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      Glyburide: A Second-generation Sulfonylurea Hypoglycemic Agent : History, Chemistry, Metabolism, Pharmacokinetics, Clinical Use and Adverse Effects

      Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy

      Wiley

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          Pharmacogenetics of tolbutamide metabolism in humans.

          This study was designed to focus on the genetic control of tolbutamide dispositon in humans and to provide insight into the potential for high accrued blood levels in individuals receiving fixed dosage regimens. Tolbutamide was administered intravenously to 42 nondiabetic subjects, eight of their relatives, and to five sets of twins. A ninefold variation in the rate of tolbutamide disappearance from plasms (Kd) was found. This variation was characterized by a trimodal frequency distribution, suggestive of monogenic inheritance and consistent with pedigree analysis, indicating autosomal transmission of rapid and slow inactivation of tolbutamide. A heritability value of 0.995 for Kd indicated little influence of environmental factors on variation of this rate. Interindividual differences in the binding of 35S-tolbutamide to serum proteins were also assessed. No correlation was found between tolbutamide serum protein binding affinity and Kd. Analysis of the metabolites of tolbutamide in urine samples provided evidence for the microsomal oxidation of the drug to hydroxytolbutamide as the primary site of genetic control. In conclusion, this study provides evidence for monogenic control of tolbutamide metabolism in man. The results suggest that fixed dosage regimens of this drug, as were prescribed in the controversial University Group Diabetes Program study, might lead to higher accrued blood levels in slow inactivators.
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            The acute and chronic effects of sulfonylurea therapy in type II diabetic subjects.

            Although sulfonylurea agents have been used in the clinical management of type II diabetes (non-insulin-dependent diabetes mellitus, NIDDM) for over two decades, the mechanisms responsible for their hypoglycemic action remain controversial. We have quantitated glycemic control, endogenous insulin secretion in response to mixed meals, adipocyte insulin binding, insulin-mediated peripheral glucose disposal, and basal hepatic glucose output in 17 type II diabetic subjects before and after 3 mo of therapy with the second-generation, sulfonylurea compound glyburide in an attempt to identify the factors responsible for the clinical response to the drug. In addition, 9 subjects were treated for an additional 15 mo to see if the response to the drug changed with time. The mean fasting serum glucose level fell from an initial value of 264 +/- 17 mg/dl to 178 +/- 16 mg/dl after 3 mo of drug therapy. Endogenous insulin secretion increased in all subjects, but the increase was most marked in those subjects who continued to exhibit fasting hyperglycemia (fasting serum glucose greater than 175 mg/dl) after 3 mo of therapy. Adipocyte insulin binding was unchanged after 3 mo of therapy, while the maximal rate of peripheral glucose disposal was increased by 23%, indicating enhancement of peripheral insulin action at a postreceptor site(s). Basal hepatic glucose output showed a significant correlation with the fasting serum glucose level both before and after therapy (r = 0.86, P less than 0.001) and fell from 141 +/- 12 mg/m2/min before therapy to 107 +/- 11 mg/m2/min after 3 mo of therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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              Clinical and pathogenic significance of pancreatic-islet-cell antibodies in diabetics treated with oral hypoglycaemic agents.

              20 out of 179 diabetics treated with oral hypoglycaemic agents (O.H.A.) within 3 mo of diagnosis had pancreatic-islet-cell antibodies (ICAb) in their sera at diagnosis or later. 13 of these 20, compared with only 14 of the remaining 159, subsequently required insulin at a mean follow-up of 2 yr 10 mo and 4 yr 11 mo, respectively (p less than 10(-7)). 5 of the 7 ICAb-positive diabetics still continuing on O.H.A. therapy after a mean follow-up of 4 yr 6 mo required maximum or near-maximum combined oral therapy, while only 34 of the 145 ICAb-negative diabetics continuing on O.H.A. did so at a mean follow-up of 5 yr 4 mo (p less than 0.02). In addition, 81 diabetics treated initially with diet for a mean time of 4 yr 7 mo before going on to O.H.A. therapy were studied. All were ICAb-negative when tested at a mean interval of 6 yr 10 mo from diagnosis. By the end of the mean follow-up period of 10 yr 3 mo, 27 were on combined oral therapy and 3 had been transferred to insulin treatment. ICAb-positive diabetics on O.H.A. had a high prevalence of a personal history of organ-specific autoimmune disease, thyrogastric antibodies, a family history of insulin-dependent diabetes and possibly of HLA-B8 comparable to that in insulin-dependent diabetes and higher than that expected in a control population or in diabetics controlled by diet alone. We believe that ICAb-positive diabetes controlled by O.H.A. is an earlier stage in the same disease process (type-I diabetes) that culminates in insulin-dependency.
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                Author and article information

                Journal
                Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy
                Wiley
                02770008
                March 04 1985
                March 04 1985
                January 24 2012
                : 5
                : 2
                : 43-62
                Article
                10.1002/j.1875-9114.1985.tb03404.x
                © 2012

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