Abstract

As the major storage site for triglycerides and free cholesterol, adipose tissue plays a central role in energy metabolism. ApoA-I is the main constituent of HDL and plays an important role in removal of excess cholesterol from peripheral tissues. Recently, multiple studies have shown beneficial effects of apoA-I on adipose metabolism and function. ApoA-I was reported to improve insulin sensitivity and exert anti-inflammatory, anti-obesity effect in animal studies. Interestingly, Uptake and resecretion of apoA-I by adipocytes has been detected. However, the significance of apoA-I recycling by adipocytes is still not clear. This article reviewed methods used to study cellular recycling of apoA-I and summarized the current knowledge on the mechanisms involved in apoA-I uptake by adipocytes. Since the main function of apoA-I is to mediate reverse cholesterol transport from peripheral tissues, the role of apoA-I internalization and re-secretion by adipocytes in intracellular cholesterol transport under physiological and pathological conditions were discussed. In addition, findings on the correlation between apoA-I recycling and obesity were discussed. Finally, it was proposed that during intracellular transport, apoA-I-protein complex may acquire cargoes other than lipids and deliver regulatory information when they were resecreted into the plasma. Although apoA-I recycling by adipocytes is still an unsolved mystery, it’s likely that it is more than a redundant pathway especially under pathological conditions.

Highlights

  • IntroductionApolipoprotein A-I (apoA-I) is synthesized and secreted by the liver and intestine

  • Apolipoprotein A-I is synthesized and secreted by the liver and intestine

  • Summary To sum up, uptake and resecretion of Apolipoprotein A-I (apoA-I) by adipocytes were detected by using different apoA-I-labeling methods

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Summary

Introduction

Apolipoprotein A-I (apoA-I) is synthesized and secreted by the liver and intestine. As the major protein constituent of high-density lipoprotein (HDL), apoA-I plays an important role in reverse cholesterol transport from peripheral tissues to the liver [1]. As the body’s largest reservoir of free cholesterol, adipose tissue contributes to apoA-I lipidation and nascent HDL biogenesis [2, 3]. ApoA-I has been reported to have reciprocal effects on adipose tissue metabolism and function. ApoA-I has been reported to promote glucose uptake [4], improve insulin sensitivity [5], upregulate the expression of adiponectin [6], and exert anti-inflammatory effect [7, 8].

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