Amin Irannejad1, Alireza Ghajar2, Mohsen Afarideh3, Elias Khajeh4, Sina Noshad5, Sadaf Esteghamati6, Khashayar Afshari7, Farima Kahe8, Morsaleh Ganji9, Mohammad Saadat10, Manouchehr Nakhjavani11, Alireza Esteghamati12. 1. Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: amin.irannejad@yahoo.com. 2. Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: ghajar.ar@gmail.com. 3. Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: mhafarideh@gmail.com. 4. Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: elyas.khajeh@gmail.com. 5. Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: sina.noshad@gmail.com. 6. Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: sadaf217@gmail.com. 7. Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: khashayarafshari@gmail.com. 8. Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: farima.kahe@yahoo.com. 9. Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: morsaleh.ganji@yahoo.com. 10. Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: saadatagah.m@gmail.com. 11. Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: nakhjavanim@tums.ac.ir. 12. Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: esteghamati@tums.ac.ir.
Abstract
BACKGROUND: Nesfatin-1 is a newly found anorectic neuropeptide with potent metabolic regulatory effects that its circulating levels are shown to be elevated in diabetes. We compared serum nesfatin-1 in patients with type 2 diabetes and microalbuminuria (30mg/day≤urinary albumin excretion (UAE) <300mg/day) with their control patients with type 2 diabetes and normoalbuminuria (UAE <30mg/day). PATIENTS AND METHODS: In a cross sectional setting, 44 adult patients with type 2 diabetes and microalbuminuria and 44 control patients with type 2 diabetes and normoalbuminuria were evaluated. Serum levels of nesfatin-1 along with demographic, clinical and biochemical factors associated with diabetes was measured. RESULTS: Mean peripheral concentrations of nesfatin-1 were significantly higher in patients with diabetes who had microalbuminuria compared to normoalbuminuric control patients (175.27±25.96pg/ml vs. 134.66±23.18pg/ml, respectively; p value<0.001). Significant positive correlations were found between circulating nesfatin-1 levels and the following case-mix variables: duration of diabetes, glycated hemoglobin, plasma creatinine, UAE and serum uric acid. In the multivariate logistic regression and after adjustment for a constellation of potentially confounding variables associated with diabetic kidney disease (DKD), circulating nesfatin-1 was the only variable significantly associated with microalbuminuria (odds ratio [95% confidence interval]=1.224 [1.007-1.487], p value=0.042). CONCLUSION: In patients with type 2 diabetes, circulating nesfatin-1 appears to be associated with microalbuminuria independent of other established risk factors of DKD. The underlying pathophysiological mechanisms and the prognostic significance of this association remain to be elucidated.
BACKGROUND:Nesfatin-1 is a newly found anorectic neuropeptide with potent metabolic regulatory effects that its circulating levels are shown to be elevated in diabetes. We compared serum nesfatin-1 in patients with type 2 diabetes and microalbuminuria (30mg/day≤urinary albumin excretion (UAE) <300mg/day) with their control patients with type 2 diabetes and normoalbuminuria (UAE <30mg/day). PATIENTS AND METHODS: In a cross sectional setting, 44 adult patients with type 2 diabetes and microalbuminuria and 44 control patients with type 2 diabetes and normoalbuminuria were evaluated. Serum levels of nesfatin-1 along with demographic, clinical and biochemical factors associated with diabetes was measured. RESULTS: Mean peripheral concentrations of nesfatin-1 were significantly higher in patients with diabetes who had microalbuminuria compared to normoalbuminuric control patients (175.27±25.96pg/ml vs. 134.66±23.18pg/ml, respectively; p value<0.001). Significant positive correlations were found between circulating nesfatin-1 levels and the following case-mix variables: duration of diabetes, glycated hemoglobin, plasma creatinine, UAE and serum uric acid. In the multivariate logistic regression and after adjustment for a constellation of potentially confounding variables associated with diabetic kidney disease (DKD), circulating nesfatin-1 was the only variable significantly associated with microalbuminuria (odds ratio [95% confidence interval]=1.224 [1.007-1.487], p value=0.042). CONCLUSION: In patients with type 2 diabetes, circulating nesfatin-1 appears to be associated with microalbuminuria independent of other established risk factors of DKD. The underlying pathophysiological mechanisms and the prognostic significance of this association remain to be elucidated.