Rapid perioperative changes in the quantitative properties of plasma lipases and lipoproteins in morbidly obese surgical patients'

Background: The impact of bariatric surgery on abnormalities in blood lipids and lipoprotein metabolism during the perioperative period has been poorly studied. Objective: We studied the impact of bariatric surgery on the composition and quantitative properties of lipoproteins and the activity of lipases in the plasma of perioperative morbidly obese patients. Methods: We examined the plasma lipoproteins and lipolytic activities of 34 morbidly obesepatients one month before surgery (OB), pre-anaesthesia (-S), post-anaesthesia ( S), and one day and one month after open Roux-en-Y gastric bypass (RYGB) surgery. Results: Surgical injury induced acute stress, as evidenced by transitory hyperglycaemia and elevated plasma levels of stress hormones. Lipid profiles revealed a significant reduction during surgery and the day after in the plasma levels of total cholesterol (p < 0.0001), which was mainly due to a decrease in low-density lipoprotein cholesterol (cLDL) and was confirmed with a significant reduction in the plasma levels of LDL (approximately 26% reduction). Significant (p < 0.0001) changes were detected in the plasma levels of high-density lipoprotein cholesterol (cHDL) as well as a significant decrease (approximately 19% reduction) in the plasma levels of HDL. A significant (p < 0.0001) rise was noted in the plasma levels of both Lipoprotein Lipase (LPL) (approximately 2.6-fold increase) and hepatic lipase (HL) (approximately 2.2-fold increase) on the day after surgery, occurring simultaneously with the maximum increase in C-reactive protein (CRP) and a day after the peak values for non-esterified fatty acid (NEFA), adrenocorticotropin hormone (ACTH), cortisol and glucose. Conclusion: The present study reveals unreported quantitative perioperative changes in plasma lipases and lipoproteins and related metabolic determinants that may contribute to the adaptive metabolic response to RYGB-induced stress

Nitric oxide and the release of lipoprotein lipase from white adipose tissue

Background/Aim: Lipoprotein lipase (LPL) is the main enzyme responsible for the distribution of circulating triacylglycerides in tissues. Its regulation via release from active sites in the vascular endothelium is poorly understood. In a previous study we reported that in response to acute immobilization (IMMO), LPL activity rapidly increases in plasma and decreases in white adipose tissue (WAT) in rats. In other stress situations IMMO triggers a generalized increase in nitric oxide (NO) production. Methods/Results: Here we demonstrate that in rats: 1) in vivo acute IMMO rapidly increases NO concentrations in plasma 2) during acute IMMO the WAT probably produces NO via the endothelial isoform of nitric oxide synthase (eNOS) from vessels, and 3) epididymal WAT perfused in situ with an NO donor rapidly releases LPL from the endothelium. Conclusion: We propose the following chain of events: stress stimulus / rapid increase of NO production in WAT (by eNOS) / release of LPL from the endothelium in WAT vessels. This chain of events could be a new mechanism that promotes the rapid decrease of WAT LPL activity in response to a physiological stimulus

Nitric oxide and the release of lipoprotein lipase from white adipose tissue

Background/Aim: Lipoprotein lipase (LPL) is the main enzyme responsible for the distribution of circulating triacylglycerides in tissues. Its regulation via release from active sites in the vascular endothelium is poorly understood. In a previous study we reported that in response to acute immobilization (IMMO), LPL activity rapidly increases in plasma and decreases in white adipose tissue (WAT) in rats. In other stress situations IMMO triggers a generalized increase in nitric oxide (NO) production. Methods/Results: Here we demonstrate that in rats: 1) in vivo acute IMMO rapidly increases NO concentrations in plasma 2) during acute IMMO the WAT probably produces NO via the endothelial isoform of nitric oxide synthase (eNOS) from vessels, and 3) epididymal WAT perfused in situ with an NO donor rapidly releases LPL from the endothelium. Conclusion: We propose the following chain of events: stress stimulus / rapid increase of NO production in WAT (by eNOS) / release of LPL from the endothelium in WAT vessels. This chain of events could be a new mechanism that promotes the rapid decrease of WAT LPL activity in response to a physiological stimulus

