat, brown fat and liver compared to HFD and controls.

TL;DR: In conclusion, metformin reduced tumor proliferation in a pre‐operative window study in obese EC patients, with dramatic effects on inhibition of the mTOR pathway.

TL;DR: Compared to a traditional HFD model, the CAF diet provides a robust model for diet-induced human obesity, which models Metabolic Syndrome-related mitochondrial dysfunction in serum, muscle, and adipose, along with pro-inflammatory metabolite alterations, and suggest that modifying the availability or metabolism of saturated fatty acids may limit the inflammation associated with obesity leading to Metabolic syndrome.

TL;DR: A novel association between ethanol-induced lipid peroxidation and the inhibition of constitutive ERK-1/2 is demonstrated, and an inhibitory mechanism mediated by the lipidperoxidation product 4-hydroxynonenal is suggested.

TL;DR: Data indicates that the CAF diet drives an increase in oxidative damage in white adipose tissue that may affect tissue homeostasis, and drives activation of inflammatory kinases that can perturb insulin signaling leading to glucose intolerance and diabetes.