Prevalence of Diabetic Retinopathy among Type Two Diabetic Patients in Arab Countries

Background Diabetes mellitus (DM) is a metabolic disorder characterized by chronic hyperglycaemia. Diabetes causes many complications like diabetic retinopathy (DR) which affects up to 80 percent of all patients who have diabetes for more than 10 years or more. Objectives To estimate the prevalence rate of diabetic retinopathy among type 2 diabetic (T2D) patients in some Arab countries and to compare the difference in the prevalence rate according to different patient’s characteristics. Patients and Methods In recent years, several studies have indicated occurrence of peripapillary retinal nerve fiber layer (RNFL) thinning in the retina of diabetic patient. We reviewed the full articles of the extracted 17 different studies across 10 Arab countries that were captured through our search strategy. Through 25 years (1991– 2016), most of the studies re-ported were carried, we captured 17 studies through our systematic search. Results The prevalence rate of diabetic retinopathy among type 2 females is 19.848%. The prevalence rate of diabetic retinopathy among type 2 males is 18.559%. Prevalence of Diabetic Retinopathy in those with up - 5 years duration of the disease is 7.597%. Prevalence of Diabetic Retinopathy in those with 5-10 years duration of the disease is 24.418%. Prevalence of Diabetic Retinopathy in those with >10 years duration of the disease is 52.913%. Prevalence of Diabetic Retinopathy in those aged <45 years is 9.505%. Prevalence of Diabetic Retinopathy in those aged 45-55 years is 20.346 %. Prevalence of Diabetic Retinopathy in those aged >55 years is 25.297%. Conclusion We present the first systematic review and meta-analysis of DR among Arab patients with T2D in 10 different Arab countries. Although our search strategy was broad, we were only able to find few reports compared to the scale of the problem in the Arab countries; our meta-analysis revealed that the prevalence is high (22.543 %) with significant variations among different Arab countries, even within the same country.

Cognition enhancing abilities of vitamin D, epalrestat and their combination in diabetic rats with and without scopolamine induced amnesia

Persistent hyperglycaemia and scopolamine were used to inflict amnesia in rats. Chronic hyperglycaemia causes metabolic impairment, neuronal dysfunction and oxidative stress causing cognitive impairment. This study aimed to determine anti amnesic activities of vitamin D, epalrestat and their combination against diabetes and scopolamine induced cognitive dysfunction. A total of eighty-eight Wistar albino rats, eleven groups, and 8 rats/Gr., were used. Type 2 diabetes mellitus was induced in all groups, except Gr.1 which was treated with 2 ml normal saline. Gr. 2 to 11 by feeding high fat diet for 28 days followed by single dose streptozotocin 35 mg/kg i.p. Hyperglycemic rats were screened with blood sugar level > 200 mg/dL. Gr. 2 rats were treated with only streptozotocin and Gr. 3 to 6 were treated with streptozotocin and test drugs donepezil 1 mg/kg, vitamin D, 27 mcg/kg, epalrestat 57 mg/kg, vitamin D + epalrestat, per oral, respectively. Gr. 7 rats were treated with only streptozotocin + scopolamine and all others from Gr. 8 to 11 were treated with streptozotocin + scopolamine and donepezil, vitamin D, epalrestat, vitamin D + epalrestat respectively. The gold standard behavioural tests were conducted by using Morris water maze and passive avoidance paradigms after 30–60 min of inj. scopolamine, 0.5 mg/kg, intra-peritoneal. Hippocampal tissue was taken for histopathological and biochemical evaluation. Rats treated with donepezil, vitamin D, epalrestat and vitamin D + epalrestat showed significant improvement in behavioural, biochemical and histopathological parameters as compared to streptozotocin and (streptozotocin + scopolamine) treated rats. This study underscores cognition enhancing abilities of vitamin D and epalrestat, and their combination in diabetic rats with and without scopolamine.

Intestinal Region-Specific and Layer-Dependent Induction of TNFα in Rats with Streptozotocin-Induced Diabetes and after Insulin Replacement

Tumour necrosis factor alpha (TNFα) is essential in neuroinflammatory modulation. Therefore, the goal of this study is to reveal the effects of chronic hyperglycaemia and insulin treatment on TNFα expression in different gut segments and intestinal wall layers. TNFα expression was mapped by fluorescent immunohistochemistry and quantitative immunogold electron microscopy in myenteric ganglia of duodenum, ileum and colon. Tissue TNFα levels were measured by enzyme-linked immunosorbent assays in muscle/myenteric plexus-containing (MUSCLE-MP) and mucosa/submucosa/submucous plexus-containing (MUC-SUBMUC-SP) homogenates. Increasing density of TNFα-labelling gold particles is observed in myenteric ganglia from proximal to distal segments and TNFα tissue levels are much more elevated in MUSCLE-MP homogenates than in MUC-SUBMUC-SP samples in healthy controls. In the diabetics, the number of TNFα gold labels is significantly increased in the duodenum, decreased in the colon and remained unchanged in the ileal ganglia, while insulin does not prevent these diabetes-related TNFα changes. TNFα tissue concentration is also increased in MUSCLE-MP homogenates of diabetic duodenum, while decreased in MUC-SUBMUC-SP samples of diabetic ileum and colon. These findings support that type 1 diabetes has region-specific and intestinal layer-dependent effects on TNFα expression, contributing to the regional damage of myenteric neurons and their intestinal milieu.

