The DiabCare Asia 2008 study – Outcomes on control and complications of type 2 diabetic patients in Indonesia.

Aim: To collect information on diabetes management, diabetes complications, and awareness of self-control in diabetic population of the country. This study also evaluated the physician perspectives, psychological aspects, and quality of life of diabetic patients. Methods: This was a non-interventional, cross-sectional study, which recruited 1832 patients from secondary and tertiary medical centers across Indonesia. Data on demography, medical history, risk factors and clinical examination reports including laboratory assessments were collected from medical records of patients. Blood samples of all patients were collected for centralized HbA1c measurements. Results: Among 1832 patients, 1785 individuals were eligible for analysis. The mean age of the patients was 58.9+9.6 years. The mean duration of diabetes was 8.5+7.0 years. Majority (97.5%) of the patients had type 2 diabetes. 67.9% had poor control of diabetes (A1c:8.1 ± 2.0%). 47.2% had FPG>130 mg/dL (161.6±14.6 mg/dL). Dyslipidemia was reported in 60% (834/1390) and 74% (617/834) of those received lipid lowering treatment. Neuropathy was most common complication (63.5%); other complications were: Diabetic retinopathy 42%, nephropathy 7.3%, severe late complications 16.9%, macrovascular complications 16%, microvascular complications 27.6%. About 81.3% of patients were on OADs (± insulin), 37.7% were on insulin (±OADs). Majority used biguanides followed by sulfonylureas. Human insulin was used by 73.2%, premix regimen 58.5%, analogues usage was 24.9%. Majority of the WHO-5 well being index responses fell in positive territory. Conclusion: Poor glycaemic control in majority of patients is a concern. There is a need for a large proportion of patients to be adjusted to more intensive pharmacotherapy and a multi-disciplinary approach for management should be adopted. The study fi ndings should be communicated to policymakers and physicians to help them provide proper healthcare and its facilities in Indonesia.

New approach in the treatment of T2DM and metabolic syndrome (focus on a novel insulin sensitizer).

Peroxisome Proliferator-Activate Receptors (PPARs) are transcription factors belonging to the nuclear receptor superfamily. The three PPARs (alpha, beta/delta, and gamma) are distributed differently in the different organs. PPARalpha is most common in the liver, but also found in kidney, gut, skeletal muscle and adipose tissue, while PPARbeta/delta, is fairly ubiquitous; it may be found in body tissues and brain (for myelination process and lipid metabolism in the brain). PPARgamma has 3 isoforms, such as PPARgamma 1, PPARgamma 2, and PPARgamma 3. The syndrome-X was firstly coined by Reaven in 1988 and then to be provided in 1999 by the name : the metabolic syndrome-X. This metabolic syndrome represents a "Cluster" of metabolic disorders and cardiovascular risk factors which has been collected and summarized by the author and such a cluster includes: insulin resistance/hyperinsulinemia, central obesity, glucose intolerance/DM, atherogenic dyslipidemia (increase TG, decrease HDL-cholesterol, increase Apo-B, increase small dense LDL), hypertension, prothrombotic state (increase PAI-1, increase F-VII, increase fibrinogen, increase vWF, increase adhesion molecules), endothelial dysfunction, hyperuricemia, and increased hsC-RP and cytokines. The metabolic syndrome-X may lead to the development of T2DM and coronary heart disease (CHD); insulin resistance plays pivotal roles in the progression of such a syndrome and cardiovascular diseases. Improvement of Insulin Resistance, therefore, is most likely to reduce the high cardiovascular event rate in T2DM. It has been generally accepted that Insulin Resistance (detected by HOMA-R) and Acute Insulin Response = AIR (by HOMA-B) are both usually present in T2DM. The Thiazolidinedions (TZDs) are Insulin Sensitizers (e.g Rosiglitazone = ROS, Pioglitazone = PIO) introduced into clinical practice in 1997; clinical evidence data showed that TZDs improved both HOMA-R, and HOMA-B. PPARgamma can be activated by TZDs and it appears to be fundamental to the pathophysiology of diabetes mellitus i.e increase GLUT-4, increase glucokinase, decrease PEPCK, increase GLUT-4, and decreases production by fat cell of several mediators that may cause insulin resistance, such as TNFalpha and resistin. PPARgamma also mediates increased production of Adiponectin and the insulin signaling intermediate PI3K, and both actions lead to increase insulin sensitivity. A "dual PPARgamma-PPARalpha agonists" (e.g PIO, but ROS poorly activate PPARalpha) might lower glucose and modulate lipids. Thus, PIO, as a stronger "dual PPARgamma-PPARalpha agonists", shows an important therapeutic pathway in diabetes mellitus and cardiovascular diseases, even in metabolic syndrome. Current evidence suggests a close relationship between activation of PPARgamma and restoration of insulin sensitivity by reductions in TNFalpha and FFAs, and the enhancement of insulin stimulation of PI3-K Pathway and also increase adiponectin & decrease resistin.