Ethyl chlorophenoxyisobutyrate (CPIB) effects in juvenile‐onset diabetes mellitus

Danowski, T. S.; Cohn, Roy; Limaye, Nisha; Novak, Jacqueline; Saul, Robert W.; Sunder, J. H.; Moses, Campbell

doi:10.1002/cpt196566716

Cited by 9 publications

(5 citation statements)

References 2 publications

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“…In patients with coronary heart disease, clofibrate has been reported not to modify (Schwandt, Weisweiler, Neureuther & Wilkening, 1976) or to significantly reduce fasting blood glucose (Enger et al, 1977;Csogor & Bornemisza, 1977). As a rule, fasting blood glucose was unchanged in diabetic patients (Danowski, Cohn, Limaye, Novak, Saul, Sunder & Moses, 1965;Danowski Novak, Saul, Vester & Moses, 1966;Jain, Ryan, McMahon, 1975;Pontirelli, Viberti & Pozza, 1976) but in one study (Ferrari et al, 1977), fasting blood glucose significantly decreased after 5 days of clofibrate administration. In 22 diabetic patients, 11 of whom being insulin-dependent, clofibrate induced a significant reduction in glycosuria (Csogor & Bornemisza, 1977).…”

Section: Discussionmentioning

confidence: 92%

Clofibrate and diabetes control in patients treated with oral hypoglycaemic agents.

Jc¹,

Daigneux²,

Bruwier³

et al. 1979

Brit J Clinical Pharma

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1. Twenty‐two maturity‐onset type diabetics treated with oral hypoglycaemic agents entered a single‐blind crossover study using placebo (periods A and C, 2 months each) and clofibrate (2 g/day; period B; 2 months). 2. In thirteen patients, under reasonably good control, clofibrate did not reduce fasting or post‐prandial blood glucose, nor 24 h glycosuria; no improvement was noted in the M‐value, an index of diabetes control. 3. In contrast, in nine patients, with poor diabetes control, clofibrate reduced 24 h glycosuria and significantly improved the M‐value. 4. In all patients, clofibrate therapy was associated with a significant 19‐23% reduction in plasma fibrinogen. 5. It is suggested that addition of clofibrate may be useful in maturity‐onset diabetics not adequately controlled by diet combined with oral hypoglycaemic agents.

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Section: Discussionmentioning

confidence: 92%

Clofibrate and diabetes control in patients treated with oral hypoglycaemic agents.

Jc¹,

Daigneux²,

Bruwier³

et al. 1979

Brit J Clinical Pharma

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“…In a study of young diabetic patients taking clofibrate for three months, no change was noted in the PBI or T3 red cell uptake. 4 Mogensen,!l however, noted a slight but significant reduction in T3 red cell uptake following clofibrate administration for 3 days, which is compatible with increased binding of thyroid hormones by protein carriers. In vitro studies with clofibrate have shown an increase in TBG binding capacity for thyroxine.…”

Section: D'iscussionmentioning

confidence: 86%

The effects of MK‐185 on thyroid function

Ryan

Jain

Maha

et al. 1971

Clin Pharma and Therapeutics

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significant reduction in serum protein-bound iodine and an increase in triiodothyroxine resin uptake in 11 patients with types III and IV hyperlipoproteinemia. The drug was administered orally at dosages of 10, 15, and 20 mg. per kilogram per day each for a period of 4 weeks, respectively. There were 4 week pre-and posttreatment periods with placebo. The free thyroxine levels and 131 124 hour thyroidal uptake before and after MK-185 therapy did not show significant change. Although thyroid-binding globulin capacity was reduced, the change was not significant. It is proposed that the drug interferes with the binding of thyroxine by plasma proteins.

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“…Data obtained in the first few months and the first year of therapy have been published previously. 4,7,27 The findings herein summarized are based on mean values recorded in the two groups prior to and at the end of 2 to 5 years of therapy. Measurements obtained several times each year were pooled and expressed as the mean value for that interval of time.…”

Section: Clinical Pharmacologymentioning

confidence: 99%