Asprosin ve Glikoz Metabolizması Üzerine Etkileri

Abstract

Adipokinler adipoz dokudan salgılanan bioaktif maddeler olup iştah, enerji, lipid, karbonhidrat metabolizması, kan basıncının düzenlenmesi ve inflammasyon üzerinde çeşitli fonksiyonlara sahiptir. Bunlardan biri de 2016 yılında keşfedilen ve beyaz adipoz dokudan salgılanan asprosindir. Asprosin, açlık süresince salınmakta ve nanomolar düzeyde sirküle olmaktadır. FBN1 geninin iki egzonu tarafından kodlanan asprosinin, glikoz metabolizması gibi bazı metabolik süreçlerde doğrudan etkili olduğu bilinmekte ve halen araştırılmaktadır. Bu çalışma, asprosin ile obezite ve tip 2 diyabet gibi bazı halk sağlığı sorunları arasındaki ilişkiyi araştırmayı amaçlamıştır.

Keywords

• asprosin
• diyabet
• obezite
• glikoz metabolizması

Asprosin and Effects on Glucose Metabolism

Abstract

Adipokines secreted from adipose tissue, are bioactive substances and have kinds of functions on appetite, energy, lipid, carbohydrate metabolism, regulation of blood pressure, inflammation, etc. One of the adipokines is asprosin discovered in 2016, is secreted by white adipose tissue. This is released during fasting and found in circulating nanomolar levels. Asprosin is encoded by two exons of the gene FBN1 and is known for its effects on many metabolic processes, especially glucose metabolism, and is still under investigation. This study was aimed to investigate the relationship between asprosin and some public health problems such as obesity and type 2 diabetes.

Keywords

• asprosin
• diabetes
• obesity
• glucose metabolism

References

1. Romere C, Duerrschmid C and Bournat J et al. Asprosin, a Fasting-Induced Glucogenic Protein Hormone. Cell. 2016; 165(3): 566-579.
2. Li E, Shan H, Chen L, Long A, Zhang Y and Liu Y et al. OLFR734 Mediates Glucose Metabolism as a Receptor of Asprosin. Cell Metabolism. 2019; 30: 319–328.
3. Duerrschmid C, He Y, Wang C, Li C, Bournat JC and Romere C et al. Asprosin is a centrally acting orexigenic hormone. Nature Medicine. 2017; 23, 1444–1453.
4. Öztürk Andaç S. Besin Alımının Düzenlenmesi. Özer C (Ed.), Diyet Çeşitlerine Bilimsel Bakış içinde, Akademisyen Kitapevi, 2020, 23-41.
5. Meguid MM and Laviano A. Basics in clinical nutrition: appetite and its control. The European e-Journal of Clinical Nutrition and Metabolism. 2008; 3: 272-274.
6. Yu JH and Kim MS. Molecular mechanisms of appetite. Regulation Diabetes Metab J. 2012;36 (6):391-398.
7. Ahima RS and Flier JS. Leptin. Annual Review of Physiol. 2000; 62: 413-437.
8. Sinha MK, Ohannesian JP, Heiman ML, Kriauciunas A, Stephens TW and Magosin S et al. Nocturnal rise of leptin in lean, obese, and non-insulin-dependent diabetes mellitus subjects. Journal of Clinical Investigation. 1996; 97(5): 1344–1347.

