Insulin-dependent treatment, diabetes mellitus

Meglitinide contains a benzamide group. Meglitinide-related compounds such as nateglinide are non-sulfonylurea oral hypoglycemic drugs used in the treatment of type 2 (non-insulin dependent) diabetes mellitus. 

The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. N Engl I Med 1993 329 977-986. 

Therapy for insulin-dependent diabetes mellitus is usually achieved by daily subcutaneous injections of insulin, and insulin-mimetics which can be orally administered may be useful for the treatment of type I diabetes (insulin dependent) if suitable complexes of low toxicity can be identified (510, 511). 

Captopr/V- Treatment of diabetic nephropathy (proteinuria greater than 500 mg/day) in patients with type 1 insulin-dependent diabetes mellitus and retinopathy. 

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%. 

In the treatment of diabetic nephropathy associated with type I insulin-dependent diabetes mellitus, captopril decreases the rate of progression of renal insufficiency and retards the worsening of renal function. 

Treatment of insulin-dependent type 1 diabetes mellitus and non-insulin-dependent type 2 diabetes mellitus when diet or weight control has failed to maintain satisfactory blood glucose levels or in event of fever, infection, surgery, ortrauma, or severe endocrine, hepatic, or renal dysfunction emergency treatment of ketoacidosis (regular insulin) to... 

It is indicated in non-insulin dependent diabetes mellitus (type II, maturityonset diabetes) whenever treatment by diet alone proves to be inadequate. 

Gentile S, Turco S, Guarino G, Oliviero B, Annunziata S, Cozzolino D, Sasso FC, Turco A, Salvatore T, Torella R. Effect of treatment with acarbose and insulin in patients with non-insulin-dependent diabetes mellitus associated with non-alcoholic liver cirrhosis. Diabetes Obes Metab 2001 3(1) 33 10. 

Chantelau E, Spraul M, Muhlhauser I, Gause R, Berger M. Long-term safety, efficacy and side-effects of continuous subcutaneous insulin infusion treatment for type 1 (insulin-dependent) diabetes mellitus a one centre experience. Diabetologia 1989 32(7) 421-6. 

Hanas R, Ludvigsson J. Side effects and indwelling times of subcutaneous catheters for insulin injections a new device for injecting insulin with a minimum of pain in the treatment of insulin-dependent diabetes mellitus. Diabetes Res Clin Pract 1990 10(l) 73-83. 

Insulin-dependent diabetes mellitus has been reported after 2 weeks to 6 months of treatment with interferon alfa in four patients with chronic hepatitis C (536). All discontinued interferon alfa, and one woman who restarted treatment had a subsequent increase in insulin requirements. 

Autoimmune polyglandular syndrome with progressive thyroid autoimmunity, type 1 diabetes mellitus, amenorrhea, and adrenal insufficiency has been reported in a 51-year-old woman treated with interferon alfa for chronic hepatitis C (545). Pancreas and pituitary gland autoantibodies, which were undetectable before interferon alfa treatment, were present at the time of diagnosis. After withdrawal, she recovered normal thyroid function, but was still insulin dependent with amenorrhea and adrenal insufficiency. 

Insulin-dependent diabetes mellitus (IDDM) is an example of a metabolic disease under active consideration for inducible gene therapy strategies. In this disorder, inflammatory cytokines have been shown to activate apoptosis in pancreatic beta cells. Experimental studies indicate that expression of insulinlike growth factor-1 (IGF-1) can prevent the cytokine-mediated destruction of beta cells of the pancreas (Giannoukakis et al., 2001). Regulated expression of IGF-1 in human pancreatic islets, to preserve beta cell function, may be a useful approach in the treatment of certain types of diabetes (Demeterco and Levine, 2001). 

The effect of PJ consumption by patients with CAS on their serum oxidative state was measured also as serum concentration of antibodies against Ox-LDL.31 A significant (p < 0.01) reduction in the concentration of antibodies against Ox-LDL by 24 and 19% was observed after 1 and 3 months of PJ consumption, respectively (from 2070 61 EU/mL before treatment to 1563 69 and 1670 52 F.lI/mL after 1 and 3 months of PJ consumption, respectively). Total antioxidant status (TAS) in serum from these patients was substantially increased by 2.3-fold (from 0.95 0.12 nmol/L at baseline up to 2.20 0.25 nmol/L after 12 months of PJ consumption). These results indicate that PJ administration to patients with CAS substantially reduced their serum oxidative status and could thus inhibit plasma lipid peroxidation. The susceptibility of the patient s plasma to free radical-induced oxidation decreased after 12 months of PJ consumption by 62% (from 209 18 at baseline to 79 6 nmol of peroxides/milliliter). The effect of PJ consumption on serum oxidative state was recently measured also in patients with non-insulin-dependent diabetes mellitus (NIDDM). Consumption of 50 mL of PJ per day for a period of 3 months resulted in a significant reduction in serum lipid peroxides and thiobarbituric acid reactive substance (TBAR) levels by 56 and 28%, respectively.32... 

Transplantation of islets of Langerhans as a means of treating insulin-dependent diabetes mellitus has become an important field of interest [217-219]. However, tissue rejection and relapse of the initial autoimmune process have limited the success of this treatment. Immunoisolation of islets in semipermeable microcapsules has been proposed to prevent their immune destruction [220, 221]. Nevertheless, a pericapsular cellular reaction eventually develops around micro-encapsulated islets, inducing graft failure [222]. Since empty microcapsules elicit a similar reaction [223], the reaction is not related to the presence of islets within the capsule but is, at least partially, caused by the capsule itself. Consequently, microcapsule biocompatibility appears to constitute a major impediment to the successful microencapsulated islet transplantation. 

---