Acute hypoxia induces hypertriglyceridemia by decreasing plasma triglyceride clearance in mice
Carregando...
Citações na Scopus
68
Tipo de produção
article
Data de publicação
2012
Título da Revista
ISSN da Revista
Título do Volume
Editora
AMER PHYSIOLOGICAL SOC
Autores
JUN, Jonathan C.
SHIN, Mi-Kyung
YAO, Qiaoling
BEVANS-FONTI, Shannon
POOLE, James
POLOTSKY, Vsevolod Y.
Citação
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, v.303, n.3, p.E377-E388, 2012
Resumo
Obstructive sleep apnea (OSA) induces intermittent hypoxia (IH) during sleep and is associated with elevated triglycerides (TG). We previously demonstrated that mice exposed to chronic IH develop elevated TG. We now hypothesize that a single exposure to acute hypoxia also increases TG due to the stimulation of free fatty acid (FFA) mobilization from white adipose tissue (WAT), resulting in increased hepatic TG synthesis and secretion. Male C57BL6/J mice were exposed to FiO(2) = 0.21, 0.17, 0.14, 0.10, or 0.07 for 6 h followed by assessment of plasma and liver TG, glucose, FFA, ketones, glycerol, and catecholamines. Hypoxia dose-dependently increased plasma TG, with levels peaking at FiO(2) = 0.07. Hepatic TG levels also increased with hypoxia, peaking at FiO(2) = 0.10. Plasma catecholamines also increased inversely with FiO(2). Plasma ketones, glycerol, and FFA levels were more variable, with different degrees of hypoxia inducing WAT lipolysis and ketosis. FiO(2) = 0.10 exposure stimulated WAT lipolysis but decreased the rate of hepatic TG secretion. This degree of hypoxia rapidly and reversibly delayed TG clearance while decreasing [H-3]triolein-labeled Intralipid uptake in brown adipose tissue and WAT. Hypoxia decreased adipose tissue lipoprotein lipase (LPL) activity in brown adipose tissue and WAT. In addition, hypoxia decreased the transcription of LPL, peroxisome proliferator-activated receptor-gamma, and fatty acid transporter CD36. We conclude that acute hypoxia increases plasma TG due to decreased tissue uptake, not increased hepatic TG secretion.
Palavras-chave
lipolysis, lipases, adipose, thermoregulation, metabolism
Referências
- Drager LF, 2010, PLOS ONE, V5, DOI 10.1371/journal.pone.0012065
- Ballart X, 2003, BIOCHIMIE, V85, P971, DOI 10.1016/j.biochi.2003.09.001
- Barnholt KE, 2006, AM J PHYSIOL-ENDOC M, V290, pE1078, DOI 10.1152/ajpendo.00449.2005
- Bartelt A, 2011, NAT MED, V17, P200, DOI 10.1038/nm.2297
- BAUM D, 1967, P SOC EXP BIOL MED, V125, P1190
- BAUM D, 1971, AM J DIS CHILD, V121, P115
- BAUM D, 1981, AM J PHYSIOL, V241, pE28
- Beigneux AP, 2009, J LIPID RES, V50, pS57, DOI 10.1194/jlr.R800030-JLR200
- Bligh G, 1959, CAN J BIOCH PHYSL, V37, P911
- BRINDLE NPJ, 1988, BIOCHEM J, V250, P363
- Brito J, 2007, HIGH ALT MED BIOL, V8, P236, DOI 10.1089/ham.2007.8310
- Cannon B, 2004, PHYSIOL REV, V84, P277, DOI 10.1152/physrev.00015.2003
- Carriere A, 2004, J BIOL CHEM, V279, P40462, DOI 10.1074/jbc.M407258200
- CHAIT A, 1979, METABOLISM, V28, P553, DOI 10.1016/0026-0495(79)90197-5
- CHIODI H., 1952, ACTA PHYSIOL LATINOAMER, V2, P228
- Davidson NO, 2000, ANNU REV NUTR, V20, P169, DOI 10.1146/annurev.nutr.20.1.169
- Drager LF, 2012, EUR HEART J, V33, P783, DOI 10.1093/eurheartj/ehr097
- Drager LF, 2010, CURR OPIN ENDOCRINOL, V17, P161, DOI 10.1097/MED.0b013e3283373624
- Farias JG, 2006, HIGH ALT MED BIOL, V7, P302, DOI 10.1089/ham.2006.7.302
- FISER RH, 1974, J NUTR, V104, P223
- Frayn KN, 2010, ACTA PHYSIOL, V199, P509, DOI 10.1111/j.1748-1716.2010.02128.x
