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An investigation on the effect of leptin on rat kidney tissue

Year 2015, Volume: 22 Issue: 1, 14 - 18, 30.03.2015

Abstract

Aim: increasing day by day obesity, one of the preventable health problems. Obese individual increases the risk of renal disease one and a half times more compared to the non-obese individuals. Leptin is a type of adipokinin hormone which is released from adipose tissue cells in proportion to the amount of adipose tissue. It is known that leptin leads to a rise in reactive oxygen radicals in the tissue. This study aimed at investigating if leptin affects renal tissue by giving leptin to the rats. Material–Method: The total of 16 Wistar albino rats (weights ranged from 250g-300g) in the study were randomly divided into groups of eight in two different cages. The first group was the Control group (intraperitoneally = i.p. 0.9% normal saline) and the second group was the leptin group (ip 0,1 mg/kg leptin). The subjects, which were given leptin i.p. for 7 days, and the ones in the control group, which were given 0.9% normal saline to trigger the same stress, were sacrificed and their kidneys were taken out for examination. The kidneys were fixed with 10% neutral form was formaldehide to routine histological procedure. The sections stained with hematoxylin-eosin = H-E were analyzed under light microscopy. Results: The sections in the control group were found to be normal hystologically. Compared to these, the renal tissue samples in the leptin group were determined to have mononuclear cell infiltration in the cortex, tubular dilatation in the medulla, degeneration and hemorrhagic areas, vacuolar degeneration in glomeruli and dilation in proximal and distal tubular. Discussion: Revealing the effects of leptin on renal damage is important for avoiding harmful effects of obesity through hormonal and behavioral arrangements. This study suggested that leptin could cause renal pathologies by damaging renal tissue. We are of the opinion that being able to explain renal damage etiology exactly will be useful to differential diagnosis and treatments

References

  • Guyton AC, Hall JE. Human Physiology and mechanisms of disease, 16th ed. WB Saunders, 1997: 486-584.
  • Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM. Positional cloning of the mouse obese gene and its human homologue. Nature 1994; 372: 425-432.
  • Gülle K, Karagöz E. Leptinler, Türkiye Klinikleri Tıp Bilimleri 2000 20: 112-121.
  • Ruige JB, Dekker JM, Blum WF, et al. Leptin and variables of body adiposity, energy balance and insulin resistance in a population based study. Diabetes Care 1999; 22: 1097- 1104.
  • Mantzoros CS, Flier JS, Lesem MD, et al. Cerebrospinal fluid leptin in anorexia nervosa:correlation with nutritional status and potential role in resistance to weight gain. J Clin Endocrinol 1997; 82: 1845-1851.
  • Tanner C.J., Barakat H.A., Dohm G.L., Pories W.J., MacDonald K.G., Cunningham P.R.G., Swanson M.S., Houmard J.A. Muscle fiber type is associated with obesity and weight loss. AJP-Endocrinol Metab. 2002; 282: 1191- 1196.
  • Hekimoglu A. Leptin ve fizyopatolojik olaylardaki rolü. Dicle Tıp Derg. 2006; 33: 259-267.
  • Özata M. Obezite tanı ve tedavisi. Gata Basımevi, Ankara. 2003; 1-19.
  • Süleymanlar G, Utaş C, Arınsoy T, et al. A population based survey of chronic renal disease in Turkey – The CREDIT study. Nephrol Dial Transplant 2011; 26: 1862-1871.
  • Abdel-Wahhab MA, Nada SA, Arbid MS. Ochratoxicosis: prevention of developmental toxicity by L-methionine in rats. Journal of applied toxicology. JAT. 1999; 19(1):7-12.
  • Peter G. Kopelman & Michael J. Stock. Klinik Obezite. Blackwell Science, Tekin yayınevi, Ankara, 1998; 120- 556.
  • Obesity and Obesity-Initiated Metabolic Syndrome: Mechanistic Links to Chronic Kidney Disease 2007; May 2(3): 550-562.
  • Rutkowski P, Klassen A, Sebekova K, et al: Renal disease in obesity: The need for greater attention. 2006; 16: 216- 223.
  • Macrea M, Martin T, Jia Z, Misra H, Leptin’s Activity on the Hydroxyl Radical: A Possible Link to the Oxidative Stress-Related Endothelial Vasodilation in Patients with Obstructive Sleep Apnea Lung 2013; 191: 391–395
  • Hall J E, Henegar JR, Dwyer TM, Liu J et al. Is obesity a major cause of chronic kidney disease. Adv Renal Replace 2004; 11: 41-54.
  • Pelleymounter MA, Cullen MJ, Baker MB, Hecht R, Winters D, Boone T, Collins F. Effects of the obese gene product on body weight regulation in ob/ob mice. Science 1995; 269: 540-543.
  • J. Ren. Leptin and hyperleptinemia from friend to foe for cardiovascular function. Endocrinol 2004; 181: 1-10.
  • Hall JE, Crook ED, Jones DW, Wofford MR and Dubbert PM. Mechanisms of obesity-associated cardiovascular and renal disease. Am J Med Sci, 2002; 324: 127-137.
  • Kayaalp O. Antihipertansif ilaçlar. Tıbbi Farmakoloji. 9. Baskı 2000; 421-459.
  • Adamopoulos S, Rosano GM, Ponikowski P, Cerquetani E, Piepoli M, Panagiota F, Collins P, Poole-Wilson P, Kremastinos D, Coats AJ. Impaired baroreflex sensitivity and sympathovagal balance in syndrome X. Am J Cardiol. 1998; 82(7): 862- 868.
  • Friedmen JM. The function of leptin in nutrition, weight and physiology, 2002; 60:51-514.
  • Wolf G, Chen Sheldon, Han DC, Ziyadeh N. Leptin and Renal Disease. AJKD, 2002; 39 (1): 1-11.
  • Praga M, Obesity a neglected culprit in renal disease. Nephrol Dial Transplant. 2002; 17: 1157-1159.

