Lipases and the stress of obesity

The existing literature regarding the effect of stress on lipid metabolism [3,4] is sparse and, in the case of LPL, contradictory [5-7]. It has been described in rats, in vivo and in vitro that adrenaline causes a decrease in the LPL activity in the vascular bed of adipocytes, but expression of the gene encoding the enzyme was not affected [8], in parallel with an increase in plasma LPL activity as well as the appearance of LPL activity in the liver [9,10], but there is still controversy about the regulatory mechanism. To further the knowledge of LPL in vivo regulation by adrenaline, a model of restraint stress in rats was used and applied either as chronic and acute conditions [11]. Both chronic and acute stresses were reported to produce significant alterations in lipid and lipoprotein metabolism [11], and these changes were accompanied by a decrease in LPL activity in white adipose tissue and an increase in plasma [8]. The possible role of blood flow in the regulation of LPL by catecholamines has also been studied. Because of its intravascular location, it is possible that LPL is sensitive to variations in the flow of blood through the capillaries. Thus, an increased flow could lead to an increase in the release of LPL from its anchor, which would lead to a decline in activity in the tissue without altering its synthesis. This would provide a mechanism for short-term regulation if the LPL (much faster than the regulation of enzyme synthesis), which has not been studied yet. It has been reported that acute immobilization stress increased blood flow in white adipose tissue (which reduces LPL activity) but not in muscle (in which LPL was unchanged) [12]. It has also been reported that LPL shows a circadian rhythm in adult rats [13] that can be modified by soft stress [14]. However, there are very few data linking stress caused by with lipolytic activity. In experimental animals, HL activity and mRNA were shown to decrease in the liver after hepatectomy, whereas activity was not detected in the plasma. However, adrenal HL activity did not vary post-surgery [15]. This is very interesting because the steroidogenic organs, such as the adrenal gland, cannot synthesize the enzyme, which originates in the liver; however, given the need to capture cholesterol for the synthesis of catecholamines and glucocorticoids, such as in a stressful situation, steroidogenic organs retain high levels of HL. It has also been observed that surgical stress leads to the recovery of the LPL activity and mRNA in the liver, and there are also changes in the expression of LPL and other proteins, such as albumin, actin, etc, in peripheral tissues [16].