The Role of the α Cell in the Pathogenesis of Diabetes: A World beyond the Mirror

Type 2 Diabetes Mellitus (T2DM) is one of the most prevalent chronic metabolic disorders, and insulin has been placed at the epicentre of its pathophysiological basis. However, the involvement of impaired alpha (α) cell function has been recognized as playing an essential role in several diseases, since hyperglucagonemia has been evidenced in both Type 1 and T2DM. This phenomenon has been attributed to intra-islet defects, like modifications in pancreatic α cell mass or dysfunction in glucagon’s secretion. Emerging evidence has shown that chronic hyperglycaemia provokes changes in the Langerhans’ islets cytoarchitecture, including α cell hyperplasia, pancreatic beta (β) cell dedifferentiation into glucagon-positive producing cells, and loss of paracrine and endocrine regulation due to β cell mass loss. Other abnormalities like α cell insulin resistance, sensor machinery dysfunction, or paradoxical ATP-sensitive potassium channels (KATP) opening have also been linked to glucagon hypersecretion. Recent clinical trials in phases 1 or 2 have shown new molecules with glucagon-antagonist properties with considerable effectiveness and acceptable safety profiles. Glucagon-like peptide-1 (GLP-1) agonists and Dipeptidyl Peptidase-4 inhibitors (DPP-4 inhibitors) have been shown to decrease glucagon secretion in T2DM, and their possible therapeutic role in T1DM means they are attractive as an insulin-adjuvant therapy.

Perturbation of the mucosa-associated anaerobic gut microbiota in streptozotocin-induced diabetic rats

Our aim was to map the gut region-specific differences of the mucosa-associated microbiome distribution in a streptozotocin-induced diabetic rat model. Tissue samples from the duodenum, ileum and colon were collected 10 weeks after the onset of hyperglycaemia to analyse the mucosa-associated microbiota using next-generation DNA sequencing. Striking differences were observed in the mucosa-associated microbiota of the duodenum between diabetic and control rats. A significant invasion of the aerobic genus Mycoplasma was apparent in diabetes, and the abundance of the anaerobic phylum Firmicutes decreased massively. It is noteworthy that insulin treatment eliminated the Mycoplasma invasion in the duodenum and apparently restored the anaerobic environment in the mucosa. In the ileum the abundance of the phylum Firmicutes increased in the diabetic samples. Although the proportion of the phylum Proteobacteria decreased moderately, its composition changed significantly, and insulin treatment induced only minor alterations. In the diabetic samples of colon, the abundance of the phylum Firmicutes decreased slightly, the relative number of the bacteria in the phylum Bacteroidetes increased strongly as compared to the control values, and after insulin treatment this increase was more significant. Chronic hyperglycaemia has the most prominent effect on the mucosa-associated microbiota in the duodenum.

Nephroprotective Effect of Coenzyme Q10 alone and in Combination with N-acetylcysteine in Diabetic Nephropathy

Aim Oxidative stress due to chronic hyperglycaemia is a key factor in the development and progression of various microvascular complications including diabetic nephropathy (DN) and associated renal injury. Treatment with antioxidants is one of the strategies to protect the kidney from oxidative tissue damage to improve renal physiology during DN. The investigation, therefore, was designed to assess the nephroprotective effect of coenzyme Q10 (CoQ10) and N-acetylcysteine (NAC), either alone or in combination in streptozotocin (STZ)-nicotinamide (NAD) induced diabetic nephropathy (DN) in rats. Methods T2DM induced by STZ (55 mg/kg, i.p.)-NAD (110 mg/kg, i.p.) in Sprague-Dawley rats (220–250 g) was confirmed by the elevated blood glucose level and glycated haemoglobin. DN was assessed by renal function tests. The diabetic rats were treated with CoQ10 (10 mg/kg, p.o.) and/or NAC (300 mg/kg, p.o.) for 8 weeks after confirmation of DN. Oxidative tissue damage due to STZ-NAD was estimated by malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT), reduced glutathione (GSH), myeloperoxidase (MPO) and nitric oxide (NO) in the renal homogenate. Results Data showed significant alteration in serum and urinary creatinine, total protein, albumin, serum urea, blood urea nitrogen (BUN) and uric acid in diabetic animals as compared to the control rats. CoQ10 and/or NAC effectively alleviated the disturbances in renal function. Diabetic rats showed increased MDA, decreased SOD and CAT activities and decreased GSH along with a significant increase in MPO activity and nitrite content. Treatment with the aforementioned antioxidants and their combination ameliorated the kidney damage as indicated by the reduced OS with improved renal function. Conclusion The investigation suggests that the chronic hyperglycaemia-induced OS leads to the development and progression of DN. The combined treatment with CoQ10 and NAC has shown a remarkable nephroprotective effect suggesting that combined antioxidant therapy with CoQ10 and NAC may be useful in the attenuation of DN.

