Postprandial regulation of blood lipids and adipose tissue lipoprotein lipase in type 2 diabetes patients and healthy control subjects.
OBJECTIVE
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).


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 approximately 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.


CONCLUSIONS
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.
Eriksson
Jan W
JW
Department of Medicine, Umeå University Hospital, Umea, Sweden. jan.eriksson@medicin.umu.se
Burén
Jonas
J
Svensson
Maria
M
Olivecrona
Thomas
T
Olivecrona
Gunilla
G
D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology; D000704:Analysis of Variance; D001774:Blood Chemical Analysis; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000378:metabolism*; D004041:Dietary Fats / Q000008:administration & dosage*; D005215:Fasting; D005260:Female; D006801:Humans; D007333:Insulin Resistance; D008071:Lipoprotein Lipase / Q000097:blood / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D019518:Postprandial Period; D011336:Probability; D012016:Reference Values; D012680:Sensitivity and Specificity; D014280:Triglycerides / Q000032:analysis / Q000378:metabolism*
D001786:Blood Glucose; D004041:Dietary Fats; D014280:Triglycerides; D008071:Lipoprotein Lipase