Aims/Introduction
Preprandial metformin administration significantly reduces postprandial plasma triglyceride levels in animal studies by reducing intestinal absorption through delayed gastric emptying. However, this effect has not been shown in a clinical study. Therefore, we planned to investigate the efficacy of preprandial metformin administration on postprandial hypertriglyceridemia and the related gastrointestinal effects in patients with type 2 diabetes mellitus.
Materials and Methods
A total of 11 patients taking single‐dose metformin at 500–1,000 mg, with non‐fasting plasma triglyceride levels of 150–1,000 mg/dL, were recruited at a single university hospital. The difference between preprandial and postprandial metformin administration on postprandial hypertriglyceridemia was examined by a meal test. The gastrointestinal effects of metformin, including stomach heaviness, heartburn and satiety, were also assessed using a visual analog scale.
Results
The mean bodyweight of patients was 80.6 kg (body mass index 27.9 kg/m2), and the mean non‐fasting plasma triglyceride level was 275.9 ± 57.0 mg/dL. The area under the curve of triglyceride during the meal test was significantly lower in the preprandial protocol than in the postprandial protocol (P < 0.05). Compared with postprandial administration, preprandial administration of metformin increased satiety (P = 0.036) without stomach heaviness or heartburn.
Conclusions
Preprandial metformin administration significantly reduced plasma triglyceride level during meal testing without marked exacerbation of gastrointestinal adverse effects. The present results suggest that a simple change in the timing of metformin administration represents a novel approach for enhancing triglyceride‐lowering strategies in patients with type 2 diabetes mellitus and postprandial hypertriglyceridemia.
We herein report a case involving a woman with type 1 diabetes and a history of metal allergy who developed a local delayed-type (type IV) allergy to zinccontaining insulin. She had been treated by continuous subcutaneous insulin infusion, but her glycemic control was poor, and she developed diabetic ketoacidosis. Her plasma insulin concentration was unexpectedly low during use of insulin lispro, but it was recovered by changing from the zinc-containing insulin lispro to the zinc-free insulin glulisine. Intradermal tests showed no reactions to various insulins except for zinc chloride. A skin biopsy at the injection site of insulin lispro showed invasion of lymphocytes, neutrophils, and eosinophils, but a skin biopsy at the injection site of insulin glulisine showed invasion of only lymphocytes. A drug lymphocyte stimulation test against polaprezinc, an antiulcer drug containing zinc, was positive. Therefore, we diagnosed the patient with local delayed allergy to zinc-containing insulin. Insulin allergy should be considered as a possible cause of poor glycemic control and diabetic ketoacidosis in patients with type 1 diabetes.
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