Ratların böbrek histomorfolojisi üzerine leptin etkisinin araştırılması

Year 2015, Volume: 22 Issue: 1, 14 - 18, 30.03.2015

Abstract

Özet
Amaç: Günümüzde gittikçe artan obezite, önlenebilir sağlık sorunlarından biridir. Obez bireylerde böbrek hastalığı riski obez olmayan bireylere göre yaklaşık 1.5 kat artmaktadır. Leptin yağ dokusu miktarıyla orantılı olarak yağ dokusu hücrelerinden salgılanan bir adipokindir.ve dokuda serbest oksijen radikallerinin artışına yol açtığı bilinmektedir. Bu çalışmada ratlara leptin vererek, hiperleptineminin böbrek histomorfolojisi üzerine etkisinin araştırılması amaçlandı.
Gereç ve Yöntem: Çalışmamızda ağırlıkları 250 gr ile 350 gr arasında değişen 16 adet Wistar albino rat kullanıldı. Ratlar, her kafeste rastgele 8 hayvan bulunan 2 gruba ayrıldı. 1.Grup; Kontrol (intraperitoneal = i.p. Serum Fizyolojik = SF) 7 gün, 2. Grup Leptin (i.p. 0,1 mg/kg leptin) 7 gün, olacak şekilde planlandı. 7 gün boyunca i.p. olarak leptin verilen hayvanlar ve aynı stresi oluşturmak amacıyla SF verilen kontrol grubundaki hayvanlar deney sonunda, anestezi altında sakrifiye edildi ve tüm ratların her iki böbreği de incelenmek üzere çıkarıldı. %10 nötral formalinde fikse edilen böbreklere rutin histolojik prosedür uygulandı. Hematoksilen-Eozin = H-E ile boyanan kesitler ışık mikroskobisi altında değerlendirildi.
Bulgular: Kontrol grubuna ait kesitlerde böbrek dokularının normal histolojik yapısında olduğu gözlendi. Kontrol grubuyla kıyaslandığında leptin grubuna ait böbrek dokusu örneklerinde, kortekste mononükleer hücre infiltrasyonu, medullada tübüler dilatasyon, dejenerasyon ve hemorajik alanlar, glomerüllerde vakuoler dejenerasyon, proksimal ve distal tübülerde dilatasyon izlendi.
Tartışma: Leptin ve böbrek hasarı arasındaki ilişkinin gösterilmesi hormonal ve davranışsal düzenlemelerle obezitenin zararlı etkilerinden korunmak için önemlidir. Bu araştırmanın sonucunda; leptinin böbrek dokusunu olumsuz etkilediğini ve böbrek dokusunda hasar meydana getirdiğini söyleyebiliriz.. Bize göre, obez bireylerde görülen böbrek hasarı etyolojisi açıklanırken leptin faktörüde gözönünde bulundurulmalıdır.
Anahtar kelimeler: Leptin, böbrek, obezite, böbrek hasarı


