Abstract
Infiltration of inflammatory cells into adipose tissue causes insulin resistance in animal models and is associated with insulin resistance in humans (1,2). Among potential therapeutic approaches, the hormone erythropoietin (EPO) exerts anti-inflammatory effects in a variety of nonerythroid tissues (3), in which the receptor for EPO (EPO-R) is widely expressed (4). Various observations suggest a relationship between EPO and diabetes. There is an increased prevalence of anemia with inadequate EPO response in diabetes (5), and treatment of anemia slows the progression of microvascular and macrovascular complications (6). EPO reduced glucose levels in nondiabetic humans (7) and reduced diet-induced obesity and suppressed gluconeogenesis in rodents (8,9). While EPO increases adipose tissue oxidative metabolism and deletion of EPO in adipocytes results in obesity (10), failure to reproduce this highlights potential genetic and environmental influences (11). EPO has cytoprotective, proliferative, and anti-inflammatory effects in a …
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