The condition of being overweight, expressed as BMI, appears to be a good indicator of risk for IGT, MS, and CVR, particularly in young non-obese subjects (BMI<30).

In the present study, we aimed to investigate the role of aspirin in preventing type 2 diabetes in rats. At 5 days old, rat pups were divided into four groups. Group I pups received citrate buffer solution and served as control; group II was treated only with streptozotocin (80 mg/kg i.p.) and served as the diabetic control; groups III and IV were treated with aspirin (10 mg/kg/day p.o.) for 1 and 2 months, respectively, after streptozotocin treatment and served as treated groups. During weeks 8 and 10, blood samples were collected from all animals and fasting blood sugar, fasting insulin, insulin resistance and insulin sensitivity were determined. Treatment of rat pups with aspirin for 1 and 2 months after streptozotocin injection produced a significant (P < 0.001) reduction in fasting blood glucose and insulin resistance levels and elevation of fasting insulin and insulin sensitivity compared with the diabetic control pups. The results of the present study suggest that aspirin treatment prevents the development of type 2 diabetes by reducing insulin resistance and elevating fasting insulin and insulin sensitivity. It also seems to protect the pancreas from damage caused by streptozotocin and maintains glucose levels near normal in diabetic rats.

Dipeptidyl peptidase-IV (DPP-IV) could serve as a potential biomarker in monitoring the disease progression and improvement on treatment. To investigate fasting & post prandial response of DPP-IV enzyme as indirect marker of incretin response failure after chronic treatment with metformin in type 2 diabetes. The study included twelve nondiabetic subjects, ten patients with glycosylated hemoglobin values (6-8 %) and fifteen patients with glycosylated hemoglobin greater than 8 % of type-2 diabetes patients of either sex with metformin treatment above 3 years were recruited. Fasting and post prandial DPP-IV levels were calculated. HbA1c was used to assess diabetes status. DPP-IV activity (fasting) in type 2 diabetic subjects with HbA1c > 8 % was significantly higher DPP-IV (44.67 ± 2.19 U/l) than in non diabetic subjects (24.39 ± 3.97 U/l). A significant correlation between DPP-IV (fasting / post prandial) and HbA1c (r = 0.821 & r = 0.732, P< 0.01) was observed in both diabetic (HbA1c 6-8, HbA1c < 8) patients. Hyperglycemia induces significant increase in serum DPP-IV activity in fasting condition and might contribute to the reduction in active glucagon like peptide-1(GLP-1) in type 2 diabetic subjects. In normal subjects during post prandial condition, there is sudden increase followed by decrease of GLP-1 due to cleavage of GLP-1 to as substrate of DPP-IV is seen as upsurge of DPP-IV. This response was lacking in diabetic patients with high HbA1c indicates indirectly metformin failure to secrete GLP-1. High fasting level and decreased post prandial of DPP-IV may indicate drug failure in type-2 diabetes mellitus.

AIM:We studied the correlations between fasting and post-lunch serum IGF-I concentrations, and insulin resistance and insulin sensitivity in subjects with various degrees of glucose tolerance.MATERIALS AND METHODS:A total of 12 nondiabetic subjects, 09 subjects with impaired glucose tolerance (IGT) and 18 patients with newly diagnosed type-2 diabetes of either sex (mean age, 46 years) were recruited. None of the participants received any drug treatment at the commencement of the study. Fasting as well as post-lunch blood samples were collected from all the subjects and anthropometric and biochemical parameters were analyzed.RESULTS:Fasting serum IGF-I concentrations were negatively correlated with fasting serum glucose, insulin, C-peptide, triglycerides, total LDL and VLDL cholesterol, homeostatic model assessment of insulin resistance (HOMA-IR), and age. Fasting serum IGF-I concentrations were positively correlated with fasting blood HDL cholesterol and homeostatic model assessment of insulin sensitivity (HOMA-S) in only diabetic subjects. Post-lunch serum IGF-I concentrations were positively correlated with HDL and LDL cholesterol. Correlations with HOMA-S with these metabolic anthropometric variables were of similar magnitude and direction as that of IGF-I concentrations. IGF-I concentrations were significantly lower in the subjects with World Health Organization-defined metabolic syndrome compared with the subjects without metabolic syndrome (P < 0.0001).CONCLUSIONS:Our data indicate that IGF-I could be a useful marker in the insulin resistance syndrome. The post-lunch low-IGF-I levels help in better identification of subjects at risk for type-2 diabetes mellitus and cardiovascular disease.

Type-2 diabetes is a chronic metabolic progressive disease, affects 200 million people worldwide will leads to increased death by more than 50% in the next 10 years. The ingested nutrients stimulate the release of gut peptides called incretins, which enhance the insulin secretion from pancreatic β cell, in addition to this, recently, another gut mediated mechanisms called intestine-brain-liver axis to regulate glucose homeostasis by a neural circuit, initiated in the intestine in response to nutrient sensing, that increases sensitivity to insulin levels. In this mini review, the underlying mechanisms of gut related glucose regulation and its impact on the management of type-2 diabetes mellitus.