Obesity-induced chronic inflammation in high fat diet challenged C57BL/6J mice is associated with acceleration of age-dependent renal amyloidosis

Scientific Reports

Volumn 5, Issue , 2015, Pages

  Van Der Heijden, Roel A ^a,f   Bijzet, Johan ^a   Meijers, Wouter C ^a   Yakala, Gopala K ^b   Kleemann, Robert ^c,f   Nguyen, Tri Q ^d   De Boer, Rudolf A ^a   Schalkwijk, Casper G ^e,f   Hazenberg, Bouke P C ^a   Tietge, Uwe J F ^a   Heeringa, Peter ^a,f  

^a UNIVERSITY MEDICAL CENTER GRONINGEN   (Netherlands)

^b NATIONAL UNIVERSITY OF SINGAPORE   (Singapore)

^c TNO   (Netherlands)

^d UNIVERSITY MEDICAL CENTER UTRECHT   (Netherlands)

^e MAASTRICHT UNIVERSITY MEDICAL CENTER   (Netherlands)

^f TOP INSTITUTE FOOD AND NUTRITION   (Netherlands)

Author keywords

[No Author keywords available]

Indexed keywords

ADIPOCYTOKINE; CYTOKINE; INSULIN; LIPID; SERUM AMYLOID A;

ADVERSE EFFECTS; AGE; AMYLOIDOSIS; ANIMAL; BLOOD; C57BL MOUSE; CHRONIC DISEASE; ENZYME LINKED IMMUNOSORBENT ASSAY; GENETICS; HOMEOSTASIS; INFLAMMATION; KIDNEY; KIDNEY DISEASES; LIPID DIET; MALE; METABOLISM; OBESITY; PATHOLOGY; PATHOPHYSIOLOGY; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; RISK FACTOR; TIME FACTOR; WESTERN BLOTTING;

ADIPOKINES; AGE FACTORS; AMYLOIDOSIS; ANIMALS; BLOTTING, WESTERN; CHRONIC DISEASE; CYTOKINES; DIET, HIGH-FAT; ENZYME-LINKED IMMUNOSORBENT ASSAY; HOMEOSTASIS; INFLAMMATION; INSULIN; KIDNEY; KIDNEY DISEASES; LIPIDS; MALE; MICE, INBRED C57BL; OBESITY; REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION; RISK FACTORS; SERUM AMYLOID A PROTEIN; TIME FACTORS;

EID: 84946944184     PISSN: None     EISSN: 20452322     Source Type: Journal    
DOI: 10.1038/srep16474     Document Type: Article

References (54)

