Background The metabolic effects and mechanism of action ofmetformin are still poorly understood, despite the fact thatit has been used to treat patients with non-insulin-dependentdiabetes mellitus (NIDDM) for more than 30 years.
Methods In 10 obese patients with NIDDM, we used a combinationof isotope dilution, indirect calorimetry, bioimpedance, andtissue-balance techniques to assess the effects of metforminon systemic lactate, glucose, and free-fatty-acid turnover;lactate oxidation and the conversion of lactate to glucose;skeletal-muscle glucose and lactate metabolism; body composition;and energy expenditure before and after four months of treatment.
Results Metformin treatment decreased the mean (±SD)glycosylated hemoglobin value from 13.2±2.2 percent to10.5±1.6 percent (P<0.001) and reduced fasting plasmaglucose concentrations from 220±41 to 155±28 mgper deciliter (12.2±0.7 to 8.6±0.5 mmol per liter)(P<0.001). Although resting energy expenditure did not change,the patients lost 2.7±1.3 kg of weight (P<0.001),88 percent of which was adipose tissue. The mean (±SE)rate of plasma glucose turnover (hepatic glucose output andsystemic glucose disposal) decreased from 2.8±0.2 to2.0±0.2 mg per kilogram of body weight per minute (15.3±0.9to 10.8±0.9 µmol per kilogram per minute) (P<0.001),as a result of a decrease in hepatic glucose output; systemicglucose clearance did not change. The rate of conversion oflactate to glucose (gluconeogenesis) decreased by 37 percent(P<0.001), whereas lactate oxidation increased by 25 percent(P<0.001). There were no changes in the plasma lactate concentration,plasma lactate turnover, muscle lactate release, plasma free-fatty-acidturnover, or uptake of glucose by muscle.
Conclusions Metformin acts primarily by decreasing hepatic glucoseoutput, largely by inhibiting gluconeogenesis. It also seemsto induce weight loss, preferentially involving adipose tissue.
Source Information
From the University of Rochester School of Medicine, Rochester, New York (M.S., N.N., G.P., J.E.G.), and the Division of Endocrinology and Metabolism, Scripps Clinic, La Jolla, Calif. (G.D.).
Address reprint requests to Dr. Gerich at the University of Rochester School of Medicine, 601 Elmwood Ave., Box Med/CRC, Rochester, NY 14642.
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