Effect of clofibrate on glucose tolerance in maturity onset diabetes.

Barnett, David A.; Craig, J.W.; Robinson, Dean W.; Rogers, Mark A.

doi:10.1111/j.1365-2125.1977.tb00761.x

Cited by 31 publications

(14 citation statements)

References 19 publications

(23 reference statements)

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“…Skeletal muscle has been suggested to be the predominant site contributing to basal metabolic rate and thermogenesis in humans. 22 Our strategy to treat obesity entails enhancing thermogenesis in skeletal muscle, potentially by the up-regulation of UCP gene expression.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional regulation of uncoupling protein-2 gene expression in L6 myotubes

Hatakeyama

Scarpace

2001

Int J Obes

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OBJECTIVE:To increase the understanding of the transcriptional regulation of UCP2 gene expression in skeletal muscle cells, we examined the effect of all-trans-retinoic acid (tRA), a ligand (after the conversion to 9-cis-RA) of the retinoid X receptor (RXR), and linolenic acid, a polyunsaturated fatty acid and peroxisome proliferator-activated receptors (PPARs) ligand, on the expression of UCP2 mRNA in cultured L 6 myotubes. RESEARCH METHODS AND PROCEDURES: UCP2 gene expression in L 6 myotubes was confirmed by Northern blot analysis. The time-and concentration-dependency of tRA and linolenic acid on UCP2 gene expression was assessed by dot blot quantification. The mRNA levels of PPAR subtypes (a, g and d) were determined by RT-PCR. RESULTS: tRA induced UCP2 gene expression in a time-and concentration-dependent manner. Similar to tRA, UCP2 mRNA was markedly increased by 0.5 mM linolenic acid. In L 6 myotubes, PPARd mRNA was abundant, whereas PPARa mRNA was lower and PPARg mRNA was minimal. CONCLUSIONS: UCP2 mRNA expression in L 6 myotubes is up-regulated by tRA and linolenic acid, possibly through a mechanism involving PPAR and RXRs.

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Section: Discussionmentioning

confidence: 99%

Transcriptional regulation of uncoupling protein-2 gene expression in L6 myotubes

Hatakeyama

Scarpace

2001

Int J Obes

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“…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: 94%

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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“…In 22 diabetic patients, 11 of whom being insulin-dependent, clofibrate induced a significant reduction in glycosuria (Csogor & Bornemisza, 1977). In 14 maturity-onset diabetics, clofibrate significantly reduced fasting blood glucose (Barnett, Craig, Robinson & Rogers, 1977) and in 12 ketosis-prone insulin-dependent diabetics, Schade, Eaton, George, Conway, Kaminsky & Sivinski (1978) reported that clofibrate treatment resulted in a significant reduction in the concentrations of plasma glucose, ketone bodies and free fatty acids.…”

Section: Discussionmentioning

confidence: 99%

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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Effect of clofibrate on glucose tolerance in maturity onset diabetes.

Cited by 31 publications

References 19 publications

Transcriptional regulation of uncoupling protein-2 gene expression in L6 myotubes

Transcriptional regulation of uncoupling protein-2 gene expression in L6 myotubes

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

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

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