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>Journals >Gaceta Médica de México >Year 2015, Issue 2


Delgadillo-Guzmán D, Quintanar-Escorza MA, Carrera-Gracia MA, Lares-Aseff I
Relation of leptin in plasma with oxidative damage in indigenous tepehuán and mestizo populations from Durango
Gac Med Mex 2015; 151 (2)

Language: Español
References: 40
Page: 216-224
PDF: 165.48 Kb.


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ABSTRACT

Background: Obesity is a multifactorial metabolic disorder that involves lipid peroxidation (LPX), activating the antioxidant systems to counteract cellular damage. Objective: To evaluate the correlation between the antioxidant capacity and LPX levels of leptin, in indigenous Tepehuán and Mestizo populations of the State of Durango. Methods: We conducted a nutritional clinical study and lipid profile to confirm the state of health of a group of 60 indigenous Tepehuán of Mezquital and 68 mestizos subjects of Durango city, aged between 18 to 59 years. We determined the concentrations of leptin, antioxidant capacity and LPX in fasting conditions on plasma of participants, comparing averages, minimum, maximum, and standard deviation through ANOVA and Kruskal-Wallis. For the correlation of variables, Pearson test was applied, getting the r value. Results: Leptin levels were lower in indigenous Tepehuán than mestizos independent of body mass index. Mestizo subjects and Tepehuán with overweight and obesity (OW/O) or both ethnic groups show a greater degree of LPX (3.39 ± 0.31, 2.72 ± 0.54 MDA µmol/l, respectively; p ‹ 0.05); however, OW/O mestizos show more activation of its (0.37±0. 03 meq/trolox) than Tepehuán normal weight (NW) and OW/O (0.32 ±0. 01 meq/trolox). The correlation between antioxidant capacity and LPX in mixed OW/O was positive (r = 0.9; p ‹ 0.001). There is a correlation between levels of leptin and the antioxidant capacity of Tepehuán subjects both NW and OW/O (r = 0.40; p ‹ 0.05 and r = -0.66; p ‹ 0.0001, respectively). Conclusion: Tepehuán groups with OW/O have less oxidative damage, while antioxidant mechanisms have a smaller activation than the top crosses of the same nutritional condition. The results suggest that antioxidant capacity has an implication on the regulation of leptin levels in Tepehuán subjects.


Key words: Obesity, Ethnic, Leptin, Oxidative stress.


REFERENCIAS

  1. Olaiz-Fernández G, Rivera- Dommarco J, Shamah-Levy T, et al. ENSANUT 2006. Cuernavaca, México: INSP; 2006.

  2. World Health Organization. Multicentre Growth Reference Study Group. WHO Child Growth Standards: Length/Height-for-age, weight-for-age, weight-for-length, weight-for-height, and body mass index-for-age: Methods and development. Ginebra, Suiza: WHO; 2006.

  3. Rosebaum M, Liebel R, Hirsch J. Obesity. N Eng J Med. 1997:337(6):396- 407.

  4. Campfied IA, Smith FJ, Guisez J, Deros R, Burn P. Recombinant mouse OB protein: Evidence for a peripheral signal linking adiposity and central neural networks. Science. 1995;269(5223):546-9.

  5. Ahima RS. Adipose tissue as an endocrine organ. Obesity. 2006;14 Suppl 5:242S-249S.

  6. Houseknecht KL, Matzoros CS, Kuliawat R, Hadro E, Flier JS, Kahn BB. Evidence for leptin binding to proteins in serum of rodents and humans; Modulation with obesity. Diabetes. 1996;45(11):1638-43.

  7. Kohno D, Gao HZ, Muroya S, Kikuyama S, Yada T. Ghrelin directly interacts with neuropeptide-Y-containing neurons in the rat arcuate nucleus: Ca2+ signalling via protein kinase A and N-type channel-dependent mechanisms and cross-talk with leptin and orexin. Diabetes. 2003;52(4):948-56.

  8. Montague CT, Farooqui IS, Whitehead JP, et al. Congenital leptin deficiency in associated with severe early-onset obesity in humans. Nature. 1997;387(6636):903-8.

  9. Simón E, Del Barrio AS. Leptina y Obesidad. Anales Sis San Navarra. 2002;25 Suppl 1:53-64.

  10. Rice-Evans C, Miller NJ. Total antioxidant status in plasma and body fluids. Methods Enzymol. 1994;234:279-93.

  11. Miller NJ, Rice-Evans C, Davies MJ. A new method for measuring antioxidant activity. Biochem Soc Trans. 1993;21(2):95S.

  12. Del Rio D, Stewart AJ, Pellegrini NA. Review of recient studies on malondialdhyde as toxic molecule and biological marker of oxidative stress. Nutr Metab Caridiovasc Dis. 2005;15(4):316-28.

  13. Furukawa S, Fujita T, Shimabukuro M, et al. Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest. 2004;114(12):1752-61.

  14. Catal F, Avci A, Karadag A, Alioglu B, Avci Z. Oxidant andantioxidant status of Turkish marasmic children: a singlecenter study. J Trace Elem Med Biol, 2007;21(2):108-12.

  15. Fridlyand LE, Philipson LH. Reactive species and early manifestation of insulin resistance in type 2 diabetes. Diabetes Obes Metab. 2006;8(2):136-45.

