![]() Use appropriate rapid-acting insulin formulation consisting of a combination of basal continuous insulin infusion rate with preprogrammed, premeal bolus doses controlled by the patient.Insulin pump (continuous SC insulin infusion) Premixed combinations are available that deliver rapid- or short-acting components at the same time as the intermediate- or long-acting component.Approximately 50-75% of the total daily insulin requirements are given as intermediate- or long-acting insulin administered in 1-2 injections rapid- or short-acting insulin should be used before or at mealtimes to satisfy the remainder balance of the total daily insulin requirements.Maintenance: 0.5-1 unit/kg/day SC divided q8hr or more frequently in insulin-resistant patients (eg, due to obesity), substantially higher daily insulin may be required.Initial: 0.2-0.4 units/kg/day SC divided q8hr or more frequently.Indicated to improve glycemic control in with diabetes mellitus SC injection 500units/mL (20mL vial) prescribe with U-500 syringes to avoid conversion for U-100 tuberculin syringes.It runs on a variety of computer platforms and can be downloaded from this site.įor queries concerning the HOMA model and its appropriate use please read the FAQ.Dosage Forms & Strengths injectable solution This provides quick and easy access to the HOMA2 model for researchers who wish to use model-derived estimates of %B and %S, rather than linear approximations. In 2004, the HOMA2 Calculator was released. The model was recalibrated also to give %B and %S values of 100% in normal young adults when using currently available assays for insulin, specific insulin or C-peptide. In 1998, Jonathan Levy et al published an updated HOMA model (HOMA2) which took account of variations in hepatic and peripheral glucose resistance, increases in the insulin secretion curve for plasma glucose concentrations above 10 mmol/L (180 mg/dL) and the contribution of circulating proinsulin. The equations have been used widely, particularly for estimates of beta cell function and insulin resistance in large-scale studies, but are not appropriate for use with currently available insulin assays. These gave approximate values of %B and, instead of %S, HOMA IR (insulin resistance) which is the reciprocal of %S (100/%S). As an alternative to running the Fortran computer model, a set of linear equations were also made available. This model, written in Fortran, took greater account of peripheral glucose uptake and could use fasting levels of specific insulin or C-peptide in addition to RIA insulin. In 1985, David Matthews et al published an expanded and more comprehensive structural model known as the Homeostasis Assessment Model (HOMA). A mathematical feedback model based on these hypotheses was constructed to estimate the degrees of beta cell function and insulin sensitivity that would equate to the steady state plasma glucose and insulin levels observed in an individual. They postulated that elevated fasting glucose levels reflected a compensatory mechanism that maintained fasting insulin levels when there was a reduced insulin secretory capacity, and that fasting insulin levels were elevated in direct proportion to diminished insulin sensitivity. In 1976, Robert Turner and Rury Holman developed the concept that fasting plasma insulin and glucose levels were determined, in part, by a hepatic-beta cell feedback loop. These measures correspond well, but are not necessarily equivalent, to non-steady state estimates of beta cell function and insulin sensitivity derived from stimulatory models such as the hyperinsulinaemic clamp, the hyperglycaemic clamp, the intravenous glucose tolerance test (acute insulin response, minimal model), and the oral glucose tolerance test (0-30 delta I/G) ![]() The Homeostasis Model Assessment (HOMA) estimates steady state beta cell function (%B) and insulin sensitivity (%S), as percentages of a normal reference population.
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