Low phosphorus status might contribute to the onset of obesity
2013
Obeid O.A. | Obeid, O.A., Department of Nutrition and Food Science, Faculty of Agricultural and Food Sciences, American University of Beirut, Beirut, Lebanon | Obeid, O.A.; Department of Nutrition and Food Science, Faculty of Agricultural and Food Sciences, American University of Beirut, PO Box 11-0236, Beirut 1107 2020, Lebanon; email: [email protected] | University: American University of Beirut; Faculty: Faculty of Agricultural and Food Sciences; Department: Nutrition and Food Sciences; | Nutrition and Food Sciences | [email protected] | Faculty of Agricultural and Food Sciences | Obeid, OA | Obeid, OA (reprint author), Amer Univ Beirut, Dept Nutr and Food Sci, Fac Agr and Food Sci, POB 11-0236, Beirut 11072020, Lebanon. | American University of Beirut
Overweight and obesity are becoming global health problems. Although genetics certainly plays a role, weight gain is ultimately the result of a failure in the balance between energy expenditure and energy intake. Obesity during the past few decades was paralleled with several changes in dietary habits favouring low phosphorus consumption. This is believed to compromise adenosine triphosphate (ATP) production that is involved in the regulation of energy metabolism. Ingestion of high-carbohydrate-low phosphorus food is known to increase insulin release, to simultaneously stimulate peripheral uptake of phosphorus and the phosphorylation of many compounds. This creates a competition for phosphorus that compromises its availability for ATP production, possibly translated into low diet-induced thermogenesis. Moreover, reduced hepatic ATP production is believed to be transmitted through neural afferents to the central nervous system, resulting in an increase in food intake. On the other hand, the positive relation between phosphorus and red blood cell 2,3-diphosphoglycerate, which reduces oxygen affinity to haemoglobin, would be expected to reduce the capacity for physical activity. In line with that, plasma phosphorus status was reported to be inversely related to body weight. Adequate intakes of phosphorus are thus potentially protective against rising obesity epidemic across the globe. © 2013 International Association for the Study of Obesity.
اظهر المزيد [+] اقل [-]Abdelmalek MF, 2012, HEPATOLOGY, V56, P952, DOI 10.1002-hep.25741; Alonso A, 2010, HYPERTENSION, V55, P776, DOI 10.1161-HYPERTENSIONAHA.109.143461; Beydoun MA, 2008, AM J CLIN NUTR, V87, P1914; Bizeau ME, 2005, METABOLISM, V54, P1189, DOI 10.1016-j.metabol.2005.04.004; Blaak EE, 2012, OBES REV, V13, P923, DOI 10.1111-j.1467-789X.2012.01011.x; Bray GA, 2004, AM J CLIN NUTR, V79, P537; Bremner K, 2002, CLIN CHIM ACTA, V323, P111, DOI 10.1016-S0009-8981(02)00165-1; Calvo MS, 2013, SEMIN DIALYSIS, V26, P54, DOI 10.1111-sdi.12042; CAMPILLO JE, 1982, DIABETES METAB, V8, P289; CARD RT, 1973, NEW ENGL J MED, V288, P388, DOI 10.1056-NEJM197302222880803; Celik N, 2011, J PEDIATR ENDOCR MET, V24, P81, DOI 10.1515-JPEM.2011.116; Chavin KD, 1999, J BIOL CHEM, V274, P5692, DOI 10.1074-jbc.274.9.5692; CLARKSON PM, 1995, MED SCI SPORT EXER, V27, P831; Cortez-Pinto H, 1999, JAMA-J AM MED ASSOC, V282, P1659, DOI 10.1001-jama.282.17.1659; Ditzel Jørn, 2010, Curr Diabetes Rev, V6, P323, DOI 10.2174-157339910793360833; Drewnowski A, 2009, NUTR REV, V67, pS36, DOI 10.1111-j.1753-4887.2009.00157.x; Drewnowski A, 1997, NUTR REV, V55, P31; Ervin RB, 2004, ADV DATA, V27, P1; Farhangi MA, 2011, BIOCHEM MEDICA, V21, P312; FELIG P, 1984, CLIN PHYSIOL, V4, P267, DOI 10.1111-j.1475-097X.1984.tb00802.x; Food and Nutrition Board Institute of Medicine, 1997, DIET REF INT CALC MA; Friedman MI, 2007, DRUG