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ORIGINAL ARTICLE
Year : 2017  |  Volume : 3  |  Issue : 2  |  Page : 59-67

Study of the association of serum level of nesfatin-1 and diabetic kidney disease in patients with type 2 diabetes


1 Department of Diabetes, Metabolism, Internal Medicine, Faculty of Medicine, University of Alexandria, Alexandria, Egypt
2 Department of Clinical and Chemical Pathology, Faculty of Medicine, University of Alexandria, Alexandria; Unit of Nephrology, Department of Internal Medicine, Faculty of Medicine, University of Alexandria, Alexandria, Egypt
3 Unit of Nephrology, Department of Internal Medicine, Faculty of Medicine, University of Alexandria, Alexandria, Egypt

Correspondence Address:
Talaat Abd-Elaaty
Unit of Diabetes and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Alexandria, Alexandria
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ejode.ejode_12_17

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Background Nesfatin-1 is a newly found anorectic neuropeptide with potent metabolic regulatory effects, whose peripheral levels are shown to be elevated in diabetes. It is a newly discovered hypothalamic neuropeptide that regulates appetite. Its discovery has generated great interest in the scientific community because of its implication in energy and glucose homeostasis. Nesfatin-1 is an amino-acid peptide originating from the cleavage of nucleobindin2. It has a molecular weight of 9.8 kDa and the half-life of nucleobindin2 mRNA is ∼6 h. Interestingly, nesfatin-1 is also expressed in pancreatic β-cells, where it is localized with insulin in secretion vesicles. The structure of nesfatin-1 is also tripartite; the segment starting from the N-terminal end and going up to 23 amino acids is called N23, the middle segment covering the amino acids from 23 to 53 is called M30, and the segment from the 53rd to 82nd amino acids toward the carboxyl terminus is called C29. Objective We compared serum nesfatin-1 in patients with type 2 diabetes with evidence of diabetic kidney disease (DKD) [urinary albumin–creatinine ratio (UACR) >300 mg/day or reduced estimated glomerular filtration rate (eGFR) <60 ml/min] with patients newly diagnosed with type 2 diabetes and who had no evidence of DKD (UACR<30 mg/day) and a control group of healthy nondiabetic individuals. Patients and methods Ninety patients attending the outpatient clinics at Alexandria Main University Hospital and Alexandria Police Hospital, Egypt, were enrolled in this cross-sectional study to determine the association of serum level of nesfatin-1 and DKD in patients with type 2 diabetes. They were divided into three groups: group I included 30 type 2 diabetic patients with DKD. Group II included 30 type 2 diabetic patients without DKD. Group III included 30 nondiabetic healthy controls matched for age and sex with group I. Assessment included a thorough assessment of history, complete clinical examination, neurological examination, fundus examination, and laboratory investigations including metabolic profile and plasma nesfatin-1 by enzyme-linked immunosorbent assay. Results The study showed a statistically significant difference between the three studied groups in terms of age (P<0.001), HbA1c and fetal bovine serum (P≤0.001), fasting insulin level (P=0.022), blood urea (P<0.001), serum creatinine (P<0.001), eGFR (P<0.001), and UACR (P<0.001). The difference between the three groups studied was not significant in serum nesfatin-1 (P<0.564). The mean peripheral concentrations of nesfatin-1 were not significantly higher in patients with diabetes who had evidence of DKD compared with newly diagnosed type 2 diabetic patients who had no evidence of DKD (P<0.001). Conclusion Serum nesfatin-1 was not significantly higher in albuminuric type 2 diabetic patients compared with normoalbuminuric patients. Serum nesfatin also did not correlate with eGFR and creatinine in the different groups studied. Serum nesfatin-1 may not be useful as an early marker of DKD instead of albuminuria. More studies are needed to identify the role and the significance of nesfatin in diabetic patients.


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