Euphorbia kansui Attenuates Insulin Resistance in Obese Human Subjects and High‐Fat Diet‐Induced Obese Mice

Abstract

Background Obesity is a main cause of insulin resistance (IR), metabolic syndrome, and fatty liver diseases. This study evaluated Euphorbia kansui radix (Euphorbia) as a potential treatment option for obesity and obesity-induced IR in obese human and high-fat diet- (HFD-) induced obese mice. Methods In the human study, we analyzed the body weight change of 14 patients who took a single dose of 6 g of Euphorbia powder. In the animal study, male mice were divided into three groups: normal chow, HFD, and Euphorbia (high-fat diet and 100 mg/Kg Euphorbia once per week). Body weight, epididymal fat pad weight, fasting blood glucose, fasting insulin, HOMA-IR, and oral glucose tolerance test were measured. Also, macrophage infiltration and expression of CD68, tumor necrosis factor- (TNF-) α, interferon- (IFN-) γ, and interleukin- (IL-) 6 genes in the liver and adipose tissue were analyzed. Results The human study showed that Euphorbia has a potential effect on body weight loss. In the in vivo study, body weight, epididymal fat weight, glucose level, IR, expression of CD68, TNF-α, IFN-r, and IL-6 genes, and macrophages in liver and adipose tissue were significantly reduced by Euphorbia. Conclusions These results suggest that Euphorbia attenuates obesity and insulin resistance via anti-inflammatory effects.

Micro‐environment and intracellular metabolism modulation of adipose tissue macrophage polarization in relation to chronic inflammatory diseases

“…Insulin resistance is characterized by the disruption of communication between insulin and its target cells. Insulin is produced by the pancreatic β‐cells in response to raised blood glucose levels, and insulin action is impaired in obese patients . Abundant evidence has established that during the development of obesity, monocytes are recruited from the circulation to the peripheral tissues, such as AT, pancreas, and liver, to become resident macrophages, and these resident macrophages play a crucial role in local tissue inflammation and insulin resistance .…”

“…Insulin is produced by the pancreatic β-cells in response to raised blood glucose levels, and insulin action is impaired in obese patients. 103,104 Abundant evidence has established that during the development of obesity, monocytes are recruited from the circulation to the peripheral tissues, such as AT, pancreas, and liver, to become resident macrophages, and these resident macrophages play a crucial role in local tissue inflammation and insulin resistance. 105 Moreover, the overproduction of pro-inflammatory signals from M1 macrophages aggravated AT function and impaired glucose tolerance in a diet-induced obese mouse model.…”