Fig. 7.

Importance of non-adipose tissue in obesity-related glucose dysregulation (and other cardiometabolic diseases). The degree the immunopathies and endocrinopathies of adiposopathy result in adverse clinical consequences (e.g., abnormalities in glucose metabolism) largely depend on crosstalk, interactions, and biometabolic responses from non-adipose body tissues. Prediabetes and type 2 diabetes mellitus (T2DM) are mostly caused by multi-organ insulin resistance in conjunction with a decline in pancreatic beta cell insulin secretory function [4] The degree that weight reduction improves body organ function (e.g., adipose tissue, liver, muscle, pancreas, kidney, brain) varies among different individuals and among different organs within the individual. For example, insulin sensitivity in the liver (insulin-mediated suppression of glucose production) and adipose tissue (insulin-mediated suppression of lipolysis) may be maximally improved with 5%–8% weight reduction, while greater amounts of weight reduction may further improve skeletal muscle insulin sensitivity [4].