An investigation on the effect of leptin on histomorphology of rat kidney Cennet Ak 1, Dilek Bayram 2, Ilkay Armagan 2, A. Cihangir Uguz 3
1 Department of Physiology, School of Medicine, Suleyman Demirel University, Isparta, Turkey
2 Department of Histology and Embryology, School of Medicine, Suleyman Demirel University, Isparta, Turkey
3Department of Biophysics, School of Medicine, Süleyman Demirel University, Isparta, Turkey.
Abstract
Aim: increasing day by day obesity, one of the preventable health problems. Obese individual increases the risk of renal disease one and a half times more compared to the non-obese individuals. Leptin is a type of adipokinin hormone which is released from adipose tissue cells in proportion to the amount of adipose tissue. It is known that leptin leads to a rise in reactive oxygen radicals in the tissue. This study aimed at investigating if leptin affects renal tissue by giving leptin to the rats.
Material – Method: The total of 16 Wistar albino rats (weights ranged from 250g-300g) in the study were randomly divided into groups of eight in two different cages. The first group was the Control group (intraperitoneally = i.p. 0.9% normal saline) and the second group was the leptin group (ip 0,1 mg/kg leptin). The subjects, which were given leptin i.p. for 7 days, and the ones in the control group, which were given 0.9% normal saline to trigger the same stress, were sacrificed and their kidneys were taken out for examination. The kidneys were fixed with 10% neutral form was formaldehide to routine histological procedure. The sections stained with hematoxylin-eosin = H-E were analyzed under light microscopy.
Results: The sections in the control group were found to be normal hystologically. Compared to these, the renal tissue samples in the leptin group were determined to have mononuclear cell infiltration in the cortex, tubular dilatation in the medulla, degeneration and hemorrhagic areas, vacuolar degeneration in glomeruli and dilation in proximal and distal tubular.
Discussion: Revealing the effects of leptin on renal damage is important for avoiding harmful effects of obesity through hormonal and behavioral arrangements. This study suggested that leptin could cause renal pathologies by damaging renal tissue. We are of the opinion that being able to explain renal damage etiology exactly will be useful to differential diagnosis and treatments.
Keywords: Leptin, kidney, obesity, renal damage

