This study tests the hypothesis that improved glycemic control decreases the postprandial plasma triglyceride (TG) response to ingestion of a saturated fat load. Fifteen normotriglyceridemic subjects with insulin-dependent diabetes mellitus (IDDM, group I) and six hypertriglyceridemic subjects with non-insulin-dependent diabetes mellitus (NIDDM, group II) were studied. Each subject was studied before and after 12 days of continuous subcutaneous insulin infusion (CSII). Each subject ingested identical meals on both study days. Plasma glucose was determined in all patients before and two hours after each meal and at 3 AM, and a mean value was calculated for each patient. CSII reduced mean plasma glucose from 252 to 140 mg/dL in group I, and from 209 to 120 mg/dL in group II (P < .001 in both groups, paired t test). Plasma TG levels were measured before and 1.5, 3, 4.5, 6, and 7.5 hours after a breakfast which contained 50 g of mostly saturated fat. A repeated-measures ANOVA was performed to assess the effects of glycemic control (factor A) and TG response (factor B) to fat ingestion. In both groups plasma TG levels increased significantly after fat ingestion (P < .001), and were significantly reduced during improved glycemic control (P < .001). The reduction was observed in 14 of 15 patients in group I and in all patients in group II. In group I the lowering of the postprandial plasma TG levels after CSII was secondary to a decrease in the fasting plasma TG levels, as shown by the unchanged mean percent TG elevation over the baseline. However, in group II, although the fasting levels also decreased, higher mean percent TG increase over the baseline was observed during improved glycemic control, suggesting that the lowering of postprandial TG levels during CSII was not secondary to the decreased baseline. In conclusion, the decrease of postprandial plasma TG observed during improved glycemic control in both IDDM and NIDDM subjects might decrease their risk for atherosclerosis since it would reflect lower levels of chylomicrons and chylomicron remnants which are potentially atherogenic.
Bibliographical noteFunding Information:
Partially supported by Public Health Service Grant RR-0003524 to the Clinical Research Center of the Johns Hopkins University School of Medicine, and by National Heart, Lung. and Blood Institute, contract 2158L (Lipid Research Clinic Program).