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American Journal of Clinical Nutrition 2000-Nov

Diet-induced change in fatty acid composition of plasma triacylglycerols is not associated with change in glucagon-like peptide 1 or insulin sensitivity in people with type 2 diabetes.

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A E Brynes
C M Edwards
A Jadhav
M A Ghatei
S R Bloom
G S Frost

Anahtar kelimeler

Öz

BACKGROUND

Polyunsaturated fatty acids (PUFAs) and monounsaturated fatty acids (MUFAs) have been shown to positively affect blood lipids; however, their comparative effects on insulin sensitivity are unclear.

OBJECTIVE

Our objective was to investigate whether chronic intake of MUFAs or PUFAs improves insulin sensitivity in people with type 2 diabetes via stimulation of the endogenous gut hormone glucagon-like peptide 1 [7-36] amide (GLP-1).

METHODS

Nine overweight people with type 2 diabetes received isoenergetic high-MUFA (20.3 +/- 3.5% of total energy) or high-PUFA (13.4 +/- 1. 3%) diets for 24 d in a randomized, double-blind crossover design.

RESULTS

Weight and glycemic control remained stable throughout the study. Despite a significant change in the plasma triacylglycerol linoleic-oleic acid ratio (L:O) with both diets (MUFA: from 0.46 +/- 0.03 to 0.29 +/- 0.02, P: < 0.005; PUFA: from 0.36 +/- 0.04 to 0.56 +/- 0.05, P: < 0.05) and the phospholipid L:O (1.7 +/- 0.1 to 2.0 +/- 0.3; P: = 0.04) during consumption of the PUFA diet, this change was not associated with a change in insulin sensitivity, measured by the short-insulin-tolerance test. There was a significant reduction in the ratio of total to HDL cholesterol during consumption of the PUFA diet (5.2 +/- 0.4 compared with 4.7 +/- 0.3; P: = 0.005) but no change with the MUFA diet. There was no change in the fasting or postprandial incremental area under the curve in response to an identical standard test meal for glucose, insulin, triacylglycerol, nonesterified fatty acids, or GLP-1.

CONCLUSIONS

Over the 3-wk intervention period, diet-induced change in the triacylglycerol or phospholipid L:O was not associated with either increased stimulation of GLP-1 or a change in insulin sensitivity in people with type 2 diabetes.

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