Steroid effect on serum leptin in Libyan children with minimal change nephritic syndrome
DOI:
https://doi.org/10.54361/ljmr.v8i1.06Keywords:
leptin, nephrotic syndrome, steroid, weight, Libya, childrenAbstract
Few studies have looked at the status of leptin in renal diseases especially nephrotic syndrome. The aim of this study was to investigate the effect of steroid therapy on serum leptin, anthropometric and appetite in patients with minimal change nephrotic syndrome (MCNS). Twenty children were recruited for this prospective study. Group I included ten children aged between 2 - 12 years with MCNS without any associated complications as impaired renal functions, hematuria, hypertension and others. Group II included ten healthy children with matching age, sex and BMI as a control group. Body weight, height, nutritional history including appetite, quantity of food, clinical examination, blood pressure and blood for kidney function parameter and serum leptin were taken before and after 3 days and after 2 weeks following prednisolone dose of 2 mg/kg/day. The same parameters were also performed for group II. Serum leptin was higher in group II than group I (1.575 ± 1.07 vs 0.575 ± 0.76 ng/ml p < 0.01). After 3 days and after 2 weeks of 2 mg/kg of prednisolone, serum leptin increased significantly in group II (t = 4.65, p < 0.014) without significant difference as it compared with group I (t = 1.65, p = 0.08). A highly significant increase in serum leptin concentration was detected in 2 weeks after prednisone therapy compared to the base line levels before therapy, compared to 3 days after therapy and to the control group (t = 5.69, p < 0.001, t = 3.95, p < 0.001 and t = 8.96, p < 0.001, respectively). In group I, serum leptin was higher in females than males (4.8 ± 2.8, p < 0.001). BMI was also higher in females compared to males. Patients' appetite improved after prednisolone for food quantity as recorded by the recall methods. Blood urea and serum creatinine in groups I and II did change significant within group II after steroid and even the changes were not significantly different from the control. Serum albumin, total serum protein, serum cholesterol concentrations and proteinuria revealed a significant difference between the two groups (t = 5.9, 8.9, 8.98 & 16.33, respectively, p < 0.01, for all). Weight, BMI in group I before and 2 weeks after intake of prednisone did not revealed any significant differences in weight, BMI before and after 2 weeks of prednisone (t = 0.99 and 0.88.8, respectively) in spite of the increase in appetite. Blood pressure had not changed significantly after the steroid therapy in MCNS patients’ group. Thus, serum leptin concentration and appetite were significantly higher especially in females without significant change in anthropometric, blood pressure and renal function indices after steroid therapy in minimal change nephropathy.
References
Zhang Y, Proenca R, Maffei M, Barone M, Leopold L and Friedman JM. Positional cloning of the mouse obese gene and its human homologue. Nature.1994, 372; 6505: 425-432. DOI: https://doi.org/10.1038/372425a0
Margetic S, Gazzola C, Pegg GG and Hill RA. Leptin: a review of its peripheral actions and interactions. Int J Obes Relat Metab Disord. 2002, 26; 11: 1407-1433. DOI: https://doi.org/10.1038/sj.ijo.0802142
Bado A, Levasseur S, Attoub S, Kermorgant S, Laigneau J, Bortoluzzi M, Moizo L, Lehy T, Guerre-Millo M, Le Marchand-Brustel Y and Lewin M. The stomach is a source of leptin. Nature. 1998, 394; 6695: 790-793. DOI: https://doi.org/10.1038/29547
Ingalls AM, Dickie MM and Snell GD. Obese, a new mutation in the house mouse. J Hered 1950, 4: 12. DOI: https://doi.org/10.1093/oxfordjournals.jhered.a106073
Jeffrey SF. What's a name? in search of leptin's Physiologic role, J Clin Endocrinol Metab. 1998, 83: 1407-1413. DOI: https://doi.org/10.1210/jc.83.5.1407
Auwerx J and Staels B. Leptin. Lancet. 1998, 351: 737-742. DOI: https://doi.org/10.1016/S0140-6736(97)06348-4
Cumin F, Baum HP, deGasparo M and Levens N. Removal of endogenous leptin from the circulation by the kidney. Int J Obes Relat Metab Disord. 1997, 21: 495-504. DOI: https://doi.org/10.1038/sj.ijo.0800428