  16. Eizirik DL, Cardozo AK, Cnop M. The role for endoplasmic reticulum stress in diabetes mellitus. Endocr Rev. 2008;29(1):42-61.

  17. Perez Bravo F, Albala C, Santotos JL, et al. Leptin leverls distribution an ethnic backgroud in two populatios from Chile: Caucasian and Mapuche groups. Int J. Obes Relat Metab Disord. 1998;22(10):943-8.

  18. Francisco Pérez B, José Luis Santos M, Cecilia Albala B, Marcelo Calvillán C, Elena Carrasco P. [Obesity and leptin association in three Chilean aboriginal populations]. Rev Méd Chile. 2000;128(1):45-52.

  19. Haffner SM, Gingerich RL, Miettinen H, Stern MP. Leptin concentration in relation to overall adiposity and regional body fat distribution in Mexican Americans. Int J Obes Relat Metab Disord. 1996;20(10):904-8.

  20. Fridlyand LE, Philipson LH. Reactive species and early manifestation of insulin resistance in type 2 diabetes. Diabetes Obes Metab. 2006;8(2):136-45.

  21. Petersen KF, Befroy D, Dufour S, et al. Mitochondrial dysfunction in the elderly: possible role in insulin resistance. Science. (Wash DC). 2003; 300(5622):1140-2.

  22. [Internet] Disponible en: http://www.salud.gob.mx/unidades/cdi/nom/ compi/rlgsmis.html.

  23. World Health Organization. Multicentre Growth Reference Study Group. WHO Child Growth Standards: «Length/Height-for-age, weight-for-age, weight-for-length, weight-for-height, and body mass index-for-age: Methods and development». Gienbra, Suiza: WHO; 2006.

  24. Rice-Evans C, Miller N. Total antioxidant status in plasma and body fluids. Methods Enzymol. 1994;234(24):279-93.

  25. Miller NJ, Rice-Evans C, Davies MJ. A new method for measuring antioxidant activity. BiochemSoc Trans. 1993;21(2):95S.

  26. Yagi K. Simple assay for the level of total lipid peroxides in serum or plasma. Methods Mol Biol. 1998;108:101-6.

  27. Graph pad Instatversión 7, software package. [Internet] Disponible en: http://www.graphpad.com/scientific-software/prism/.

  28. Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM. Positional cloning of the mouse obese gene and its human homologue. Nature (London). 1994;372(6505):425-32.

  29. Qatanani M, Lazar MA. Mechanisms of obesity associated insulin resistance: many choices on the menu. Genes Dev. 2007;21(12):1443-55.

  30. Wauters M, Considine RV, Van Gaal LF. Human leptin: from and adipocyte hormone to an edocrine mediator. Eur J Endocrinol. 2000;143(3): 293-311.

  31. Loffe E, Moon B, Connolly E, Friedman JA. Abnormal regulation of the leptin gene in the pathogenesis of obesity. Pro Nat Acad Sci USA. 1998;95(20):11852-7.

  32. Yang RL, Shi YH, Hao G, Li W, Le GW. Increasing oxidative stress with progressive hyperlipidemia in human: relation between malondialdehyde and atherogenic index. J Clin Biochem Nutr. 2008;43(3):154-8.

  33. Zanella AM, Nakazone MA, Pinhel MA, Souza DR. Lipid profile, apolipoprotein A-I and oxidative stress in professional footballers, sedentary individuals, and their relatives, Arq. Bras. Endocrinol. Metabol. 2011;55(2):121-6.

  34. Hoffman JR, Im J, Kang J, et al. Comparison of low- and high-intensity resistance exercise on lipid peroxidation: Role of muscle oxygenation. J Strength Cond Res. 2007;21(1):118-22.

  35. Bos,nak M, Kelekçi S, Yel S, Koçyig˘it Y, S,en V, Ece A. Oxidative Stress in Marasmic Children:Relationships with Leptin. Eur J Gen Med. 2010;7(1):1-8.

  36. Squali Houssaini FZ, Foulon T, Payen N, Iraqi MR, Arnaud J, Groslambert P. Plasma fatty acid status in Moroccan children: increased lipid peroxidation and impaired polyunsaturated fatty acid metabolism in protein-calorie malnutrition. Biomed Pharmacother. 2001;55(3):155-62.8

  37. Ashour MN, Salem SI, El-Gadban HM, Elwan NM, Basu TK. Antioxidant status in children with protein-energy malnutrition (PEM) living in Cairo, Egypt. Eur J Clin Nutr. 1999;53(8):669-73.

  38. Reyes Valdez JA. Tepehuanes del sur. México: Comisión Nacional para el Desarrollo de los pueblos indígenas; 2006. p. 12.

  39. Ashfaq S, Abramson JL, Jones DP, et al. The relationship between plasma levels of oxidized and reduced thiols and early atherosclerosis in healthy adults. J Am Coll Cardiol. 2006;47(5):1005-11.

  40. Wu LL, Chiou CC, Chang PY, Wu JT. Urinary 8-OHdG: a marker of oxidative stress to DNA and a risk factor for cancer, atherosclerosis and diabetics. Clin Chim Acta. 2004;339(1-2):1-9.






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