ABSTRACT
Type 2 Diabetes mellitus is characterized by insulin resistance and defects in insulin secretion. These variables have been studied by the euglycemic/hyperinsulinemic clamp and MinMod, which difficult the insulin resistance and b cell failure study in clinical practice. The aim of this study was to evaluate three different anti-diabetic therapeutic options using a mathematical model (Homeostasis model assessment, HOMA). Seventy type 2 diabetic patients were randomly assigned one of the next therapeutic options: A) Metformin + ADA Diet + Physical activity (Walk, 60 minutes/day). B) Metformin + Glimepiride + ADA Diet + Physical activity. C) Only ADA diet + Physical activity. A blood sample was taken before and after the treatment to determine basal and post-prandial blood glucose, basal insulin and HbA1c and to calculate HOMAbcell and HOMAIR. Before treatment basal and post-prandial levels of glucose, HbA1c, basal insulin and HOMAIR and HOMAbcell were significantly different when compared to after treatment levels for each group (p<0.01). Significant differences were also found when comparing basal blood glucose reduction (51.8 per cent; p<0.01), post-prandial blood glucose (55.0 per cent; p<0.05), and HOMAIR (65.3 per cent; p<0.01) of group B (Metformin + low glimepiride dose) with the other therapeutic options. We conclude that metformin plus glimepiride at a low dose is a more effective treatment for type 2 diabetes than other therapeutic options. HOMAIR and HOMAbcell are inexpensive and reliable methods to study IR and b cell function in DM2
Subject(s)
Humans , Medicine , VenezuelaABSTRACT
Dietary saturated fatty acids are implicated as a risk factor for atherosclerosis. The conversion of the major dietary saturated fatty acids stearic acid (18:0) and palmitic acid (16:0) to monounsaturated fatty acids in whole plasma and lipoprotein fractions is reported for seven healthy adult humans over 6 d using [U-13C]stearic acid (18:0*) and [U-13C]palmitic acid (16:0*) and high-precision mass spectrometry. A tracer dose (28-32 mg) of 18:0* or 16:0* was loaded into an emulsion and orally administered before breakfast. Serial blood samples were collected on day 1 and fasting blood was drawn daily until day 7. Overall conversion of 18:0 to 18:1 was approximately 14%, whereas that of 18:0 to 16:0 was approximately 2% in plasma up to 144 h. Conversion of 16:0 to 16:1 was < 2%, whereas conversion of 16:0 to 18:0 was approximately 6%. No other fatty acid metabolites were detected for 18:0* or 16:0*. The conversion products were observed mainly in chylomicrons and very-low-density lipoproteins, indicating that the intestine and liver have comparable roles in desaturating 18:0 and 16:0. Overall, these data indicate that dietary 18:0 desaturation is severalfold greater than 16:0 desaturation. The low level (14%) of 18:0 desaturation in omnivorous adults may have little influence on blood lipid profiles relevant to atherosclerosis risk.
