Insulin resistance initiation

The drug improves the responsiveness to insulin in sueh patients that experience Type 2 diabetes mellitus problems of insulin resistance initiated and sustained by a unique mechanism of action whieh is fairly comparable with those of other similar drugs. Importantly, it is at present only approved for use with insulin. 

Symptomatic patients may initially require insulin or combination oral therapy to reduce glucose toxicity (which may reduce /1-cell insulin secretion and worsen insulin resistance). 

Initially the level of insulin decreases, favouring increased rates of lipolysis, fatty acid oxidation, muscle protein degradation, glycogenolysis and gluconeogenesis. It soon increases, however, as a result of insulin resistance, when the stimulation of the above processes will depend on the cytokine levels. For details of endocrine hormone effects, see Chapter 12. For details of cytokines see Chapter 17. 

The most common adverse effects of indinavir are indirect hyperbilirubinemia and nephrolithiasis due to crystallization of the drug. Nephrolithiasis can occur within days after initiating therapy, with an estimated incidence of approximately 10%. Consumption of at least 48 ounces of water daily is important to maintain adequate hydration. Thrombocytopenia, elevations of serum aminotransferase levels, nausea, diarrhea, insomnia, dry throat, dry skin, and indirect hyperbilirubinemia have also been reported. Insulin resistance may be more common with indinavir than with the other Pis, occurring in 3-5% of patients. There have also been rare cases of acute hemolytic anemia. 

Plaque ruptures in the ACS setting are often involved with a diffuse process, Inflammation is involved in plaque growth and development in addition to complications of plaque rupture. These could be considered the result of injury, Well-known coronary risk factors can provide the impetus for plaque development. Cigarette smoking, hypertension, hyperlipidemia, hyperglycemia, or insulin resistance are noxious stimuli. The stimuli can facilitate monocyte attachment to endothelial cells. Eventually monocytes migrate to the subintimal space and become foam cells to initiate plaque development. 

P-Cells in the pancreas normally respond to peripheral insulin resistance by increasing basal and stimulated insulin secretion to compensate for the insulin-resistant state. Initially, this compensation maintains normal or impaired glucose tolerance in the prediabetic insulin-resistant state and delays deterioration of glucose homeostasis and type 2 diabetes. In patients destined to develop type 2 diabetes, P-cells can no longer com-... 

Diabetes mellitus ( sweet urine ) involves relative over-production of glucose by the liver and under-utilization by other organs. Diabetes is the most serious metabolic disease in terms of its social impact. Obesity and the indulgent Western diet correlates with mature age diabetes. Type 1 diabetes (juvenile diabetes) typically manifests at less than 20 years from autoimmune destruction of the insulin-producing pancreatic (3 cells. Type 1 diabetes is insulin-dependent diabetes mellitus (IDDM) and is fatal without exogenous insulin. Type 2 diabetes mellitus (mature age diabetes) occurs later in life and typically involves both deficient insulin production and insulin resistance , that is, the target cells are less responsive to insulin. Type 2 diabetes is initially non-insulin-dependent diabetes (NIDDM) but insulin therapy (in addition to oral antidiabetics) may eventually be required. Hyperglycaemia due... 

The use of oral antidiabetic drugs may be necessary. Insuhn production is initially only moderately impaired in type 2 diabetes, so oral medication can often be used to improve insulin production (e.g. sulphonylureas), to regulate inappropriate release of glucose by the liver and attenuate insulin resistance to some extent (e.g. metformin), and to substantially attenuate insulin resistance (e.g. thiazohdinediones). A Hnal resort is insuhn therapy to maintain normal or near-normal glucose levels. 

It is important to prevent nocturnal hypoglycaemia, not only to protect brain function, but also to prevent insulin resistance. This may easily result in exaggerated hyperglycaemia and initiate the vicious circle -hypoglycaemia, hyperglycaemia, increase in insulin dose and risk of subsequent hypoglycaemia (Bolli and Perriello, 1990). The mechanism, frequency and even the existence of the Somogyi phenomenon, however, are all still controversial. 

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