Howard JK, Lord GM, Clutterbuck EJ, Ghatei MA and Pusey CD. Plasma immune-reactive leptin concentration in end-stage renal disease. Clin Sci.1997, 93: 119-126. DOI: https://doi.org/10.1042/cs0930119
Saad MF, Riad-Gabriel M, Khan A, Sharma A, Michael R, Jinagouda SD, Boyadjian R and Steil GM. Diurnal and ultradian rhythm city of plasma leptin: effect of gender and adiposity. J Clin Endocrinol Metab. 1998, 83: 453. DOI: https://doi.org/10.1210/jcem.83.2.4532
Ostlund RE, Yang JW, Klein S and Gingerich R. Relation between plasma leptin concentration and body fat, gender, diet, age and metabolic covariates. J Clin Endocrinol Metab. 1996, 81: 3909-3913. DOI: https://doi.org/10.1210/jcem.81.11.8923837
Carlsson B, Ankarberg C, Rosberg S, Norjavaara E, Albertsson-Wikland K and Carlsson LMS. Serum leptin concentrations in relation to pubertal development. Arch Dis Child 1997, 77: 396-400. DOI: https://doi.org/10.1136/adc.77.5.396
James NR and Alan DR. Role of leptin during childhood growth and development. J Clin Endocrinol Metab. 1999, 28: 749-764. DOI: https://doi.org/10.1016/S0889-8529(05)70100-6
Blum WF, Englaro P, Hanitsch S, Juul A, Hertel N, Müller J, Skakkebæk NE, Heiman ML, Birkett M and Attanasio AM. Plasma leptin levels in healthy children and adolescents: Dependence on body mass index, body fat mass, gender, pubertal stage and testosterone. J Clin Endocrinol Metab. 1997, 82: 2904. DOI: https://doi.org/10.1210/jcem.82.9.4251
Rentsch J and Chiesi M. Regulation of ob gene mRNA levels in cultured adipocytes. FEBS let. 1996, 379: 55-59. DOI: https://doi.org/10.1016/0014-5793(95)01485-3
Halleux CM, Servais I, Reul BA, Detry R and Brichar SM. Multihormonal control of ob gene expression and leptin secretion from cultured human visceral adipose tissue: increased responsiveness to glucocorticoids in obesity. J Clin Endocrinol Metab. 1998, 83: 902-910. DOI: https://doi.org/10.1210/jc.83.3.902
Wabitsch M, Jensen P, Blum WF, Christoffersen CT, Englaro P, Heinze E, Rascher W, Teller W, Tornqvist H and Hauner H. Insulin and cortisol promote leptin production in cultured human fat cells. Diabetes. 1996, 45: 1435-1438. DOI: https://doi.org/10.2337/diab.45.10.1435
Considine RV, Nyce MR, Kolaczynski JW, Zhang PL, Ohannesian JP, Moore JH Jr, Fox JW and Caro JF. Dexamethasone stimulates leptin release from human adipocytes: Unexpected inhibition by insulin. J Cell Biochem. 1997, 65: 254-258. DOI: https://doi.org/10.1002/(SICI)1097-4644(199705)65:2<254::AID-JCB10>3.0.CO;2-I
Kolaczynski JW, Considine RV, Ohannesian J, Marco C, Opentanova I, Nyce MR, Myint M and Caro JF. Response of leptin to short-term fasting and refeeding in humans: a link with ketogenesis but not ketones themselves. Diabetes. 1996, 45: 1511-1515. DOI: https://doi.org/10.2337/diabetes.45.11.1511
Mendoza SA and Tune BM. Management of the difficult nephrotic patient. Pediatr Clin North Am. 1995, 42: 1459-1468. DOI: https://doi.org/10.1016/S0031-3955(16)40093-3
Nash MA, Edelmann Jr. CM, Bernstein J, Meadow SR, Spitzer A and Travis LB (eds). Pediatric Kidney Disease. 2nd Edition. Boston: Little, Brown and Company. 1992,1247-1266.
Vernier RL. Primary (idiopathic) nephrotic syndrome. In: Holliday MA, Barratt TM, Vernier RL (eds). Pediatric Nephrology. 2nd Edition, Baltimore: Wiliams and Wilikins. 1987, 445- 456.
Habib R and Kleinknecht C. The primary nephrotic syndrome of childhood: Classification and clinicopathologic study of 406 cases. Pathol Annu. 1971, 6: 417.
White RHR, Glasgow EF and Mills RJ. Clinicopathologic study of nephrotic syndrome on childhood. Lancet. 1970, 1: 1353. DOI: https://doi.org/10.1016/S0140-6736(70)91268-7
International Study of Kidney Disease in Children: Nephrotic syndrome in children. Prediction of histopathology from clinical and laboratory characteristics at time of diagnosis. Kidney Int. 1978, 13: 159. DOI: https://doi.org/10.1038/ki.1978.23
Nash MA, Edelmann JR, CM, Bernstein J and Barnett HL. Minimal change nephrotic syndrome, diffuse mesangial hypercellularity, and focal glomerular sclerosis. In Edelmann JR, CM, Bernstein J, Meadow SR, Spitzer A and Travis LB (eds). Pediatric Kidney Disease. 2nd Edition. Boston: Little, Brown and Company. 1992, 1267-1290.
