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Comparison of clofibrate with halofenate in diabetics with hyperlipidaemia
Insights
Clofibrate and halofenate showed modest triglyceride and urate reductions in maturity-onset diabetics with hyperlipidaemia. Neither drug is recommended due to limited efficacy and adverse reactions.
Area of Science:
- Endocrinology
- Metabolic Diseases
- Pharmacology
Background:
- Hyperlipidaemia is a common comorbidity in maturity-onset diabetes.
- Effective management of dyslipidemia in diabetic patients is crucial for preventing cardiovascular complications.
Purpose of the Study:
- To compare the efficacy and safety of clofibrate and halofenate in treating hyperlipidaemia in maturity-onset diabetics.
- To evaluate the effects of these agents on serum lipids, urate levels, and glycemic control.
Main Methods:
- A 48-week, double-blind, randomized study.
- Inclusion of maturity-onset diabetic patients with hyperlipidaemia.
- Administration of clofibrate and halofenate, with assessment of clinical and biochemical parameters.
Main Results:
- Both drugs slightly lowered serum cholesterol and modestly, transiently reduced triglyceride levels.
- Both significantly reduced serum urate, with halofenate showing a greater effect.
- Halofenate demonstrated a notable hypoglycaemic effect, unlike clofibrate.
- Adverse reactions led to premature discontinuation in approximately 20% of patients.
Conclusions:
- Neither clofibrate nor halofenate demonstrated sufficient efficacy or safety for managing hyperlipidaemia in maturity-onset diabetics.
- The observed adverse effects and limited lipid-lowering capacity do not support their use in this patient population.
Abstract:
In a double-blind, randomized study which lasted 48 weeks the effects of clofibrate and halofenate were compared in maturity-onset diabetics with hyperlipidaemia. With the use of both clofibrate and halofenate serum cholesterol values were lowered only slightly. Both agents significantly reduced triglyceride values, but the decreases were modest and transient. Both drugs significantly lowered serum urate values, although the effect of halofenate was distinctly greater. Halofenate, but not clofibrate, had a considerable hypoglycaemic effect on the patients, most of whom were also receiving oral antidiabetic medicines. The drugs produced a number of clinical and biochemical adverse reactions, and in about 20% of all patients the trial had to be discontinued prematurely. The management of hyperlipidaemia in maturity-onset diabetics is briefly discussed, and it is concluded that neither clofibrate nor halofenate is to be recommended.
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