Abstract
Relative hypoxia has been shown to develop in white adipose tissue depots of different types of obese mouse (genetic, dietary), and this leads to substantial changes in white adipocyte function. These changes include increased production of inflammation-related adipokines (such as IL-6, leptin, Angptl4, and VEGF), an increase in glucose utilization and lactate production, and the induction of fibrosis and insulin resistance. Whether hypoxia also occurs in brown adipose tissue depots in obesity has been little considered. However, a recent study has reported low pO2 in brown fat of obese mice, this involving mitochondrial loss and dysfunction. We suggest that obesity-linked hypoxia may lead to similar alterations in brown adipocytes as in white fat cells – particularly changes in adipokine production, increased glucose uptake and lactate release, and insulin resistance. This would be expected to compromise thermogenic activity and the role of brown fat in glucose homeostasis and triglyceride clearance, underpinning the development of the metabolic syndrome. Hypoxia-induced augmentation of lactate production may also stimulate the “browning” of white fat depots through recruitment of UCP1 and the development of brite adipocytes.
Highlights
Oxygen is rarely considered as an essential nutrient in mammals and this is primarily because it is delivered through the lungs rather than in the diet via the gastrointestinal tract
We suggest that obesity-linked hypoxia may lead to similar alterations in brown adipocytes as in white fat cells – changes in adipokine production, increased glucose uptake and lactate release, and insulin resistance
We provide a perspective on the effects of hypoxia on the function of white adipocytes and consider, in particular, whether hypoxia occurs in brown adipose tissue (BAT)
Summary
Oxygen is rarely considered as an essential nutrient in mammals and this is primarily because it is delivered through the lungs rather than in the diet via the gastrointestinal tract. We suggest that obesity-linked hypoxia may lead to similar alterations in brown adipocytes as in white fat cells – changes in adipokine production, increased glucose uptake and lactate release, and insulin resistance.
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