Rohner-Jeanrenaud F, Jeanrenaud B. Obesity, leptin, and the brain, N Engl J Med. 1996, 334: 324-325. DOI: https://doi.org/10.1056/NEJM199602013340511
Fried SK, Russell CD, Grauso NL and Brolin RE. Lipoprotein lipase regulation by insulin and gloucocorticoid in subcutaneous and omental adipose tissues of obese women and men. J Clin Invest. 1993, 92: 2191-2198. DOI: https://doi.org/10.1172/JCI116821
Hajduch E, Hainault I, Meunier C, Jardel C, Hainque B, Guerre-Millo M and Lavau M. Regulation of glucose transporters in cultured rat adipocytes: synergistic effect of insulin and dexamethasone on GLUT4 gene expression through promoter activation. Endocrinol. 1995, 126: 4782-4789. DOI: https://doi.org/10.1210/endo.136.11.7588207
Slieker LJ, Sloop KW, Surface PL, Kriauciunas A, LaQuier F, Manetta J, Bue-Valleskey J and Stephens TW. Regulation of expression of ob mRNA and protein by glucocorticosteroids and cAMP. J Biol Chem. 1996, 271: 5301-5304. DOI: https://doi.org/10.1074/jbc.271.10.5301
De Vos P, Saladin R, Auwerx J and Staels B. Induction of ob gene expression by corticosteroids is accompanied by weight loss and reduced food intake. J Biol Chem. 1995, 270: 15958-15961. DOI: https://doi.org/10.1074/jbc.270.27.15958
Meill JP, Englaro P and Blum WF. Dexamethasone induces an acute and sustained rise in circulating leptin levels in normal human subjects. Horm Metab Res. 1996, 28: 704-707. DOI: https://doi.org/10.1055/s-2007-979882
Kiess W, Englaro P, Hanistsch S, Rascher W, Attanasio A and Blum WF. High leptin concentrations in serum of very obese children are further stimulated by dexamethasone. Horm Metab Res. 1996, 28: 708-710. DOI: https://doi.org/10.1055/s-2007-979883
Larsson H and Ahren BO. Short-term dexamethasone treatment increases plasma leptin independently of changes in insulin sensitivity in healthy women. J Clin Endocrinol Metab 1996, 81: 4428-4432. DOI: https://doi.org/10.1210/jc.81.12.4428
Kolaczynski JW, Goldstein BJ, Considine RV, dexamethasone, ob gene and leptin in humans: effect of exogenous hyperinsulinemia. J Clin Endocrinol Metab. 1997, 82: 3895- 3897. DOI: https://doi.org/10.1210/jc.82.11.3895
Elimam A, Knutsson U and Bronnegard M. variations in glucocorticoid levels within the physiological range affect plasma leptin levels. Eur J Endocrinol. 1998, 139: 615-620. DOI: https://doi.org/10.1530/eje.0.1390615
Merabet E, Dagogo-Jack S, Coyne DW, Klein S, Santiago JV, Hmiel SP and Landt M. Increased plasma leptin concentration in end-stage renal disease. J Clin Endocrinol Metabol. 1997, 82; 3: 847-850 DOI: https://doi.org/10.1210/jc.82.3.847
Valle M, Gascon F, Martos R, Bermudo F, Ceballos P and Suanes A. Relationship between high plasma leptin concentrations and metabolic syndrome in obese pre-pubertal children. Inter J Obesity. 2003, 27: 13-18. DOI: https://doi.org/10.1038/sj.ijo.0802154
Wasilewska A, Tomaszewska B, Zoch-Zwierz W, Biernacka A, Klewinowska K and Koput A. Serum and urine leptin concentration in children with nephrotic syndrome. Pediatr Nephrol. 2005, 20; 5: 597-602. DOI: https://doi.org/10.1007/s00467-004-1772-x
Ricardo V, Andrade M, Rios M, Lage M and Felipe FC. Serum leptin levels in normal children: relationship to age, gender, body mass index, pituitary-gonadal hormones and pubertal stage. J Clin Endocrinol Metab. 1997, 82: 2849-1858. DOI: https://doi.org/10.1210/jc.82.9.2849
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Copyright (c) 2014 Atwatif Alboashie, Elmukhtar Habas, Amnna Rayani (Author)
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