Diabetes insulin release

FIGURE 12 Effect of insulin released from microspheres of PCPP-SA 50 50 injected subcutaneously in streptozotocin-diabetic rats. Details were as described in the text. 

Galanin GAL1 Human cDNA Alzheimer s disease, feeding diabetes, growth disorders, pain, stroke, obesity, Parkinson s disease Inhibition of acetylcholine release, regulation of motility, inhibition of insulin release, stimulation of growth hormone, inhibition of LH-RH secretion... 

K+ channels K-atp Rat brain Diabetes, asthma, cardiac arrythmia, angina, cardiac and cerebral ischemia, thrombosis, hypertension, incontinence, pain, neurogenic inflammation, epilepsy, stroke, hair growth Control of insulin release, vasodilatation, protection against cell ischemia... 

Repaglinide is a newer oral hypoglycaemic agent, indicated in type 2 diabetes either in combination with metformin or as monotherapy. Repaglinide stimulates insulin release. 

Diabetes mellitus and hypoglycemia -blockade may prevent the appearance of premonitory signs and symptoms of acute hypoglycemia. -blockade also reduces insulin release it may be necessary to adjust antidiabetic drug dose. 

Repaglinide en nateglinide are not sulfonylurea agents but their mechanism of action is very alike. Repaglinide is the first carbamoylmethyl-benzoic acid derivative that has been registred for the treatment of diabetes mellitus. It closes ATP-dependent potassium channels in the beta cell membrane with consequent depolarization, opening of calcium channels and increased insulin release. It is rapidly absorbed with peak plasma levels after 1 hour. It has a protein binding of over 98%. 

Hypolipidemic activity. Seed hull, administered to mice at a dose of 2.5% of diet for 18 weeks, was inactive " . The husk, administered orally to male Hartley guinea pigs at doses of 7.5 or 10 g/100 g of Plantago ovata for 4 weeks, exerted a hypolipidemic effect by affecting bile acid absorption and altering hepatic cholesterol metabolism Insulin release inhibition. Seed administered orally to 18 patients with noninsulin-dependent diabetes at a dose of 13.6 g/day lowered insulin levels by 17% . 

For persons with type 1 diabetes, insulin replacement therapy is necessary to sustain life. Pharmacologic insulin is administered by injection into the subcutaneous tissue using a manual injection device or an insulin pump that continuously infuses insulin under the skin. Interruption of the insulin replacement therapy can be life-threatening and can result in diabetic ketoacidosis or death. Diabetic ketoacidosis is caused by insufficient or absent insulin and results from excess release of fatty acids and subsequent formation of toxic levels of ketoacids. 

Insulin resistance and type 2 diabetes Insulin resistance alone will not lead to type 2 diabetes. Rather, type 2 diabetes develops in insulin-resistant individuals who also show impaired p cell function. Insulin resistance and subsequent development of type 2 diabetes is commonly observed in the elderly, and in individuals who are obese, physically inactive, or in women who are pregnant. These patients are unable to sufficiently compensate for insulin resistance with increased insulin release. Figure 25.8 shows the time course for the develpment of hyperglycemia and the destruction of P cells. 

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