NEWS PERSPECT, V20, P573, DOI 10.1358-dnp.2007.20.9.1162243; GOLAY A, 1982, DIABETES, V31, P1023; Gong ZW, 2012, INT J ENDOCRINOL, DOI 10.1155-2012-320482; Haap M, 2006, EUR J CLIN NUTR, V60, P734, DOI 10.1038-sj.ejcn.1602375; Haglin L, 2001, EUR J CLIN NUTR, V55, P493, DOI 10.1038-sj.ejcn.1601209; Haglin L, 2001, MED HYPOTHESES, V56, P657, DOI 10.1054-mehy.2000.1272; Halton TL, 2004, J AM COLL NUTR, V23, P373; Heaney RP, 2002, J AM COLL NUTR, V21, P239; Holecki M, 2011, INT J ENDOCRINOL, DOI 10.1155-2011-707126; Hong J, 2000, AM J PHYSIOL-REG I, V278, pR1579; JAEDIG S, 1991, INT J OBESITY, V15, P429; JAEDIG S, 1994, MINER ELECTROL METAB, V20, P147; Jenkins DJA, 2002, DIABETES CARE, V25, P1522, DOI 10.2337-diacare.25.9.1522; Kaciuba-Uściłko H, 1993, J Physiol Pharmacol, V44, P425; Kalaitzidis R, 2005, AM J KIDNEY DIS, V45, P851, DOI 10.1053-j.ajkd.2005.01.005; KALOFOUTIS A, 1975, CLIN CHEM, V21, P1414; KARCZMAR GS, 1989, BIOCHIM BIOPHYS ACTA, V1012, P121, DOI 10.1016-0167-4889(89)90084-0; Khattab M, 2011, P NUTR SOC, V70, pE60, DOI 10.1017-S0029665111001005; Kristensen M, 2012, J NUTR, V142, P710, DOI 10.3945-jn.111.142315; Kritzer MD, 1955, AMA ARCH INT MED, V97, P62; Langhans W, 1992, World Rev Nutr Diet, V70, P1; Latner JD, 1999, APPETITE, V33, P119, DOI 10.1006-appe.1999.0237; Lim WJ, 2005, ARCH INTERN MED, V165, P910, DOI 10.1001-archinte.165.8.910; LIND L, 1993, EUR J CLIN INVEST, V23, P307, DOI 10.1111-j.1365-2362.1993.tb00779.x; LINDGARDE F, 1977, ACTA MED SCAND, V202, P307; Litchman MA, 1971, ANN INTERN MED, V74, P562; Maloney EM, 2010, METABOLISM, V59, P1351, DOI 10.1016-j.metabol.2009.12.019; MONTI M, 1974, ACTA MED SCAND, V195, P287; Morris JRC, 1978, J CLIN INVEST, V61, P209; Nair S, 2003, AM J GASTROENTEROL, V98, P466, DOI 10.1016-S0002-9270(02)05889-6; Nazar K, 1996, J PHYSIOL PHARMACOL, V47, P373; Nowicki M, 1996, J CLIN ENDOCR METAB, V81, P156, DOI 10.1210-jc.81.1.156; Obeid OA, 2010, INT J OBESITY, V34, P1446, DOI 10.1038-ijo.2010.74; OBERHAENSLI RD, 1986, BRIT J RADIOL, V59, P695; Park W, 2009, DIABETES RES CLIN PR, V83, P119, DOI 10.1016-j.diabres.2008.08.018; Paula FJA, 1998, HORM METAB RES, V30, P281, DOI 10.1055-s-2007-978884; Pollack H, 1934, AM J PHYSIOL, V110, P117; Polymeris AD, 2011, ENDOCR RES, V36, P45, DOI 10.3109-07435800.2010.496761; Popkin BM, 2004, INT J OBESITY, V28, pS2, DOI [10.1038-sj.ijo.0802804, 10.1038-sj.ijo.0802557]; Popkin BM, 2006, AM J CLIN NUTR, V84, P289; Ravussin E, 1996, DIABETES REV, V4, P403; RAWSON NE, 1994, AM J PHYSIOL, V266, pR1792; RIQUELME PT, 1984, J BIOL CHEM, V259, P5115; SEGAL KR, 1985, J CLIN INVEST, V76, P1107, DOI 10.1172-JCI112065; SEGAL KR, 1990, METABOLISM, V39, P985, DOI 10.1016-0026-0495(90)90312-Z; SEGAL KR, 1990, AM J CLIN NUTR, V51, P14; SOLOMON SM, 1990, JPEN-PARENTER ENTER, V14, P90, DOI 10.1177-014860719001400190; Swinburn BA, 2004, PUBLIC HEALTH NUTR, V7, P123, DOI 10.1079-PHN2003585; Teegarden D, 2005, J NUTR, V135, P2749; THORNE A, 1989, CLIN PHYSIOL, V9, P481, DOI 10.1111-j.1475-097X.1989.tb01002.x; THORNE A, 1990, CLIN PHYSIOL, V10, P99, DOI 10.1111-j.1475-097X.1990.tb00087.x; TRAVIS SF, 1971, NEW ENGL J MED, V285, P763, DOI 10.1056-NEJM197109302851402; Wagner G, 2007, J AM COLL NUTR, V26, P456; Wlodek D, 2003, J THEOR BIOL, V225, P33, DOI 10.1016-S0022-5193(03)00218-2; Wycherley TP, 2012, AM J CLIN NUTR, V96, P1281, DOI 10.3945-ajcn.112.044321; Xie WS, 2000, BIOCHEM J, V352, P227, DOI 10.1042-0264-6021:3520227; Yanovski JA, 2009, ANN INTERN MED, V150, P821; Ye EQ, 2012, J NUTR, V142, P1304, DOI 10.3945-jn.111.155325
اظهر المزيد [+] اقل [-]الكلمات المفتاحية الخاصة بالمكنز الزراعي (أجروفوك)
المعلومات البيبليوغرافية
تم تزويد هذا السجل من قبل American University of Beirut