Atromid in the treatment of post-climacteric diabetes

Miller, R. David

doi:10.1016/s0368-1319(63)80054-x

Cited by 17 publications

(7 citation statements)

References 4 publications

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“…I t has been known that clofibrate may improve glucose tolerance in diabetic subjects (1)(2)(3)(4). However, most of these studies were not performed systematically on NIDDM subjects, and the effect of diet therapy may cause improvement of glucose metabolism.…”

Section: Discussionmentioning

confidence: 99%

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Improvement of Glucose Tolerance in NIDDM by Clofibrate Randomized Double-Blind Study

et al. 1988

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A randomized double-blind study was performed to examine the effect of clofibrate on glucose tolerance in subjects with non-insulin-dependent diabetes mellitus (NIDDM). Clofibrate (1.5 g/day) or placebo was administered to 70 patients and an oral glucose tolerance test (OGTT) was performed before and 12 wk after treatment. Blood glucose levels were significantly improved in clofibrate-treated groups at all time points during OGTT, whereas there was no change in insulin levels. Improvement of fasting glucose levels required 8 wk of clofibrate treatment. Insulin binding to erythrocytes demonstrated no significant change in the clofibrate-treated subjects. These results suggest that clofibrate improves glucose tolerance in NIDDM subjects without a change in insulin receptors and that clofibrate increases insulin sensitivity through an unknown postreceptor mechanism.

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Section: Discussionmentioning

confidence: 99%

“…It has been reported by several investigators that treatment with clofibrate improves glucose tolerance (1)(2)(3)(4), but other investigators reported that clofibrate did not have any effect on glucose tolerance (5,6). However, except for the study on insulin-dependent diabetic (IDDM) subjects re-…”

mentioning

confidence: 99%

Improvement of Glucose Tolerance in NIDDM by Clofibrate Randomized Double-Blind Study

et al. 1988

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“…An improvement of glucose tolerance in diabetics treated with clofibrate was first reported in 1963 (Miller, 1963;Herriot, Percy-Robb, Strong & Thompson, 1963). This and subsequent evidence (Berkowitz, 1971;Danowski, Cohn, Limaye, Novak, Saul, Sunder & Moses, 1965;Danowski, Novak, Saul, Vester & Moses, 1966; Narduzzi, Danowski, Weir, Alley, Vester & Moses, 1967;Vester, Sunder, Aarons & Danowski, 1970) has not led to general use of clofibrate as a specific treatment of diabetes because the effect has not been reliably reproduced.…”

Section: Introductionmentioning

confidence: 88%

Effect of clofibrate on glucose tolerance in maturity onset diabetes.

Barnett¹,

Craig²,

Robinson³

et al. 1977

Brit J Clinical Pharma

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1 Fourteen maturity onset diabetics showed improvement of glucose tolerance while on treatment with clofibrate. Fasting blood glucose levels were reduced by 20% after treatment for 14 and 28 days. 2 The effect was found to be independent of concurrent treatment with oral hypoglycaemic drugs. 3 Plasma insulin levels were also lower during clofibrate treatment. 4 Clofibrate may prove to be a useful adjunct to the treatment of maturity onset diabetes.

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“…The glucose-lowering effect of clofibrate in normal (Ferrari et al, 1978), non-insulin dependent diabetic (Bamett et al, 1977) and in insulin dependent diabetic patients (Miller, 1963, Schade et al, 1978 has been recognized, but its mechanism remains unknown. The study reported here was designed to clarify the glucoselowering mechanism by clofibrate in non-insulin dependent diabetics receiving diet therapy alone.…”

Section: Introductionmentioning

confidence: 99%

Clofibrate enhances the affinity of insulin receptors in non‐insulin dependent diabetes mellitus.

Murakami¹,

Nambu²,

Koh³

et al. 1984

Brit J Clinical Pharma

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Glucose-lowering mechanism by clofibrate was studied in non-insulin dependent diabetics managed with dietary therapy alone. Clofibrate 1500 mg was administered for 1 month to 15 patients, and 75 g oral glucose tolerance test and insulin tolerance test were carried out before and after 1 month of the treatment. Fasting plasma glucose values were decreased from 9.34 + 0.53 mmol/l to 7.58 ± 0.33 mmol/l (P < 0.01), and fasting insulin levels were decreased from 13.8 ± 1.7 ,uu/ml to 10.1 + 1.5 5,u/ml (P < 0.05). However, insulinogenic index and 2IRI/Eglucose ratio during 75 g oral glucose tolerance test were not changed. Enhanced glucose fall in insulin tolerance test was also observed. As these results suggested the enhanced tissue sensitivity to insulin, we examined the insulin binding to erythrocytes before and at 3 months' treatment of clofibrate in 10 non-insulin dependent diabetics. Insulin bindings were increased from 3.41 ± 0.17% to 4.11 + 0.20% in the presence of 1 ng/ml of native insulin (P < 0.01). This increased binding was due to an increased affinity without a change in the number of insulin receptors. These results suggest that improved glucose tolerance by clofibrate might be derived from the enhanced tissue sensitivity to insulin, probably through an enhanced affinity of insulin receptors.

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Atromid in the treatment of post-climacteric diabetes

Cited by 17 publications

References 4 publications

Improvement of Glucose Tolerance in NIDDM by Clofibrate Randomized Double-Blind Study

Improvement of Glucose Tolerance in NIDDM by Clofibrate Randomized Double-Blind Study

Effect of clofibrate on glucose tolerance in maturity onset diabetes.

Clofibrate enhances the affinity of insulin receptors in non‐insulin dependent diabetes mellitus.

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