1. Zhou, X. J. et al. The aging kidney. Kidney Int. 74, 710-720 (2008).
2. Kaplan, C., Pasternack, B., Shah, H. & Gallo, G. Age-related incidence of sclerotic glomeruli in human kidneys. Am. J. Pathol. 80, 227-234 (1975).
3. Coresh, J., Astor, B. C., Greene, T., Eknoyan, G. & Levey, A. S. Prevalence of chronic kidney disease and decreased kidney function in the adult US population: Third National Health and Nutrition Examination Survey. Am. J. Kidney Dis. 41, 1-12 (2003).
4. Rule, A. D. et al. The association between age and nephrosclerosis on renal biopsy among healthy adults. Ann. Intern. Med. 152, 561-567 (2010).
5. Vorster, H. H., Bourne, L. T., Venter, C. S. & Oosthuizen, W. Contribution of Nutrition to the Health Transition in Developing Countries: A Framework for Research and Intervention. Nutr. Rev. 57, 341-349 (1999).
6. Popkin, B. M., Adair, L. S. & Ng, S. W. NOW AND THEN: The Global Nutrition Transition: The Pandemic of Obesity in Developing Countries. Nutr. Rev. 70, 3-21 (2012).
7. Collins, A. J. et al. US renal data system 2011 Annual data report. Am. J. Kidney Dis. 59, 6386 (2012).
8. Foley, R. N. & Collins, A. J. The USRDS: What you need to know about what it can and can't tell us about ESRD. Clin. J. Am. Soc. Nephrol. 8, 845-851 (2013).
9. Oberg, B. P. et al. Increased prevalence of oxidant stress and inflammation in patients with moderate to severe chronic kidney disease. Kidney Int. 65, 1009-1016 (2004).
10. Hotamisligil, G. S. Inflammation and metabolic disorders 1. Nature 444, 860-867 (2006).
11. Vlassara, H. et al. Role of oxidants/inflammation in declining renal function in chronic kidney disease and normal aging. Kidney Int. Suppl. 76, S3-S11 (2009).
12. Wellen, K. E. & Hotamisligil, G. S. Obesity-induced inflammatory changes in adipose tissue. J. Clin. Invest. 112, 1785-1788 (2003).
13. Norris, A. L. et al. Circulating oxidized LDL and inflammation in extreme pediatric obesity. Obesity (Silver Spring). 19, 1415-1419 (2011).
14. Liu, Y. Renal fibrosis: new insights into the pathogenesis and therapeutics. Kidney Int. 69, 213-217 (2006).
15. Wahba, I. M. & Mak, R. H. Obesity and obesity-initiated metabolic syndrome: Mechanistic links to chronic kidney disease. Clin. J. Am. Soc. Nephrol. 2, 550-562 (2007).
16. Westermark, P. et al. A primer of amyloid nomenclature. Amyloid 14, 179-183 (2007).
17. Malle, E. & De Beer, F. C. Human serum amyloid A (SAA) protein: a prominent acute-phase reactant for clinical practice. Eur. J. Clin. Invest. 26, 427-435 (1996).
18. Tietge, U. J. F. et al. Human secretory phospholipase A2 mediates decreased plasma levels of HDL cholesterol and ApoA-I in response to inflammation in human ApoA-I transgenic mice. Arterioscler. Thromb. Vasc. Biol. 22, 1213-1218 (2002).
19. Schmitt, R. et al. Ageing mouse kidney-not always the SAME old story. Nephrol. Dial. Transplant 24, 3002-3005 (2009).
20. Hall, J. E. et al. Is Obesity a Major Cause of Chronic Kidney Disease? Advances in Renal Replacement Therapy 11, 41-54 (2004).
21. Kramer, H. Obesity and chronic kidney disease. Contributions to Nephrology 151, 1-18 (2006).
22. Tzanetakou, I. P., Katsilambros, N. L., Benetos, A., Mikhailidis, D. P. & Perrea, D. N. Is obesity linked to aging? Adipose tissue and the role of telomeres. Ageing Res. Rev. 11, 220-229 (2012).
23. Carlsen, H. et al. Diet-induced obesity increases NF-κB signaling in reporter mice. Genes Nutr. 4, 215-222 (2009).
24. Kisilevsky, R. & Tam, S. Acute phase serum amyloid a, cholesterol metabolism, and cardiovascular disease. Pediatr. Pathol. Mol. Med. 21, 291-305 (2002).
25. Tan, C. Y. & Vidal-Puig, A. Adipose tissue expandability: the metabolic problems of obesity may arise from the inability to become more obese. Biochem. Soc. Trans. 36, 935-940 (2008).
26. Jiang, T. et al. Diet-induced obesity in C57BL/6J mice causes increased renal lipid accumulation and glomerulosclerosis via a sterol regulatory element-binding protein-1c-dependent pathway. J. Biol. Chem. 280, 32317-32325 (2005).
27. Schrijvers, B. F., De Vriese, A. S. & Flyvbjerg, A. From hyperglycemia to diabetic kidney disease: The role of metabolic, hemodynamic, intracellular factors and growth factors/cytokines. Endocrine Reviews 25, 971-1010 (2004).
28. Garud, M. S. & Kulkarni, Y. A. Hyperglycemia to Nephropathy via Transforming Growth Factor Beta. Curr. Diabetes Rev. 10, 182-9 (2014).