Changes in lipoprotein lipase modulate tissular energy supply during stress

We studied the variations caused by stress in lipoprotein lipase (LPL) activity, LPL-mRNA, and local blood flow in LPL-rich tissues in the rat. Stress was produced by body immobilization (Immo): the rat's limbs were taped to metal mounts, and its head was placed in a plastic tube. Chronic stress (2 h daily of Immo) decreased total LPL activity in mesenteric and epididymal white adipose tissue (WAT) and was accompanied by a weight reduction of these tissues. In limb muscle, heart, and adrenals, total LPL activity and mRNA levels increased, and, in plasma, LPL activity and mass also increased. Acute stress (30-min Immo) caused a decrease in total LPL activity only in retroperitoneal WAT and an increase in preheparin plasma active LPL, but the overall weight of this tissue did not vary significantly. We propose an early release of the enzyme from this tissue into the bloodstream by some unknown extracellular pathways or other local mechanisms. These changes in this key energy-regulating enzyme are probably induced by catecholamines. They modify the flow of energy substrates between tissues, switching the WAT from importer to exporter of free fatty acids and favoring the uptake by muscle of circulating triacylglycerides for energy supply. Moreover, we found that acute stress almost doubled blood flow in all WAT studied, favoring the export of free fatty acids

Rapid perioperative changes in the quantitative properties of plasma lipases and lipoproteins in morbidly obese surgical patients'

Background: The impact of bariatric surgery on abnormalities in blood lipids and lipoprotein metabolism during the perioperative period has been poorly studied. Objective: We studied the impact of bariatric surgery on the composition and quantitative properties of lipoproteins and the activity of lipases in the plasma of perioperative morbidly obese patients. Methods: We examined the plasma lipoproteins and lipolytic activities of 34 morbidly obesepatients one month before surgery (OB), pre-anaesthesia (-S), post-anaesthesia ( S), and one day and one month after open Roux-en-Y gastric bypass (RYGB) surgery. Results: Surgical injury induced acute stress, as evidenced by transitory hyperglycaemia and elevated plasma levels of stress hormones. Lipid profiles revealed a significant reduction during surgery and the day after in the plasma levels of total cholesterol (p < 0.0001), which was mainly due to a decrease in low-density lipoprotein cholesterol (cLDL) and was confirmed with a significant reduction in the plasma levels of LDL (approximately 26% reduction). Significant (p < 0.0001) changes were detected in the plasma levels of high-density lipoprotein cholesterol (cHDL) as well as a significant decrease (approximately 19% reduction) in the plasma levels of HDL. A significant (p < 0.0001) rise was noted in the plasma levels of both Lipoprotein Lipase (LPL) (approximately 2.6-fold increase) and hepatic lipase (HL) (approximately 2.2-fold increase) on the day after surgery, occurring simultaneously with the maximum increase in C-reactive protein (CRP) and a day after the peak values for non-esterified fatty acid (NEFA), adrenocorticotropin hormone (ACTH), cortisol and glucose. Conclusion: The present study reveals unreported quantitative perioperative changes in plasma lipases and lipoproteins and related metabolic determinants that may contribute to the adaptive metabolic response to RYGB-induced stress

Changes in lipoprotein lipase modulate tissular energy supply during stress

We studied the variations caused by stress in lipoprotein lipase (LPL) activity, LPL-mRNA, and local blood flow in LPL-rich tissues in the rat. Stress was produced by body immobilization (Immo): the rat's limbs were taped to metal mounts, and its head was placed in a plastic tube. Chronic stress (2 h daily of Immo) decreased total LPL activity in mesenteric and epididymal white adipose tissue (WAT) and was accompanied by a weight reduction of these tissues. In limb muscle, heart, and adrenals, total LPL activity and mRNA levels increased, and, in plasma, LPL activity and mass also increased. Acute stress (30-min Immo) caused a decrease in total LPL activity only in retroperitoneal WAT and an increase in preheparin plasma active LPL, but the overall weight of this tissue did not vary significantly. We propose an early release of the enzyme from this tissue into the bloodstream by some unknown extracellular pathways or other local mechanisms. These changes in this key energy-regulating enzyme are probably induced by catecholamines. They modify the flow of energy substrates between tissues, switching the WAT from importer to exporter of free fatty acids and favoring the uptake by muscle of circulating triacylglycerides for energy supply. Moreover, we found that acute stress almost doubled blood flow in all WAT studied, favoring the export of free fatty acids