9. Licinio J, Mantzoros C, Negrão AB, Cizza G, Wong ML and Bongiorno PB. Human leptin levels are pulsatile and inversely related to pituitary-adrenal function. Nature Medicine. 1997; 3(5):575-9.
10. Martin R, Cordova C, Gutierrez B, Hernandez M, Nieto ML. A dangerous liaison: Leptin and Spla2-IIA join forces to induce proliferation and migration of astrocytoma cells. PLoS One. 2017;12(3):0170675.
11. Cummings DE, Purnell JQ, Frayo RS, Schmidova K, Wisse BE and Weigle DS. A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans. Diabetes. 2001;50(8):1714-9.
12. Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H and Kangawa K. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999; 402: 656–660.
13. Segal-Lieberman G, Rubinfeld H, Glick M, Kronfeld-Schor N and Shimon I. Melanin-concentrating hormone stimulates human growth hormone secretion: a novel effect of MCH on the hypothalamic-pituitary axis. American Journal of Physiology-Endocrinology and Metabolism. 2006; 290: 982–988.
14. Holzer P, Reichmann F and Farzi A. Neuropeptide Y, peptide YY and pancreatic polypeptide in the gut-brain axis. Neuropeptides. 2012;46(6):261-74.
15. Kose S, Gulec MY, Ozalmete OA, Ozturk M, Gulec H and Sayar K. Plasma neuropeptide Y levels in medication naive adolescents with major depressive disorder. Klinik Psikofarmakoloji Bulteni. 2010; 20: 132-138.
16. Baggio LL, Drucker DJ. Biology of incretins: GLP-1 and GIP. Gastroenterology. 2007; 132(6): 2131–57.
17. Hermann C, Goke R, Richter G, Fehmann HC, Arnold R and Goke B. Glucagon-like peptide-1 and glucose-dependent insulin-releasing polypeptide plasma levels in response to nutrients. Digestion. 1995; 56: 117–26.
18. Schirra J, Wank U, Arnold R, Goke B and Katschinski M. Effects of glucagon-like peptide-1 (7–36) amide on motility and sensation of the proximal stomach in humans. Gut. 2002; 50: 341–8.
19. Aea A. Peripheral motor action of glucagon-like peptide-1 through enteric neuronal receptors. Journal of Neurogastroenterol and Motility. 2010; 22: 664–e203.
20. Pocai A. Action and therapeutic potential of oxyntomodulin. Molecular Metabolism. 2014; 3: 241–251.
21. Brubaker PL. A beautiful cell (or two or three?). Endocrinology. 2012; 153:2945–2948.
22. Habib AM, Richards P, Cairns LS, Rogers, GJ, Bannon, CA and Parker HE et al. Overlap of endocrine hormone expression in the mouse intestine revealed by transcriptional profiling and flow cytometry. Endocrinology. 2012; 153:3054–3065.
23. Drucker DJ. Biologic actions and therapeutic potential of the glucagonlike peptides. Nature Clinical Practice. Endocrinology and Metabolism. 2005; 1: 22–31.
24. Wynne K and Bloom SR. The role of oxyntomodulin and peptide tyrosine–tyrosine (PYY) in appetite control. Nature Clinical Practice Endocrinology& Metabolism. 2006; 2(11): 612-20.
25. Rocha M, Bing C, Williams G and Puerta M. Pregnancy-induced hyperphagia is associated with increased gene expression of hypothalamic agouti-related peptide in rats. Regulatory Peptides. 2003;114:159–65.
26. Ge Y, Ohta T, Driscoll DJ, Nicholls RD and Kalra SP. Anorexigenic melanocortin signaling in the hypothalamus is augmented in association with failure-to-thrive in a transgenic mouse model for Prader-Willi syndrome. Brain Research. 2002; 957: 42–5.
27. Claycombe KJ, Wang Y, Jones BH, Kim S, Wilkison WO and Zemel MB et al. Transcriptional regulation of the adipocyte fatty acid synthase gene by agouti: interaction with insulin. Physiological Genomics.2000 a;3: 157–62.
28. Claycombe KJ, Xue BZ, Mynatt RL, Zemel MB and Moustaid-Moussa N. Regulation of leptin by agouti. Physiological Genomics.2000 b;2: 101–5.
29. Hoggard N, Hunter L, Duncan JS and Rayner DV. Regulation of adipose tissue leptin secretion by alphamelanocyte-stimulating hormone and agouti-related protein: further evidence of an interaction between leptin and the melanocortin signalling system. Journal of Molecular Endocrinology.2004;32: 145–53.
