| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Department of Clinical and Experimental Medicine (A.A.R., C.D.N., L.D.M., L.P., C.I., S.C., G.R., G.A.), Federico II University, 80131 Naples, Italy; and Department of Endocrinology and Metabolism, University of Pisa (S.D.P.), 56124 Pisa, Italy
Address all correspondence and requests for reprints to: Dr. Angela A. Rivellese, Department of Clinical and Experimental Medicine, Medical School, Federico II University, Via S. Pansini 5, 80131 Naples, Italy. E-mail: rivelles{at}unina.it.
The aim of this study was to evaluate exogenous and endogenous lipoprotein responses to a standard fat-rich meal in type 2 diabetic patients with optimal fasting triglyceridemia and optimal blood glucose control. Seven type 2 diabetic patients and five nondiabetic controls (age, 49 ± 7 and 48 ± 4 yr; body mass index, 28.3 ± 3.6 and 25.1 ± 3.6 kg/m2; mean ± SD) were given, after at least 12 h of fasting, a standard fat-rich meal. Before and over the 6 h after the meal, serial blood samples were taken for determination of glucose, insulin, lipids, lipoproteins, apolipoprotein B-48 (apo B-48), apo B-100, free fatty acids, and lipoprotein lipase activity. The main abnormality in the postprandial lipid response of diabetic patients involved large very low density lipoproteins. In these particles, apo B-48, apo B-100, cholesterol, and triglyceride incremental areas were, in fact, significantly higher in diabetics compared with controls [7.08 ± 2.65 vs. 1.17 ± 0.88 mg/liter·h, 65.5 ± 11.5 vs. 12.4 ± 1.77 mg/liter·h, 29.7 ± 3.9 vs. 13.1 ± 3.1 mg/dl·h (0.77 ± 0.10 vs. 0.34 ± 0.08 mmol/liter·h), 170 ± 31 vs. 94 ± 22 mg/dl·h (1.93 ± 0.35 vs. 1.06 ± 0.25 mmol/liter·h)] (all P < 0.05; mean ± SEM). Postprandial preheparin lipoprotein lipase plasma activity was, if anything, higher in diabetic patients. In conclusion, even with fasting normotriglyceridemia and optimal blood glucose control, type 2 diabetic patients are characterized, in the postprandial period, by a significant increase in large very low density lipoproteins of both endogenous and exogenous origins.
This work was supported by a grant from the Ministry of Health (ICS 110.1/RF 98.97).
Abbreviations: apo, Apolipoprotein; FFA, free fatty acid; HDL, high-density lipoprotein; HL, hepatic lipase; IDL, intermediate-density lipoprotein; LDL, low-density lipoprotein; LPL, lipoprotein lipase; Sf, Svedberg flotation unit; VLDL, very LDL.
This article has been cited by other articles:
![]() |
S. S Lund, L. Tarnow, M. Frandsen, U. M Smidt, O. Pedersen, H.-H. Parving, and A. A Vaag Impact of metformin versus the prandial insulin secretagogue, repaglinide, on fasting and postprandial glucose and lipid responses in non-obese patients with type 2 diabetes Eur. J. Endocrinol., January 1, 2008; 158(1): 35 - 46. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Shah, B. Adams-Huet, L. Brinkley, S. M. Grundy, and A. Garg Lipid, Glycemic, and Insulin Responses to Meals Rich in Saturated, cis-Monounsaturated, and Polyunsaturated (n-3 and n-6) Fatty Acids in Subjects With Type 2 Diabetes Diabetes Care, December 1, 2007; 30(12): 2993 - 2998. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. L. Isley, J. M. Miles, B. W. Patterson, and W. S. Harris The effect of high-dose simvastatin on triglyceride-rich lipoprotein metabolism in patients with type 2 diabetes mellitus J. Lipid Res., January 1, 2006; 47(1): 193 - 200. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Annuzzi, C. De Natale, C. Iovine, L. Patti, L. Di Marino, S. Coppola, S. Del Prato, G. Riccardi, and A. A. Rivellese Insulin Resistance Is Independently Associated With Postprandial Alterations of Triglyceride-Rich Lipoproteins in Type 2 Diabetes Mellitus Arterioscler. Thromb. Vasc. Biol., December 1, 2004; 24(12): 2397 - 2402. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |