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Clinical Chemistry 50: 2316-2322, 2004. First published September 30, 2004; 10.1373/clinchem.2004.037556
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Right arrow Lipids, Lipoproteins, and Cardiovascular Risk Factors
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(Clinical Chemistry. 2004;50:2316-2322.)
© 2004 American Association for Clinical Chemistry, Inc.


Lipids, Lipoproteins, and Cardiovascular Risk Factors

Relationship between Serum Lipoprotein Ratios and Insulin Resistance in Obesity

Attila Brehm1, Georg Pfeiler1, Giovanni Pacini2, Heinrich Vierhapper1 and Michael Roden1,3,a

1 Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
2 Metabolic Unit, Institute of Biomedical Engineering (ISIB-CNR), Padova, Italy.
3 First Medical Department, Hanusch Hospital, Vienna, Austria.

aAddress correspondence to this author at: First Medical Department, Hanusch Hospital, Heinrich Collin Strasse 30, A-1140 Vienna, Austria. Fax 43-1-91021-85019; e-mail michael.roden{at}meduniwien.ac.at.

Background: The fasting serum lipid profile [triglycerides (TGs), total cholesterol (TC), and LDL- and HDL-cholesterol (LDL-C and HDL-C)] is used to calculate lipid ratios (TC/HDL-C, LDL-C/HDL-C, TG/HDL-C) that allow identification of individuals at increased risk for cardiovascular disease. Because these individuals are also frequently insulin resistant, this study analyzed the relationships between lipid ratios and insulin sensitivity.

Methods: In 132 obese [mean (SE) body mass index, 37.5 (0.6) kg/m2] outpatients without known diabetes mellitus, fasting serum lipid profiles and 75-g oral glucose tolerance tests were performed. Insulin sensitivity was assessed from surrogate estimates for fasting (QUICKI) and dynamic (OGIS) conditions.

Results: After exclusion of other endocrine diseases (n = 35), the remaining patients were classified as glucose tolerant (n = 56), glucose intolerant (n = 22), or as having type 2 diabetes (n = 19). QUICKI and OGIS indicated severe insulin resistance in all individuals with type 2 diabetes and impaired glucose tolerance compared with glucose-tolerant individuals: QUICKI, glucose tolerant, 0.302 (0.002); glucose intolerant, 0.290 (0.002); type 2 diabetes, 0.281 (0.005); P <0.001; OGIS (mL · m–2 · min–1), glucose tolerant, 343 (7), glucose intolerant, 293 (9); type 2 diabetes, 256 (12); P <0.001. Serum TG (P <0.005) and TG/HDL-C ratios (P <0.05) were increased in individuals with impaired glucose tolerance. TG/HDL-C ratios negatively correlated with QUICKI (r = –0.370; P < 0.001) and OGIS (r = –0.333; P < 0.005) in nondiabetic individuals (glucose tolerant plus glucose intolerant), but not in patients with type 2 diabetes (not significant).

Conclusions: This study demonstrates that the TG/HDL-C ratio positively correlates with insulin resistance in severely obese nondiabetic individuals.




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