30. Dhillo WS, Small CJ, Gardiner JV, Bewick GA, Whitworth EJ and Jethwa PH et al. Agouti-related protein has an inhibitory paracrine role in the rat adrenal gland. Biochemical and Biophysical Research Communications. 2003;301:102–7.
31. Doghman M, Delagrange P, Blondet A, Berthelon MC, Durand P and Naville D et al. Agouti Related Protein Antagonizes Glucocorticoid Production Induced through Mc4-R Activation in Bovine Adrenal Cells: A Possible Autocrine Control. Endocrinology. 2003;145(2):541-7.
32. Katsuki A, Sumida Y, Gabazza EC, Murashima S, Tanaka T and Furuta M et al. Plasma levels of agouti-related protein are increased in obese men. The Journal of Clinical Endocrinology & Metabolism. 2001;86: 1921–4.
33. Shen CP, Wu KK, Shearman LP, Camacho R, Tota MR and Fong TM et al. Plasma agouti-related protein level: a possible correlation with fasted and fed states in humans and rats. Journal of Neuroendocrinology. 2002; 14: 607– 610.
34. Gavrila A, Chan JL, Miller LC, Heist K, Yiannakouris N and Mantzoros CS. Circulating melaninconcentrating hormone, agouti-related protein, and alpha-melanocyte-stimulating hormone levels in relation to body composition: alterations in response to food deprivation and recombinant human leptin administration. The Journal of Clinical Endocrinology & Metabolism. 2005;90: 1047–54.
35. Bencze J, Pocsai K, Murnyak B, Gergely P, Juhász B and Szilvássy Z et al. The Melanin-concentrating Hormone System in Human, Rodent and Avian Brain. Open Medicine. 2018; 13(1):264-269.
36. Arora S and Anubhuti. Role of neuropeptides in appetite regulation and obesity - a review. Neuropeptides.2006; 40 (6): 375-401.
37. Boutin JA, Suply T, Audinot V, Rodriguez M, Beauverger P and Nicolas JP et al. Melanin-concentrating hormone and its receptors: state of the art. Canadian Journal of Physiology and Pharmacology. 2002;80, 388–395.
38. Oh-I S, Shimizu H, Satoh T, Okada S, Adachi S and Inoue K et al. Identification of nesfatin- 1 as a satiety molecule in the hypothalamus. Nature. 2006; 443(7112): 709-712.
39. Stengel A, Goebel M, Yakubov I, Wang L,Witcher D and Coskun T et al. Identification and characterization of nesfatin-1 immunoreactivity in endocrine cell types of the rat gastric oxyntic mucosa. Endocrinology. 2009; 150: 232–238.
40. Zhang AQ, Li XL, Jiang CY, Lin L and Shi RH et al. Expression of nesfatin1/NUCB2 in rodent digestive system. World J Gastroenterolgy. 2010; 16: 1735–1741.
41. Algül S, Erkeç ÖE, Kara M, Kara B and Özçelik O. Şiddetli Depresyonda Nesfatin-1 ve Ghrelin Hormonunun İncelenmesi. Van Tıp Dergisi. 2017; 24(3):141-145.
42. World Health Organization. BMI Classification. Global Database on Body Mass Index. Available
43. Ritchie H and Roser M. Obesity. Access adress: https://ourworldindata.org/obesity
44. Edrees HM and Morgan EN. Asprosin: A Risk Factor For Obesity and Metabolic Disturbance. International Journal of Current Research. 2018; 10(9):73319-23.
45. Sahoo K, Sahoo B, Choudhury AK, Sofi NY, Kumar R and Bhadoria AS. Childhood obesity: causes and consequences. Journal of Family Medicine and Primary Care. 2015; 4(2):187-92.
46. Silistre Sünnetçi E and Hatiğoplu HU. Increased Serum Circulating Asprosin Levels in Children with Obesity. Japon Pediatric Society. 2020; 62(4):467-476.
47. Long W, Xie X, Du C, Zhao Y, Zhang C and Zhan D et al. Decreased Circulating Levels of Asprosin in Obese Children. Hormone Research Paediatrics. 2019;91(4):271-277.
48. Wang C, Lin T, Liu K, Liao C, Liu Y and Wu VC et al. Serum asprosin levels and bariatric surgery outcomes in obese adults. International Journal of Obesity. 2019; 43: 1019–1025.
