Epidemiology of type 2 diabetes in the Middle East and North Africa: Challenges and call for action

Type 2 diabetes continues to be a serious and highly prevalent public health problem worldwide. In 2019, the highest prevalence of diabetes in the world at 12.2%, with its associated morbidity and mortality, was found in the Middle East and North Africa region. In addition to a genetic predisposition in its population, evidence suggests that obesity, physical inactivity, urbanization, and poor nutritional habits have contributed to the high prevalence of diabetes and prediabetes in the region. These risk factors have also led to an earlier onset of type 2 diabetes among children and adolescents, negatively affecting the productive years of the youth and their quality of life. Furthermore, efforts to control the rising prevalence of diabetes and its complications have been challenged and complicated by the political instability and armed conflict in some countries of the region and the recent coronavirus disease 2019. Broad strategies, coupled with targeted interventions at the regional, national, and community levels are needed to address and curb the spread of this public health crisis

Younger adult type 2 diabetic patients have poorer glycaemic control: A cross-sectional study in a primary care setting in Singapore

10.1186/1472-6823-13-18BMC Endocrine Disorders13-BEDM

Oxidative stress in type 2 diabetes: the role of fasting and postprandial glycaemia

Oxidative stress, through the production of reactive oxygen species (ROS), has been proposed as the root cause underlying the development of insulin resistance, β-cell dysfunction, impaired glucose tolerance and type 2 diabetes mellitus (T2DM). It has also been implicated in the progression of long-term diabetes complications, including microvascular and macrovascular dysfunction. Excess nourishment and a sedentary lifestyle leads to glucose and fatty acid overload, resulting in production of ROS. Additionally, reaction of glucose with plasma proteins forms advanced glycation end products, triggering production of ROS. These ROS initiate a chain reaction leading to reduced nitric oxide availability, increased markers of inflammation and chemical modification of lipoproteins, all of which may increase the risk of atherogenesis. With the postulation that hyperglycaemia and fluctuations in blood glucose lead to generation of ROS, it follows that aggressive treatment of fasting and postprandial hyperglycaemia is important for prevention of micro and macrovascular complications in T2DM

Arachidonic acid stimulates glucose uptake in 3T3-L1 adipocytes by increasing GLUT1 and GLUT4 levels at the plasma membrane: Evidence for involvement of lipoxygenase metabolites and peroxisome proliferator-activated receptor

Exposure of insulin-sensitive tissues to free fatty acids can impair glucose disposal through inhibition of carbohydrate oxidation and glucose transport. However, certain fatty acids and their derivatives can also act as endogenous ligands for peroxisome proliferator-activated receptor gamma (PPARgamma ), a nuclear receptor that positively modulates insulin sensitivity. To clarify the effects of externally delivered fatty acids on glucose uptake in an insulin-responsive cell type, we systematically examined the effects of a range of fatty acids on glucose uptake in 3T3-L1 adipocytes. Of the fatty acids examined, arachidonic acid (AA) had the greatest positive effects, significantly increasing basal and insulin-stimulated glucose uptake by 1.8- and 2-fold, respectively, with effects being maximal at 4 h at which time membrane phospholipid content of AA was markedly increased. The effects of AA were sensitive to the inhibition of protein synthesis but were unrelated to changes in membrane fluidity. AA had no effect on total cellular levels of glucose transporters, but significantly increased levels of GLUT1 and GLUT4 at the plasma membrane. While the effects of AA were insensitive to cyclooxygenase inhibition, the lipoxygenase inhibitor, nordihydroguaiaretic acid, substantially blocked the AA effect on basal glucose uptake. Furthermore, adenoviral expression of a dominant-negative PPARgamma mutant attenuated the AA potentiation of basal glucose uptake. Thus, AA potentiates basal and insulin-stimulated glucose uptake in 3T3-L1 adipocytes by a cyclooxygenase-independent mechanism that increases the levels of both GLUT1 and GLUT4 at the plasma membrane. These effects are at least partly dependent on de novo protein synthesis, an intact lipoxygenase pathway and the activation of PPARgamma with these pathways having a greater role in the absence than in the presence of insulin

High frequency of viridians group streptococci bacteremia in pediatric neuroblastoma high-risk patients during induction chemotherapy

Existing literature on febrile neutropenia (FN) has categorized patients with acute leukemia or those undergoing allogeneic stem cell transplantation (SCT) as being high risk for severe infection, bacteremia, and poor outcomes. Comprehensive studies of infection risk in pediatric high-risk neuroblastoma (NB-HR) during induction chemotherapy are limited, and mostly merged within the solid tumor (ST) group. Therefore, it is unclear whether infectious complications and outcomes for NB-HR are the same as in other ST groups. We conducted a retrospective medical record review of pediatric FN patients in a single center from March 2009 to December 2016. FN episodes were categorized into five groups based on underlying diagnosis (acute myelogenous leukemia (AML), acute lymphocytic leukemia (ALL), NB-HR during induction chemotherapy, other solid tumors, and SCT). Comparative analyses of infectious complications between patients with NB-HR and those with other types of cancer diagnoses were performed. A total of 667 FN episodes (FNEs) were identified in 230 patients. FNEs occurred in 82 episodes with NB-HR. Bloodstream infection (BSI) occurred in 145 (21.7%) of total FN episodes. The most isolated organisms were the viridians group streptococci (VGS) (25%). NB-HR patients have higher rates of VGS bacteremia (OR 0.15, 95% [CI 0.04, 0.56]) and are more likely to be admitted to the Pediatric Intensive Care Unit (PICU) compared to patients with other solid tumors (OR 0.36, 95% [CI 0.15, 0.84]). Interestingly, there is no difference in VGS rates between patients with NB-HR and those with AML despite the fact that NB-HR patients do not receive a cytosine arabinoside (AraC)-based regimen. This large neuroblastoma cohort showed that patients with NB-HR during induction chemotherapy are at higher risk for VGS bacteremia and PICU admissions compared with patients with other solid tumors. Further prospective studies are needed to investigate infection-related complications in this high-risk group and to improve morbidity and mortality