Journals / European Journal of Biology / 2022 / Cilt: 81 - Sayı: 1

Leptin Enhances Nitric Oxide Production and Decreases Blood Flow in Rat Skeletal Muscle

Pages
18–25
Publication Date
2022-10-12
DOI
—
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AI Summary & Key Takeaways

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⚡ TL;DR(Too Long; Didn't Read)

Conclusion: Although NO synthesis is inhibited by L-NAME, it is concluded that leptin partially enhances NO production and leptin uses NO as a mediator in its physiological effects.

📌 3 Key Takeaways

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Objective & Hypothesis:Objective: There are a few studies related to nitric oxide (NO) and leptin interaction in the regulation of physiological events in skeletal muscle.
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Key Findings & Data:Materials and Methods: Twenty-four adult-male Wistar albino rats were divided into 4 groups: control (C), Leptin (LP) (50 μg/kg), L-NG-nitroarginine methyl ester (LN) (a non-specific nitric oxide synthase inhibitor, 10 mg/kg,) and L-NAME+Leptin (LN+LP) administrated groups.
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Conclusion & Impact:Conclusion: Although NO synthesis is inhibited by L-NAME, it is concluded that leptin partially enhances NO production and leptin uses NO as a mediator in its physiological effects.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Blood flow · leptin · nitric oxide

Abstract

Objective: There are a few studies related to nitric oxide (NO) and leptin interaction in the regulation of physiological events in skeletal muscle. Therefore, the aim of the present study is to investigate the interaction of leptin and NO in response to blood flow and nitric oxide synthase (NOS) distribution on rat skeletal muscle. Materials and Methods: Twenty-four adult-male Wistar albino rats were divided into 4 groups: control (C), Leptin (LP) (50 μg/kg), L-NG-nitroarginine methyl ester (LN) (a non-specific nitric oxide synthase inhibitor, 10 mg/kg,) and L-NAME+Leptin (LN+LP) administrated groups. Drugs were administered via the right jugular vein. Hemodynamic parameters: mean arterial pressure, heart rate and blood flow were recorded during the experiment and at the end blood samples for biochemical analyses of leptin and nitrite/nitrate levels and gastrocnemius muscle tissues from the right hindlimb for NOS distribution were taken. Results: Leptin infusion after L-NAME administration significantly decreased heart rate and blood flow (p<0.05, p<0.001). In addition, there was no change in the mean arterial pressure in the leptin group and leptin-administered L-NAME group. Leptin levels were the highest in the LP+LN group (p<0.01). Decreased nitrate/nitrate levels with L-NAME administration (p<0.01 vs C) reached control values by leptin infusion. Both endothelial NOS (eNOS) and neuronal NOS (nNOS) distributions were observed in the skeletal muscle cells of the leptin group. Conclusion: Although NO synthesis is inhibited by L-NAME, it is concluded that leptin partially enhances NO production and leptin uses NO as a mediator in its physiological effects.

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Cite This Article

KAPUCU, A., USTUNOVA, S., TANSEL, C. D. (2022). Leptin Enhances Nitric Oxide Production and Decreases Blood Flow in Rat Skeletal Muscle. European Journal of Biology, Cilt: 81 - Sayı: 1, 18–25. https://ajindex.com/articles/510546

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References (17)

  1. Paz-Filho G, Mastronardi CA, Licinio J. Leptin treatment: facts and xpectations. Metabolism 2015; 64(1): 146-56
  2. Zhang Y, Chua S, Jr. Leptin Function and Regulation. Compr Physiol 2017; 8(1): 351-69
  3. Kokta TA, Dodson MV, Gertler A, Hill RA. Intercellular signaling between adipose tissue and muscle tissue. Domest Anim Endocrinol 2004; 27(4): 303-31
  4. Sletten AC, Peterson LR, Schaffer JE. Manifestations and mechanisms of myocardial lipotoxicity in obesity. J Intern Med 2018; 284(5): 478-91
  5. Minokoshi Y, Toda C, Okamoto S. Regulatory role of leptin in glucose and lipid metabolism in skeletal muscle. Indian J Endocrinol Metab 2012; 16(Suppl 3): S562
  6. Ciriello J. Leptin in nucleus of the solitary tract alters the cardiovascular responses to aortic baroreceptor activation. Peptides 2013; 44: 1-7
  7. Smith PM, Ferguson AV. Cardiovascular actions of leptin in the subfornical organ are abolished by diet‐induced obesity. J Neuroendocrinol 2012; 24(3): 504-10
  8. Hassan MJM, Bakar NS, Aziz MA, Basah NK, Singh HJ. Leptin-induced increase in blood pressure and markers of endothelial activation during pregnancy in Sprague Dawley rats is prevented by resibufogenin, a marinobufagenin antagonist. Reprod Biol 2020; 20(2): 184-90
  9. Rahmouni K, Jalali A, Morgan DA, Haynes WG. Lack of dilator effect of leptin in the hindlimb vascular bed of conscious rats. Eur J Pharmacol 2005; 518(2-3): 175-81
  10. Winters B, Mo Z, Brooks-Asplund E, Kim S, Shoukas A, Li D, et al. Reduction of obesity, as induced by leptin, reverses endothelial dysfunction in obese (Lepob) mice. J Appl Physiol 2000; 89(6): 2382-90
  11. Robbins RA, Grisham MB. Nitric oxide. Int J Biochem Cell Biol 1997; 29(6): 857-60
  12. Buchwalow IB, Minin EA, Samoilova VE, Boecker W, Wellner M, Schmitz W, et al. Compartmentalization of NO signaling cascade in skeletal muscles. Biochem Biophys Res Commun 2005; 330(2): 615-21
  13. Grozdanovic Z. NO message from muscle. Microsc Res Tech 2001; 55(3): 148-53
  14. Stamler JS, Meissner G. Physiology of nitric oxide in skeletal muscle. Physiol Rev 2001; 81(1): 209-37
  15. Frühbeck G. Pivotal role of nitric oxide in the control of blood pressure after leptin administration. Diabetes 1999; 48(4): 903-8
  16. Fuhrich DG, Lessey BA, Savaris RF. Comparison of HSCORE assessment of endometrial beta3 integrin subunit expression with digital HSCORE using computerized image analysis (ImageJ). Anal Quant Cytopathol Histpathol 2013; 35(4): 210-6
  17. Arneth W, Herold B. Nitrat