49. Hu Y, Xu Y, Zheng Y, Kang Q, Lou Z and Liu Q et al. Increased plasma asprosin levels in patients with drug‑naive anorexia nervosa. Eating and Weight Disorders- Studies on Anorexia, Bulimia and Obesity.2020.
50. WHO, World Health Organization. Diabetes. 2016. Access Adress: https://www.who.int/diabetes/global report/WHD2016_Diabetes_Infographic_v2.pdf
51. Zimmet P, Alberti KG, Magliano DJ and Bennett PH. Diabetes mellitus statistics on prevalence and mortality: facts and fallacies. Nature Reviews Endocrinolology. 2016;12(10):616.
52. TEMD, Türkiye Endokrinoloji ve Metabaolizma Derneği. Diabetes Mellitus ve Komplikasyonlarının Tanı, Tedavi ve İzlem Kılavuzu;2020.
53. Groener JB, Valkanou A, Kender Z, Pfeiffenberger J, Kihm L and Fleming T et al. The asprosin response in hypoglycemia is not due to unawareness of hypoglycemia, but rather to insulin resistance in type 1 diabetes. PLoS ONE. 2019; 14 (9): e0222771.
54. DeFronzo RA. Lilly lecture 1988. The triumvirate: Beta‐cell, muscle, liver. A collusion responsible for NIDDM. Diabetes. 1988; 37(6), 667–687.
55. DeFronzo RA. Pathogenesis of type 2 diabetes mellitus. Medical Clinics of North America. 2004; 88(4), 787–835.
56. Lebovitz HE. Insulin resistance: Definition and consequences. Experimental and Clinical Endocrinology & Diabetes. 2001; 109(2): 135–148.
57. Lillioja S, Mott DM, Howard BV, Bennett PH, Yki‐Jarvinen H and Freymond D et al. Impaired glucose tolerance as a disorder of insulin action. Longitudinal and cross‐sectional studies in Pima Indians. New England Journal of Medicine. 1988; 318(19): 1217–1225.
58. Jung TW, Kim H, Kim HU, Park T, Park J and Kim U et al. Asprosin attenuates insulin signaling pathway through PKCδ‐activated ER stress and inflammation in skeletal muscle. Journal of Cellular Physiology. 2019; 234:20888–20899.
59. Petersen MC, Vatner DF, and Shulman GI. Regulation of hepatic glucose metabolism in health and disease. Nature Reviews Endocrinology. 2017; 13572–587.
60. Lin HV and Accili D. Hormonal regulation of hepatic glucose production in health and disease. Cell Metabolism. 2011; 14, 9–19.
61. Li X, Liao M, Shen R, Zhang L, Hu H and Wu J et al. Plasma Asprosin Levels Are Associated with Glucose Metabolism, Lipid, and Sex Hormone Profiles in Females with Metabolic-Related Diseases. Hindawi Mediators of Inflammation. 2018; 2018:1-12.
62. Zhang X, Jiang H, Ma X and Wu H. Increased serum level and impaired response to glucose fluctuation of asprosin is associated with type 2 diabetes mellitus. Journal Diabetes Investigation. 2020; 11(2) :349-355.
63. Naiemian S, Naeemipour M, Zarei M, Najaf ML, Gohari A and Behroozikhah MR et al. Serum concentration of asprosin in new-onset type 2 diabetes. Diabetology& Metabolic Syndrome. 2020; 12: 65.
64. Zhanga L, Chena C, Zhoub N, Fub Y and Cheng X. Circulating asprosin concentrations are increased in type 2 diabetes mellitus and independently associated with fasting glucose and triglyceride. Clinica Chimica Acta. 2019; 489: 183-188.
65. Kasprzyk M, Wudarczyk B, Czyz R, Szarpak L and Jankowska-Polanska B. Ischemic heart disease – definition, epidemiology, pathogenesis, risk factors and treatment. Postępy Nauk Medycznych. 2018; XXXI(6): 358-360.
66. Kocaman N and Kuloğlu T. Expression of asprosin in rat hepatic, renal, heart, gastric, testicular and brain tissues and its changes in a streptozotocin-induced diabetes mellitus model. Tissue and Cell. 2020; 66: 101397.
67. Acara AC, Bolatkale M, Kızıloğlu İ, İbişoğlu E and Can Ç. A novel biochemical marker for predicting the severity of ACS with unstable angina pectoris: Asprosin. The American Journal of Emergency Medicine. 2018; 36(8):1504-1505.
68. Zhang Z, Tanb Y, Zhub L, Zhangb B, Fengb P, Gaod E et al. Asprosin improves the survival of mesenchymal stromal cells in myocardial infarction by inhibiting apoptosis via the activated ERK1/2-SOD2 pathway. Life Sciences. 2019; 5 (231):116554.