Diabetes is estimated to be responsible for 3.96 million adult deaths per year at global level. By 2025, the number of people with diabetes in India is estimated to rise to 70 million. In spite of well-defined treatment for type 2 diabetes, in majority of the people, disease is poorly controlled. Hence controlling the disease is a major issue to prevent complications, increase the life expectancy and improve the quality of life. To find out the factors associated with poor control of diabetes, a systematic review and meta-analysis was carried out. The data source was Published and unpublished studies from 1980 to October 2010. Two of the authors applied selection criteria to get the relevant studies. Glycated hemoglobin level was the measure for outcome. Meta-analysis was performed by pooling the results of selected studies. Mantel - Haenszel Odds Ratios, standardized mean differences and 95 % Confidence Intervals of estimates were calculated for Meta-analysis. The results were presented using forest plot. Meta-analysis showed that, elderly people and males had better control on diabetes. Presence of coronary heart disease and non-adherence to diet, exercise, medication and glucose monitoring are the factors associated with poor control of diabetes. Neuropathy, retinopathy, renal failure and neurological disorders are the complications of poor control. In spite of our sincere attempt to consolidate all studies, which give evidence of factors responsible for poor control of diabetes, we did not find this as the primary objective in many well-conducted studies. Hence, this area requires more attention of diabetes researchers.

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Aim of the study was to find out the prevalence of long-term diabetic complications among type 2 diabetic patients in Benghazi. It was a cross-sectional study and included 952 type 2 diabetic patients (410 male subjects) aged 29-85 years. The patients were examined for evidence of coronary heart disease, diabetic retinopathy, macroproteiuria, peripheral arterial disease, peripheral neuropathy, cataract and amputations due to diabetes and diabetic foot. Hypertension was present in 33.4% of the subjects. The majority of the patients (58.3 %) were on oral hypoglycemic drugs, and only 3 patients were on diet control. About eighty per cent of the patients were poorly controlled. 27.7% percent of the patients were current smokers. 68.7% of the patients had complications, while 31.3% percent did not have any complication. 36.7% had one, 20.1 % had two, 9.6 % had three and 2.3 % had four or more complications. The overall prevalence of coronary heart disease was 14.9%, diabetic retinopathy 30.6%, peripheral neuropathy 47.1%, macroalbuminuria 25.8%, peripheral arterial disease 15.2% and cataract 13.1%, 1.1% of patients had their legs amputed below knee and 0.7% of them were blind. The prevalence of long-term diabetic complications was higher among poorly controlled than well-controlled patients. Stepwise logistic regression analysis showed that the age of the patients and duration of diabetes were independent risk factors for the development of long term diabetic complications. This study provides a baseline data on long term complications of diabetes, among Libyans. Age, duration of diabetes and poor glycemic control were independent risk factors for the development of long-term diabetic complications.

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With increasing prevalence rates of diabetes mellitus in tropical countries, malaria and diabetes often coincide. The study was designed to investigate the effects of glucose and insulin upon in vitro proliferation of Plasmodium falciparum, the causative agent of malaria tropica. Plasmodium falciparum proliferation was determined via the Malstat™ assay, following incubation of the parasites at varying concentrations of glucose (0 - 27.7mM) or insulin (10 pM - 100μM) for 24 and 48 hrs. While Plasmodium falciparum proliferation was unaffected at concentrations of 5.5 - 27.7mM glucose, growth was impaired below a threshold of 5.5mM. No effect was seen following incubation of the parasites in the presence of 10pM - 100μM insulin. Insulin levels did not affect parasite proliferation whilst glucose levels below 5.5mM reduced parasite growth. The Malstat™ assay was identified as a suitable screening assay to assess the effects of glycemic control upon Plasmodium falciparum growth.

