Pajouhi M, Shaban Nejad Khas Z, Mohajeri Tehrani M R,
Volume 65, Issue 3 (6-2007)
Abstract
Background: Diabetic neuropathy is an incapacitating disease that afflicts almost 50 percent of patients with diabetes. A late finding in type 1 diabetes, diabetic neuropathy can be an early finding in non insulin-dependent diabetes. Diabetic neuropathies are divided primarily into two groups, sensorimotor and autonomic. Patients may acquire only one type of diabetic neuropathy or may present with combinations of neuropathies, such as autonomic neuropathy or distal symmetric polyneuropathy, the latter of which the most common form. Motor deficits, orthostatic hypotension, silent cardiac ischemia, hyperhidrosis, vasomotor instability, gastroparesis, bladder dysfunction, and sexual dysfunction can also result from diabetic neuropathy. Strict control of blood sugar, combined with proper daily foot care, is essential to avoid the complications of this disorder. With the potential to afflict any part of the nervous system, diabetic neuropathy should be suspected in all patients with type 2 diabetes as well as patients who have had type 1 diabetes for over five years. Although some patients with diabetic neuropathy notice few symptoms, upon physical examination mild to moderately severe sensory loss may be noted by the physician. Idiopathic neuropathy has been known to precede the onset of type 2 diabetes.
Azim Adibmanesh , Narges Mohammad Taghvaei , Mehrnoosh Zakerkish , Hamid Yaghooti ,
Volume 77, Issue 12 (3-2020)
Abstract
Background: Nitric oxide (NO) produced by endothelial NO synthase (eNOS) mediates a large range of processes, and abnormality in the production of NO has been implicated in diabetic complications including diabetic nephropathy (DN). G894T polymorphism in the eNOS gene has been shown to decreased activity the NO levels of plasma. The association between eNOS Glu298Asp gene polymorphism and DN risk is still controversial. The present study investigated the effect of eNOS gene G894T polymorphism on susceptibility to type 2 diabetes (T2D) and DN and measures of kidney function in a population with and without diabetes.
Methods: This case-control study was carried out at the diabetes specialist clinic of Golestan Hospital of Ahvaz Jundishapur University of Medical Sciences, Iran, from September 2016 to December 2017. The study comprised 132 patients with T2D (with and without nephropathy). They were compared to 66 normal subjects. The subjects were genotyped for the eNOS G894T polymorphism by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Blood glucose, HbA1c, BUN, creatinine and urinary albumin were evaluated by a biochemistry analyzer.
Results: Higher prevalence of the mutant T allele and homozygous TT genotypes and biochemical parameters) like FBS, TG, and BUN) were seen in T2D patients compared to healthy subjects. For T2DM, the odds ratios (ORs) for the TT genotype and the T allele carrier were 3.1 (P=0.0001) and 2.6 (P=0.0001), respectively. In contrast to the significant association between the eNOS G894T polymorphism and T2D, we could not find a significant correlation to the DN. For DN, the ORs for the TT genotype and the T allele carrier were 1.1 (P=0.76) and 0.8 (P=0.6). For decreased epidermal growth factor receptor (EGFR) below 60 ml/min/ 1.73 m2 in diabetic patients, the OR for TT was 0.8 (P=0.7).
Conclusion: Our results confirm that the risk of T allele and TT genotype of the eNOS G894T polymorphism were significantly associated with T2D, The TT genotype of this polymorphism also conferred the risk of developing T2D, but they were not correlated with DN and decreased eGFR.
Hamed Alizadeh Pahlavani , Mitra Tajari, Mohadese Hozouri,
Volume 82, Issue 2 (4-2024)
Abstract
Background: In people with diabetes, metabolic changes can affect the body's response to physical activity. On the other hand, for people with diabetes, exercise can be a powerful tool to manage diabetes and improve overall health through key regulatory proteins such as adenosine monophosphate-activated protein kinase (AMPKα1/2), dynamin-like protein (DLP1), and autophagy-related protein 13 (ATG13). In diabetes, AMPK regulation is often disrupted, contributing to the metabolic imbalances that characterize diabetes. In diabetes, disruption of DLP1 protein as a key regulator of mitochondrial fission leads to the accumulation of damaged mitochondria and metabolic imbalance. ATG13, as an autophagy regulator causes the recycling of damaged cells and damaged components.
Methods: This study was conducted in May to July 2023. In this experimental research, 12 two-month-old male Sprague-Dawley rats with an average weight of 280±30 grams participated. To induce type two diabetes, nicotinamide solution with a dose of 110 mg/kg and streptozotocin (STZ) with a dose of 60 mg/kg were injected, and blood glucose between 126 and 260 mg/dl was determined as the index of diabetes induction. Then the diabetic rats were randomly divided into training (six heads) and control groups (six heads). The moderate-intensity interval training (MIIT) group trained for 4 weeks and four sessions every week. The MIIT program consisted of 4 rounds of 3 minutes with an intensity equal to 55-75% of the maximum speed and active rest periods of two minutes with an intensity of 35-45% of the maximum speed. After 24 hours from the last training, the rats were anesthetized and the soleus muscle tissue was isolated and the proteins were measured by western blot methods.
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Results: The results showed that MIIT causes a non-significant increase in AMPK protein (P=0.29) and ATG13 (P=0.079), while it has a significant decrease in DLP1 (P=0.002).
Conclusion: It seems that MIIT, through decreasing DLP1, can have a beneficial effect on energy metabolism and autophagy process in order to optimize cells mitochondria in the soleus muscle of diabetic rats.
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