Six weeks' sebacic acid supplementation improves fasting plasma glucose, HbA1c and glucose tolerance in db/db mice

• Published in: Diabetes, obesity & metabolism Vol. 12; no. 12; pp. 1120 - 1126
• Main Authors: Membrez, M, Chou, C.J, Raymond, F, Mansourian, R, Moser, M, Monnard, I, Ammon‐Zufferey, C, Mace, K, Mingrone, G, Binnert, C
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.12.2010; Wiley Subscription Services, Inc
• Subjects: Animals; Blood glucose; Blood Glucose - drug effects; Blood Glucose - metabolism; Decanoic Acids - pharmacology; Diabetes; Diabetes mellitus (non-insulin dependent); Diabetes Mellitus, Type 2 - drug therapy; Diabetes Mellitus, Type 2 - metabolism; Dicarboxylic Acids - pharmacology; Dietary supplements; Disease Models, Animal; Fasting; Gene expression; Glucose; glucose metabolism; Glucose tolerance; Glycated Hemoglobin A - metabolism; Hyperglycemia; Insulin secretion; Liver; Male; Mice; Original; Transcriptomics; type 2 diabetes
• ISSN: 1462-8902; 1463-1326
• DOI: 10.1111/j.1463-1326.2010.01308.x

Aim: To investigate the impact of chronic ingestion of sebacic acid (SA), a 10‐carbon medium‐chain dicarboxylic acid, on glycaemic control in a mouse model of type 2 diabetes (T2D). Methods: Three groups of 15 db/db mice were fed for 6 weeks either a chow diet (Ctrl) or a chow diet supplemented with 1.5 or 15% (SA₁.₅% and SA₁₅%, respectively) energy from SA. Fasting glycaemia was measured once a week and HbA1c before and after supplementation. An oral glucose tolerance test (OGTT) was performed at the end of the supplementation. Gene expression was determined by transcriptomic analysis on the liver of the Ctrl and SA₁₅% groups. Results: After 42 days of supplementation, fasting glycaemia and HbA1c were ∼70 and 25% lower in the SA₁₅% group compared with the other groups showing a beneficial effect of SA on hyperglycaemia. During OGTT, plasma glucose area under the curve was reduced after SA₁₅% compared with the other groups. This effect was associated with a tendency for an improved insulin response. In the liver, Pck1 and FBP mRNA were statistically decreased in the SA₁₅% compared with Ctrl suggesting a reduced hepatic glucose output induced by SA. Conclusion: Dietary supplementation of SA largely improves glycaemic control in a mouse model of T2D. This beneficial effect may be due to (i) an improved glucose‐induced insulin secretion and (ii) a reduced hepatic glucose output.