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Adiponectin and resistin are inversely associated with type 2 diabetes but it is not yet concluded whether adiponectin and resistin are the causal factors of diabetes. The present study was undertaken to evaluate the association of serum adiponectin and resistin with insulin secretory capacity and insulin resistance in subjects with impaired glucose regulation (IGR). Twenty four subjects with impaired fasting glucose (IFG), 58 with impaired glucose tolerance (IGT) and 30 with IFG-IGT were recruited in this study. Forty four non-diabetic healthy controls with on family history of diabetes or prediabetes were also recruited. Serum insulin, adiponectin and resistin levels were measured using ELISA technique. Serum adiponectin and resistin levels were not significantly different among the study groups. Ratios of fasting insulin with adiponectin and resistin were increased, both in IGT and IFG-IGT subjects. Binary logistic regression analysis have shown that ratio of fasting glucose to Adiponectin was significantly associated (=1.085, p=0.031) with IGR subjects when age and body mass index were adjusted. Ratios of fasting glucose to adiponectin and resistin were also increased in IFG-IGT subjects. Multiple regression analysis have shown that ratio of fasting insulin to Adiponectin was negatively associated (=-0.201, p=0.034) with insulin sensitivity (HOMA% S) and positively (=0.507, p=0.0001) with insulin secretory capacity (HOMA% B) in IGR subjects. On the other hand, ratio of fasting insulin to Resistin showed significant negative association (=-0.237, p=0.015) with HOMA% S and positive association with HOMA% B, (=0.506, p=0.001) in IGR subjects. The findings indicate that ratio of fasting glucose to adiponectin may be an important factor for the development of type2 diabetes.

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Atherosclerosis constitutes a major cause of complications of diabetes. The mechanisms involved include, oxidative modification of low density lipoproteins (LDL) through a multitude of endogenous mediators including homocysteine and angiotensin II. Assessment of supplementation with either low-dose ACE inhibitor or a combination of antioxidants to the treatment regimens of type 2 diabetics with CAD on some markers of atherosclerosis. Thirty subjects, of the same socio-economic background, were recruited and divided into 3 groups. Group I included 10 healthy individuals. The 20 diabetic subjects with CAD were randomly distributed into of group II and group III. Treatment of patients in group II was supplemented by a once daily tablet containing antioxidant combination. Supplementation in group III patients consisted of 12.5 mg daily dose of the ACE inhibitor, captopril. Compared to the healthy individuals, diabetic patients showed hyperglycemia, elevated glycated hemoglobin, increased oxidative stress, depressed antioxidant defense, hyperhomocysteinemia and elevated levels of oxidized LDL autoantibodies. The results of a three month follow-up of type 2 diabetic patients indicated that both adjunct treatments improved all parameters tested, including glycemic control, oxidative stress, and hyperhomocysteinemia. However, the titer of circulating ox-LDL autoantibodies, which declined very rapidly, was not a good prognostic indicator for atherosclerosis. Conclusion: The observed shift in the disease indices towards normal levels make the use of both adjuvant therapies in type 2 diabetics with atherosclerotic CAD worth pursuing in a larger clinical study.

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Oxidative stress resulting from enhanced free radical formation or defect in anti-oxidant defence mechanism, implicates in the development of various disorders including impairment of vasodilatation, neuro degeneration, ventricular dysfunction and changes in cardiac muscle cells morphology. Oxidative stress activates renin aldosterone angiotensin system and inflammatory cytokines that induce apoptosis in heart muscles. It also decreases ATP formation that leads to apoptosis in myocyte. As a consequence, the physical force in the heart is increased that may guide to programme cardiac muscle cell death. The net effect of oxidative stress leads to an architectural rearrangement of the myocardium involving side to side slippage called myocyte disarray. Single myocyte cell death allows side by side translocation of cells. However, multiple cells death causes sliding of the myocyte bundle. No work has yet been done to correlate the myocardial cell slippage and oxidative stress in diabetes, in which heart muscles apoptosis are evident. Thus the present review is done to scrutinize if there is any role of oxidative stress on development of myocyte disarray in diabetes.

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