29. DeFronzo, R. A. & Ferrannini, E. Insulin Resistance: A Multifaceted Syndrome Responsible for NIDDM, Obesity, Hypertension, Dyslipidemia, and Atherosclerotic Cardiovascular Disease. Diabetes Care 14, 173-194 (1991).
30. Paneni, F., Beckman, J. A., Creager, M. A. & Cosentino, F. Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I. Eur. Heart J. 34, 2436-43 (2013).
31. Van der Heijden, R. A. et al. High fat diet induced obesity primes inflammation in adipose tissue prior to liver in C57BL/6j mice. Aging (Albany NY) 7, 256-268 (2015).
32. Dember, L. M. Amyloidosis-associated kidney disease. J. Am. Soc. Nephrol. 17, 3458-3471 (2006).
33. Bollée, G. et al. Presentation and outcome of patients with systemic amyloidosis undergoing dialysis. Clin. J. Am. Soc. Nephrol. 3, 375-381 (2008).
34. Lachmann, H. J. et al. Natural history and outcome in systemic AA amyloidosis. N. Engl. J. Med. 356, 2361-2371 (2007).
35. Kisilevsky, R. & Subrahmanyan, L. Serum amyloid A changes high density lipoprotein's cellular affinity. A clue to serum amyloid A's principal function. Lab. Invest. 66, 778-785 (1992).
36. Tam, S. P., Kisilevsky, R. & Ancsin, J. B. Acute-phase-HDL remodeling by heparan sulfate generates a novel lipoprotein with exceptional cholesterol efflux activity from macrophages. PLoS One 3, (2008).
37. Poitou, C.et al. Serum amyloid A: Production by human white adipocyte and regulation by obesity and nutrition. Diabetologia 48, 519-528 (2005).
38. Den Hartigh, L. J. et al. Deletion of Serum Amyloid A3 Improves High Fat High Sucrose Diet-Induced Adipose Tissue Inflammation and Hyperlipidemia in Female Mice. PLoS One 9, e108564 (2014).
39. Yang, R. Z. et al. Acute-phase serum amyloid A: An inflammatory adipokine and potential link between obesity and its metabolic complications. PLoS Med. 3, 0884-0894 (2006).
40. Zhao, Y. et al. Association between serum amyloid A and obesity: A meta-analysis and systematic review. Inflamm. Res. 59, 323-334 (2010).
41. Shibasaki, T. et al. A case of renal amyloidosis associated with hepatic adenoma: the pathogenetic role of tumor necrosis factor-alpha. Nephron 75, 350-353 (1997).
42. Alsina, E., Martin, M., Panadés, M. & Fernández, E. Renal AA amyloidosis secondary to morbid obesity? Clinical nephrology 72, 312-314 (2009).
43. Barbara Kluve-Beckerman, Lijing & Du, J. H. Obesity as a determinant in the development and progression of AA amyloidosis. Abstr. XIVth Int. Symp. Amyloidoisis.
44. Targońska-Stȩpniak, B. & Majdan, M. Serum Amyloid A as a Marker of Persistent Inflammation and an Indicator of Cardiovascular and Renal Involvement in Patients with Rheumatoid Arthritis. Mediators Inflamm. 2014, 1-7 (2014).
45. Luo, H. et al. Extracellular deposition of mouse senile AApoAII amyloid fibrils induced different unfolded protein responses in the liver, kidney, and heart. Lab. Investig. 95, 320-333 (2014).
46. Wheeler, D. C. & Bernard, D. B. Lipid abnormalities in the nephrotic syndrome: causes, consequences, and treatment. Am. J. Kidney Dis. 23, 331-346 (1994).
47. Mcmahon, E., Campbell, K., Bauer, J. & Mudge, D. Altered dietary salt intake for people with chronic kidney disease (Review). (2015).
48. Karalius, V. P. & Shoham, D. A. Dietary Sugar and Artificial Sweetener Intake and Chronic Kidney Disease: A Review. Advances in Chronic Kidney Disease 20, 157-164 (2013).
49. Martin, W. F., Armstrong, L. E. & Rodriguez, N. R. Dietary protein intake and renal function. Nutr. Metab. (Lond). 2, 25 (2005).
50. Meems, L. M. G. et al. The vitamin D receptor activator paricalcitol prevents fibrosis and diastolic dysfunction in a murine model of pressure overload. J. Steroid Biochem. Mol. Biol. 132, 282-289 (2012).
51. Yakala, G. K. et al. Beneficial Effects of an Alternating High- Fat Dietary Regimen on Systemic Insulin Resistance, Hepatic and Renal Inflammation and Renal Function. PLoS One 7, (2012).
52. Sipe, J. D. et al. Amyloid fibril protein nomenclature: 2010 recommendations from the nomenclature committee of the International Society of Amyloidosis. Amyloid 17, 101-104 (2010).
53. Puchtler, H., Sweat, F. & Levine, M. ON THE BINDING OF CONGO RED BY AMYLOID. J. Histochem. Cytochem. 10, 355-364 (1962).
54. Tietge, U. J. F. et al. Lipids and Lipoproteins: Overexpression of Secretory Phospholipase A2 Causes Rapid Catabolism and Altered Tissue Uptake of High Density Lipoprotein. 275, 10077-10084 (2000).