Clustering effects on postprandial insulin secretion and sensitivity in response to meals with different fatty acid compositions

• Published in: Food & function 2014-07, Vol.5 (7), p.1374-138
• Main Authors: Bermudez, Beatriz, Ortega-Gomez, Almudena, Varela, Lourdes M, Villar, Jose, Abia, Rocio, Muriana, Francisco J. G, Lopez, Sergio
• Format: Article
• Language: English
• Subjects: Adult; Blood Glucose - metabolism; Body Mass Index; Cluster Analysis; Diabetes Mellitus, Type 2 - blood; Diet; Dietary Fats - administration & dosage; Fatty Acids, Unsaturated - administration & dosage; Healthy Volunteers; Humans; Hyperlipoproteinemias - blood; Insulin - metabolism; Insulin Resistance; Insulin Secretion; Insulin-Secreting Cells - metabolism; Male; Meals; Oleic Acid - administration & dosage; Palmitic Acid - administration & dosage; Postprandial Period; Triglycerides - blood
• ISSN: 2042-6496; 2042-650X
• DOI: 10.1039/c4fo00067f

Dietary fatty acids play a role in glucose homeostasis. The aim of this study was to assess the individual relationship between dietary saturated (SFA), monounsaturated (MUFA) and polyunsaturated (PUFA) fatty acids with postprandial β-cell function and insulin sensitivity in subjects with normal and high fasting triglycerides. We assessed postprandial β-cell function (by the insulinogenic index and the ratio of the insulin to glucose areas under the time-concentration curve) and insulin sensitivity (by the oral glucose and the minimal model insulin sensitivity indices) over four nonconsecutive, randomly assigned, high-fat meals containing a panel of SFA (palmitic and stearic acids), MUFA (palmitoleic and oleic acids) and PUFA (linoleic and α-linolenic acids) in 14 subjects with normal and in 14 subjects with high fasting triglycerides. The proportions of each fatty acid in the meals and the values for surrogate measures of postprandial β-cell function and insulin sensitivity were subjected to a Pearson correlation and hierarchical cluster analysis, which revealed two classes of dietary fatty acids for regulating postprandial glucose homeostasis. We successfully discriminated the adverse effects of SFA palmitic acid from the beneficial effects of MUFA oleic acid on postprandial β-cell function ( r ≥ 0.84 for SFA palmitic acid and r ≥ −0.71 for MUFA oleic acid; P < 0.05) and insulin sensitivity ( r ≥ −0.92 for SFA palmitic acid and r ≥ 0.89 for MUFA oleic acid; P < 0.001) both in subjects with normal and high fasting triglycerides. In conclusion, dietary MUFA oleic acid, in contrast to SFA palmitic acid, favours the tuning towards better postprandial glycaemic control in subjects with normal and high fasting triglycerides. Postprandial glycaemic control may be at risk from dietary SFA palmitic acid but not SFA stearic acid and may be protected by dietary MUFA oleic acid but not MUFA palmitoleic acid.