Brainstem Auditory Evoked Potentials in Type 2 Diabetes Mellitus

Diabetes mellitus is a group of metabolic diseases characterized by hyperglycaemia resulting from defects in insulin secretion, insulin action or both. Diabetes affects many systems and produces complications in the human body, in those complications one is diabetic central neuropathy. The pathological mechanisms involved in the central neuropathy include chronic hyperglycaemia, hypoglycaemic episodes, angiopathy and blood–brain barrier dysfunction. Diabetic central neuropathy is detected by using of brainstem auditory evoked response (BAER), Visual evoked potential (VEP), somatosensory evoked potential (SEP). These abnormalities are present at different levels and may appear before appearance of overt complications. The central nervous system abnormalities are more frequent in patients with peripheral neuropathy but evoked potentials can be abnormal even in patients without neuropathy. The BAER is a physiological recording technique to study the auditory pathway and does not require subject’s attention and generates waves during the first 10 ms after the sound stimulus. Each BAER wave is generated by the activation of a sub-cortical component of the auditory pathway with 90% sensitivity and 70–90% of specificity.

ROLE OF SARVANGA UDVARTANA AND SARVANGA TAKRADHARA IN THE MANAGEMENT OF DIABETIC PERIPHERAL NEUROPATHY WITH SPECIAL REFERENCE TO MADHUMEHA: A CLINICAL STUDY

Diabetes mellitus is a global health problem of this era. Presently India is having the largest diabetic population of 50.8 million. In 2015, diabetes was the direct cause of 1.6 million deaths. Diabetes Mellitus is a metabolic disorder of multiple aetiology characterized by chronic hyperglycaemia with disturbances of carbohydrates, fat and protein metabolism resulting from defects in insulin secretion. Diabetes, particularly type 2 is associated with various long-term complications like Diabetic retinopathy, nephropathy, neuropathy, etc., Globally diabetic neuropathy affects approximately 132 million people as of 2010 (1.9% of population). There is a higher prevalence (60.4%) and incidence (8.76%) of sensory peripheral neuropathy among the observed diabetic patients. In Ayurveda, the symptoms of Diabetic neuropathy are explained under the headings of Purvaroopa and upadrava of Prameha. Madhumeha is a bahudrava shleshma condition. So, Sarvanga Udvartana and Sarvanga Takradhara is been adopted to counteract the Samprapti of Prameha. A minimum of 20 subjects who fulfilled the diagnostic and inclusion criteria was subjected to the intervention. The overall results in the study revealed statistically highly significant result after the treatment on reducing symptoms and blood sugar levels.

Current and future therapies for type 1 diabetes

In type 1 diabetes, insulin remains the mature therapeutic cornerstone; yet, the increasing number of individuals developing type 1 diabetes (predominantly children and adolescents) still face severe complications. Fortunately, our understanding of type 1 diabetes is continuously being refined, allowing for refocused development of novel prevention and management strategies. Hitherto, attempts based on immune suppression and modulation have been only partly successful in preventing the key pathophysiological feature in type 1 diabetes: the immune-mediated derangement or destruction of beta cells in the pancreatic islets of Langerhans, leading to low or absent insulin secretion and chronic hyperglycaemia. Evidence now warrants a focus on the beta cell itself and how to avoid its dysfunction, which is putatively caused by cytokine-driven inflammation and other stress factors, leading to low insulin-secretory capacity, autoantigen presentation and immune-mediated destruction. Correspondingly, beta cell rescue strategies are being pursued, which include antigen vaccination using, for example, oral insulin or peptides, as well as agents with suggested benefits on beta cell stress, such as verapamil and glucagon-like peptide-1 receptor agonists. Whilst autoimmune-focused prevention approaches are central in type 1 diabetes and will be a requirement in the advent of stem cell-based replacement therapies, managing the primarily cardiometabolic complications of established type 1 diabetes is equally essential. In this review, we outline selected recent and suggested future attempts to address the evolving profile of the person with type 1 diabetes. Graphical abstract