References

  • Guyton AC, Hall JE. Human Physiology and mechanisms of disease, 16th ed. WB Saunders, 1997: 486-584.
  • Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM. Positional cloning of the mouse obese gene and its human homologue. Nature 1994; 372: 425-432.
  • Gülle K, Karagöz E. Leptinler, Türkiye Klinikleri Tıp Bilimleri 2000 20: 112-121.
  • Ruige JB, Dekker JM, Blum WF, et al. Leptin and variables of body adiposity, energy balance and insulin resistance in a population based study. Diabetes Care 1999; 22: 1097- 1104.
  • Mantzoros CS, Flier JS, Lesem MD, et al. Cerebrospinal fluid leptin in anorexia nervosa:correlation with nutritional status and potential role in resistance to weight gain. J Clin Endocrinol 1997; 82: 1845-1851.
  • Tanner C.J., Barakat H.A., Dohm G.L., Pories W.J., MacDonald K.G., Cunningham P.R.G., Swanson M.S., Houmard J.A. Muscle fiber type is associated with obesity and weight loss. AJP-Endocrinol Metab. 2002; 282: 1191- 1196.
  • Hekimoglu A. Leptin ve fizyopatolojik olaylardaki rolü. Dicle Tıp Derg. 2006; 33: 259-267.
  • Özata M. Obezite tanı ve tedavisi. Gata Basımevi, Ankara. 2003; 1-19.
  • Süleymanlar G, Utaş C, Arınsoy T, et al. A population based survey of chronic renal disease in Turkey – The CREDIT study. Nephrol Dial Transplant 2011; 26: 1862-1871.
  • Abdel-Wahhab MA, Nada SA, Arbid MS. Ochratoxicosis: prevention of developmental toxicity by L-methionine in rats. Journal of applied toxicology. JAT. 1999; 19(1):7-12.
  • Peter G. Kopelman & Michael J. Stock. Klinik Obezite. Blackwell Science, Tekin yayınevi, Ankara, 1998; 120- 556.
  • Obesity and Obesity-Initiated Metabolic Syndrome: Mechanistic Links to Chronic Kidney Disease 2007; May 2(3): 550-562.
  • Rutkowski P, Klassen A, Sebekova K, et al: Renal disease in obesity: The need for greater attention. 2006; 16: 216- 223.
  • Macrea M, Martin T, Jia Z, Misra H, Leptin’s Activity on the Hydroxyl Radical: A Possible Link to the Oxidative Stress-Related Endothelial Vasodilation in Patients with Obstructive Sleep Apnea Lung 2013; 191: 391–395
  • Hall J E, Henegar JR, Dwyer TM, Liu J et al. Is obesity a major cause of chronic kidney disease. Adv Renal Replace 2004; 11: 41-54.
  • Pelleymounter MA, Cullen MJ, Baker MB, Hecht R, Winters D, Boone T, Collins F. Effects of the obese gene product on body weight regulation in ob/ob mice. Science 1995; 269: 540-543.
  • J. Ren. Leptin and hyperleptinemia from friend to foe for cardiovascular function. Endocrinol 2004; 181: 1-10.
  • Hall JE, Crook ED, Jones DW, Wofford MR and Dubbert PM. Mechanisms of obesity-associated cardiovascular and renal disease. Am J Med Sci, 2002; 324: 127-137.
  • Kayaalp O. Antihipertansif ilaçlar. Tıbbi Farmakoloji. 9. Baskı 2000; 421-459.
  • Adamopoulos S, Rosano GM, Ponikowski P, Cerquetani E, Piepoli M, Panagiota F, Collins P, Poole-Wilson P, Kremastinos D, Coats AJ. Impaired baroreflex sensitivity and sympathovagal balance in syndrome X. Am J Cardiol. 1998; 82(7): 862- 868.
  • Friedmen JM. The function of leptin in nutrition, weight and physiology, 2002; 60:51-514.
  • Wolf G, Chen Sheldon, Han DC, Ziyadeh N. Leptin and Renal Disease. AJKD, 2002; 39 (1): 1-11.
  • Praga M, Obesity a neglected culprit in renal disease. Nephrol Dial Transplant. 2002; 17: 1157-1159.
There are 23 citations in total.

Details

Primary Language Turkish
Subjects Dentistry
Journal Section Research Articles
Authors

Cennet Ak

Dilek Bayram

İlkay Armağan This is me

A. Cihangir Uğuz

Publication Date March 30, 2015
Submission Date May 7, 2015
Published in Issue Year 2015 Volume: 22 Issue: 1

Cite

Vancouver Ak C, Bayram D, Armağan İ, Uğuz AC. Ratların böbrek histomorfolojisi üzerine leptin etkisinin araştırılması. Med J SDU. 2015;22(1):14-8.

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