Publications
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Author:
Eriksson, Jan. W. (Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine)
Burén, Jonas (Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine)
Svensson, Maria (Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine)
Olivecrona, Thomas (Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry)
Olivecrona, Gunilla (Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry)
Title:
Postprandial regulation of blood lipids and adipose tissue lipoprotein lipase in type 2 diabetes patients and healthy control subjects
Department:
Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine
Publication type:
Article in journal (Refereed)
Language:
English
Publisher: Elsevier
Status:
Published
In:
Atherosclerosis(ISSN 0021-9150)(EISSN 1879-1484)
Volume:
166
Issue:
2
Pages:
359-367
Year of publ.:
2003
URI:
urn:nbn:se:umu:diva-3934
Permanent link:
http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-3934
Subject category:
Endocrinology and Diabetes
Keywords(en) :
Type 2 diabetes, Adipose tissue, Lipoprotein lipase, Insulin resistance, Glucose uptake, Triglycerides, Free fatty acids, Postprandial
Abstract(en) :

Background/aim: In type 2 diabetes and other insulin-resistant conditions, postprandial hypertriglyceridaemia is an important metabolic perturbation. To further elucidate alterations in the clearance of triglyceride-rich lipoproteins in type 2 diabetes we focused on the nutritional regulation of adipose tissue lipoprotein lipase (LPL).

Subjects and methods: Eight subjects with type 2 diabetes and eight age-, sex- and body mass index (BMI)-matched control subjects underwent subcutaneous abdominal adipose tissue biopsies in the fasting state and 3.5 h following a standardized lipid-enriched meal. LPL activity and mass were measured in adipose tissue and also in plasma after an intravenous injection of heparin.

Results: Postprandial, but not fasting, triglycerides were significantly higher in the diabetic subjects than in the control subjects (3.0±0.4 vs 2.0±0.2 mmol/l, P=0.028). Adipose tissue LPL activity was increased following the meal test by ∼35–55% (P=0.021 and 0.004, respectively). There was no significant difference between the groups in this respect. The specific enzyme activity of LPL was not altered in the postprandial state. Fasting and postprandial adipose tissue LPL activity as well as post-heparin plasma LPL activity tended to be lower among the diabetes patients (NS). There was a significant and independent inverse association between insulin resistance (homeostasis model assessment insulin resistance (HOMA-IR) index) vs post-heparin plasma LPL activity and postprandial triglyceride levels, respectively. Adipose tissue LPL activity was related to insulin action in vitro on adipocyte glucose transport, but not to HOMA-IR.

Conclusion: Following food intake adipose tissue LPL activity is enhanced to a similar degree in patients with type 2 diabetes and in healthy control subjects matched for BMI, age and gender. If LPL dysregulation is involved in the postprandial hypertriglyceridaemia found in type 2 diabetes, it should occur in tissues other than subcutaneous fat.

Available from:
2002-12-06
Created:
2002-12-06
Last updated:
2012-05-16
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