Evaluation of the Serum Levels of IL-1 in Type 2 Diabetic Patients with and without Diabetic Nephropathy

Background: Diabetic nephropathy (DN) has been regarded as an important cause of morbidity in patients with type 2 diabetes (T2D). Immune system components are modulated during T2D, with the most apparent modifications in adipose tissue, pancreatic islets, liver, and circulating leukocytes. The aim of this survey was to evaluate the role of IL-1 in the etiopathogenesis of nephropathic T2D. Methods: In this case-control investigation, the study population consisted of 58 T2D patients with proteinuria (nephropathy T2D cases) as the case group and 76 T2D cases without proteinuria (non-nephropathy T2D cases) as the control group. Blood samples were obtained from all individuals and ELISA approach was carried out to measure IL-1 levels in samples. Results: Our experiments demonstrated that T2D patients with nephropathy had significantly increased levels of IL-1 in their blood in comparison to T2D patients without nephropathy. Conclusions: It seems that IL-1 plays a role in the etiopathogenesis of nephropathy in T2D patients, requiring further implementation to vivid disclose of the inflammation in this context.

[1]  H. Joller-jemelka,et al.  Glucose-induced β cell production of IL-1β contributes to glucotoxicity in human pancreatic islets. , 2002, The Journal of clinical investigation.

[2]  H. Parving,et al.  Predictors for the development of microalbuminuria and macroalbuminuria in patients with type 1 diabetes: inception cohort study , 2004, BMJ : British Medical Journal.

[3]  F. Locatelli,et al.  End-stage renal failure in type 2 diabetes: A medical catastrophe of worldwide dimensions. , 1999, American journal of kidney diseases : the official journal of the National Kidney Foundation.

[4]  S. Shoelson,et al.  Type 2 diabetes as an inflammatory disease , 2011, Nature Reviews Immunology.

[5]  R. Foley,et al.  End-stage renal disease in the United States: an update from the United States Renal Data System. , 2007, Journal of the American Society of Nephrology : JASN.

[6]  J. Nerup,et al.  Cytotoxicity of human pI 7 interleukin-1 for pancreatic islets of Langerhans. , 1986, Science.

[7]  G. Hotamisligil,et al.  Inflammation and metabolic disorders , 2006, Nature.

[8]  M. Donath,et al.  Glucose induces beta-cell apoptosis via upregulation of the Fas receptor in human islets. , 2001, Diabetes.

[9]  A. Whitehead,et al.  The major acute phase reactants: C-reactive protein, serum amyloid P component and serum amyloid A protein. , 1994, Immunology today.

[10]  D. Wesson,et al.  Primary hypertension and nephropathy. , 2006, Current opinion in nephrology and hypertension.

[11]  G. Jerums,et al.  3: Preventing complications of diabetes , 2003, The Medical journal of Australia.

[12]  T. Mandrup-Poulsen,et al.  The role of interleukin-1 in the pathogenesis of IDDM , 1996, Diabetologia.

[13]  Allan Vaag,et al.  Interleukin-1-receptor antagonist in type 2 diabetes mellitus. , 2007, The New England journal of medicine.

[14]  J. Navarro-González,et al.  The role of inflammatory cytokines in diabetic nephropathy. , 2008, Journal of the American Society of Nephrology : JASN.

[15]  Richard A. Flavell,et al.  Inflammasomes in health and disease , 2012, Nature.

[16]  J. Pickup Inflammation and activated innate immunity in the pathogenesis of type 2 diabetes. , 2004, Diabetes care.

[17]  G. Rossi,et al.  Diagnosis and Classification of Diabetes Mellitus The information that follows is based largely on the reports of the Expert Committee on the Diagnosis and Classification of Diabetes (Diabetes Care 20:1183–1197, 1997, and Diabetes Care 26:3160–3167, 2003). , 2008, Diabetes Care.

[18]  G. Eknoyan,et al.  National Kidney Foundation Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification , 2003, Annals of Internal Medicine.

[19]  J. Sturis,et al.  Glucose- and interleukin-1beta-induced beta-cell apoptosis requires Ca2+ influx and extracellular signal-regulated kinase (ERK) 1/2 activation and is prevented by a sulfonylurea receptor 1/inwardly rectifying K+ channel 6.2 (SUR/Kir6.2) selective potassium channel opener in human islets. , 2004, Diabetes.

[20]  M. Crook Type 2 diabetes mellitus: a disease of the innate immune system? An update , 2004, Diabetic medicine : a journal of the British Diabetic Association.

[21]  Rury R Holman,et al.  Development and progression of nephropathy in type 2 diabetes: the United Kingdom Prospective Diabetes Study (UKPDS 64). , 2003, Kidney international.