Purpose of review
The present review aims to address the role of adipose tissue oxygen partial pressure (PO2) in the metabolic and endocrine derangements in conditions characterized by insulin resistance.
The balance between adipose tissue oxygen supply and its metabolic rate seems to determine adipose tissue PO2. Studies in ob/ob and dietary-induced obese mice have provided evidence for adipose tissue hypoxia in obesity, which has been explained by insufficient adipose tissue angiogenesis during the massive and rapid weight gain in these animals. However, conflicting data have been reported in humans, showing both increased and decreased adipose tissue PO2 in obese compared with lean individuals. Both low and high adipose tissue PO2 may induce a proinflammatory phenotype in (pre)adipocytes, but most studies have been performed under rather extreme PO2 levels, not reflecting human adipose tissue physiology. Furthermore, adipose tissue PO2 may affect glucose and lipid metabolism as well as adipogenic differentiation, but many issues still need to be addressed.
Adipose tissue hypoxia has been demonstrated in animal models of obesity, but findings in humans are controversial and require further investigation. Although adipose tissue PO2 seems to be involved in metabolic and endocrine derangements in human adipose tissue, future studies should investigate how low and high adipose tissue PO2 within the human physiological range (3–11% O2) relates to adipose tissue blood flow and oxygen consumption, cellular metabolic responses, and the inflammatory phenotype.