- FRAYN KN, 1995, ADV ENZYME REGUL, V35, P163, DOI 10.1016/0065-2571(94)00011-Q
- FREDHOLM B B, 1970, Acta Physiologica Scandinavica, V80, P567, DOI 10.1111/j.1748-1716.1970.tb04824.x
- FRIED SK, 1987, INT J OBESITY, V11, P129
- Gauthier MS, 2008, J BIOL CHEM, V283, P16514, DOI 10.1074/jbc.M708177200
- Gautier H, 1996, J APPL PHYSIOL, V81, P521
- Goldberg IJ, 2009, J LIPID RES, V50, pS86, DOI 10.1194/jlr.R800085-JLR200
- Goudriaan JR, 2005, J LIPID RES, V46, P2175, DOI 10.1194/jlr.M500112-JLR200
- Havel R, J LIPID RES, V1, P1959
- HILL JR, 1959, J PHYSIOL-LONDON, V149, P346
- Jun J, 2010, ATHEROSCLEROSIS, V209, P381, DOI 10.1016/j.atherosclerosis.2009.10.017
- Jun J, 2009, ILAR J, V50, P289
- Kahn BB, 2005, CELL METAB, V1, P15, DOI 10.1016/j.cmet.2004.12.003
- KAYSER B, 1992, INT J SPORTS MED, V13, pS129, DOI 10.1055/s-2007-1024616
- Kim KH, 2005, BIOCHEM BIOPH RES CO, V333, P1178, DOI 10.1016/j.bbrc.2005.06.023
- KUWAHIRA I, 1993, J APPL PHYSIOL, V74, P211
- Lafontan M, 2009, PROG LIPID RES, V48, P275, DOI 10.1016/j.plipres.2009.05.001
- Li JG, 2007, J APPL PHYSIOL, V102, P557, DOI 10.1152/japplphysiol.01081.2006
- Li JG, 2005, CIRC RES, V97, P698, DOI 10.1161/01.RES.000018379.60089.a9
- Li JG, 2007, PHYSIOL GENOMICS, V31, P273, DOI 10.1152/physiolgenomics.00082.2007
- Liu LP, 2006, MOL CELL, V21, P521, DOI 10.1016/j.molcel.2006.01.010
- Livak KJ, 2001, METHODS, V25, P402, DOI 10.1006/meth.2001.1262
- LOUHIJA A, 1969, EXPERIENTIA, V25, P248, DOI 10.1007/BF02034371
- MCELROY WT, 1961, J APPL PHYSIOL, V16, P760
- MCGARRY JD, 1973, J BIOL CHEM, V248, P270
- Motojima K, 1998, J BIOL CHEM, V273, P16710, DOI 10.1074/jbc.273.27.16710
- Muratsubaki H., 2003, Archives of Physiology and Biochemistry, V111, P449, DOI 10.3109/13813450312331342319
- Newman AB, 2001, AM J EPIDEMIOL, V154, P50, DOI 10.1093/aje/154.1.50
- NILSSONEHLE P, 1976, J LIPID RES, V17, P536
- OLIVECRONA G, 1995, CURR OPIN LIPIDOL, V6, P291, DOI 10.1097/00041433-199510000-00009
- Phillips CL, 2011, AM J RESP CRIT CARE, V184, P355, DOI 10.1164/rccm.201102-0316OC
- Ranganathan G, 2002, J BIOL CHEM, V277, P43281, DOI 10.1074/jbc.M202560200
- Ricart-Jane D, 2005, J APPL PHYSIOL, V99, P1343, DOI 10.1152/japplphysiol.00971.2004
- RICHES AC, 1973, J PHYSIOL-LONDON, V228, P279
- Roberts AC, 1996, J APPL PHYSIOL, V81, P1762
- ROSELL S, 1966, ACTA PHYSIOL SCAND, V67, P343, DOI 10.1111/j.1748-1716.1966.tb03320.x
- Schmittgen TD, 2008, NAT PROTOC, V3, P1101, DOI 10.1038/nprot.2008.73
- SCHNAKEN.DD, 1972, EXPERIENTIA, V28, P1172, DOI 10.1007/BF01946150
- Schoonjans K, 1996, EMBO J, V15, P5336
- Schweiger M, 2006, J BIOL CHEM, V281, P40236, DOI 10.1074/jbc.M608048200
- Sharma SK, 2011, NEW ENGL J MED, V365, P2277, DOI 10.1056/NEJMoa1103944
- STREJA DA, 1977, METABOLISM, V26, P505, DOI 10.1016/0026-0495(77)90094-4
- Tansey JT, 2004, IUBMB LIFE, V56, P379, DOI 10.1080/15216540400009968
- Usui S, 2002, J LIPID RES, V43, P805
- Wang B, 2008, J ENDOCRINOL, V198, P127, DOI 10.1677/JOE-08-0156
- Wang SP, 2008, MOL GENET METAB, V95, P117, DOI 10.1016/j.ymgme.2008.06.012
- Way JM, 2001, ENDOCRINOLOGY, V142, P1269, DOI 10.1210/en.142.3.1269
- Weinstein MM, 2008, J BIOL CHEM, V283, P34511, DOI 10.1074/jbc.M806067200
- White UA, 2010, MOL CELL ENDOCRINOL, V318, P10, DOI 10.1016/j.mce.2009.08.023
- Yoshida K, 2002, J LIPID RES, V43, P1770, DOI 10.1194/jlr.C200010-JLR200
- YOUNG PM, 1989, J APPL PHYSIOL, V66, P1430
- Yun Z, 2002, DEV CELL, V2, P331, DOI 10.1016/S1534-5807(02)00131-4