Adipose (fat) tissue inflammation is directly linked to obesity-induced insulin resistance, while gut imbalance and mitochondrial dysfunction are not required. These are the findings of new research published in Function, the latest addition to the American Physiological Society’s collection of journals. The study was performed in mice to determine the importance of fat tissue inflammation, mitochondrial dysfunction and gut imbalance for obesity-induced insulin resistance using a spontaneously obese mouse model.
Researchers found a spontaneous mutation in some mice that resulted in profound obesity, whole-body insulin resistance, fat tissue enlargement, inflammation and redox imbalance. The findings suggest gut imbalance and skeletal mitochondrial dysfunction may be linked to high fat diet feeding and, therefore, not required for a certain level of obesity-induced insulin resistance. However, several aspects of fat tissue inflammation appear intrinsic to the obese phenotype. The full article may be found here.
