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Lipoprotein lipase: new roles for an 'old' enzyme.
Chang, CL
Current opinion in clinical nutrition and metabolic care. 2019;(2):111-115
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Abstract
PURPOSE OF REVIEW Lipoprotein lipase (LpL) is well known for its lipolytic action in blood lipoprotein triglyceride catabolism. This article summarizes the recent mechanistic and molecular studies on elucidating the 'unconventional' roles of LpL in mediating biological events related to immune cell response and lipid transport in the pathogenesis of cardiovascular disease (CVD) and tissue degenerative disorders. RECENT FINDINGS Several approaches to inactivate the inhibitors that block LpL enzymatic activity have reestablished the importance of systemic LpL activity in reducing CVD risk. On the other hand, increasing evidence suggests that focal arterial expression of LpL relates to aortic macrophage levels and inflammatory processes. In the hematopoietic origin, LpL also plays a role in modulating hematopoietic stem cell proliferation and circulating blood cell levels and phenotypes. Finally, building upon the strong genetic evidence on the association with assorted brain disorders, a new era in exploring the mechanistic insights into the functions and activity of LpL in brain that impacts central nerve systems has begun. SUMMARY A better understanding of the molecular action of LpL will help to devise novel strategies for intervention of a number of diseases, including blood cell or metabolic disorders, as well to inhibit pathways related to CVD and tissue degenerative processes.
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Postprandial monocyte activation in response to meals with high and low glycemic loads in overweight women.
Motton, DD, Keim, NL, Tenorio, FA, Horn, WF, Rutledge, JC
The American journal of clinical nutrition. 2007;(1):60-5
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Abstract
BACKGROUND Recent data show that atherosclerosis is initiated and perpetuated by inflammatory events. Activation of immune cells such as monocytes initiates inflammation, a key step in atherosclerosis. OBJECTIVE We hypothesize that a high-glycemic load meal activates inflammatory cells, and that this is mediated by elevated circulating triacylglycerol-rich lipoproteins. DESIGN Sixteen women [body mass index (in kg/m2): 25.7-29.6], aged 20-48 y, consumed meals with a high or a low glycemic load in a crossover fashion. Blood samples were collected before and up to 8 h after the meals. Samples were measured for glucose, insulin, triacylglycerols, and circulating cytokines, and expression of tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta) was measured by flow cytometry. RESULTS At 3.5 h after the test meals, we observed a significant increase in monocytes expressing TNF-alpha with both high-and low-glycemic load meals. Also, expression of IL-1beta in monocytes tended to increase, but the change was not significant. The glycemic load of the meal did not influence circulating cytokines and had only a minimal effect on postprandial triacylglycerol concentrations despite marked postprandial changes in glycemia and circulating insulin concentrations. CONCLUSIONS In the postprandial state, monocytes can be activated by both high-and low-glycemic load meals. The glycemic load of a single meal did not have a significant effect on the degree of activation of the monocytes in women who displayed only a modest increase in circulating triacylglycerols in response to test meals. Future studies should examine the effect of glycemic load in subjects who have a hyperlipemic response to dietary carbohydrate.