![]() | Only 14 pages are availabe for public view |
Abstract Diabetes mellitus is the most frequent cause of chronic kidney disease in both developed and developing countries. Diabetic kidney disease occurs in 30%~50% of patients with type 1 or types 2 diabetes respectively. Screening for DKD must be a routine component of diabetes care. The ADA recommends yearly screening for individuals with type 2 diabetes at the diagnosis and five years after diagnosis of type 1diabetes. Because urinary albumin excretion is recognized as an early predictor of diabetic nephropathy in addition to cardiovascular disease, it has become an important screening target. Morphological changes in DKD are known to begin more early than laboratory abnormalities. Also, some patients with albuminuria have normal renal structure, while some normoalbuminuric diabetics have evident nephropathic lesions. Also, albumin excretion rate is a predictor of nephropathy in hypertension and cardiovascular diseases, so it is not a specific marker for diabetic nephropathy. Thus, we are still in need to identify earlier markers for DKD instead of albuminuria. Nesfatin-1 is a newly discovered hypothalamic neuropeptide that controls appetite. It is an 82 amino-acid peptide originating from the cleavage of nucleobindin2 NUCB2. Nesfatin-1 is present in neurons of various brain areas including hypothalamic nuclei such as PVN, ARC, LHA and the NTS and DMNX at the brain stem level, and is also present in pancreatic b-cells, where it is co-localized with insulin in secretion vesicles. It is the middle segment covering the amino acids from 23 to 53 which is called M30, that responsible for the dose-dependent inhibition of food intake, whose amino acid sequencing is similar to that of alpha-MSH and Agouti-related peptides (AgRP). Nesfatin-1 has been observed to possess an anti-hyperglycemic effect which is peripheral and time, dose and insulin-dependent. Recent studies have also linked nesfatin-1 to enhanced peripheral and hepatic insulin sensitivity, through promoting peripheral glucose uptake and decreasing gluconeogenesis via different pathways. Nesfatin-1 has been investigated in several metabolic dysregulations such as diabetes, epilepsy, and inflammation. Raised nesfatin-1 levels were significantly associated with BMI, HbA1c, FBG, and 2-h postprandial plasma glucose. Studies have investigated nesfatin-1 as a potential cause of feeding disturbance in patients with CKD, suggesting that nesfatin-1 may have a negative correlation with total protein intake in these patients. The present work aimed to determine the changes in the circulating plasma levels of nesfatin-1 in type 2 diabetic patients with different grades of diabetic nephropathy compared to control subjects, as measured by urinary albumin creatinine ratio (UACR) and estimated GFR, and to investigate the possible association of Nesfatin-1 with some anthropometric and metabolic parameters in such diabetic patients. This study was done on 120 subjects divided into four subgroups, group І included30 type 2 diabetic patients with (UACR less than 30 mg /day), group ІІ included 30 types 2 diabetic patients (UACR 30-300 mg / 24), group ІIІ included 30 types 2 diabetic patients (UACR more than300 mg / 24) and group VI included 30 healthy subjects as a control form period February 2019 to February 2020 and include 96 male and 24 female. |