Flaxseed oil prevents trans-10, cis-12-conjugated linoleic acid-induced insulin resistance in mice.

Key Findings:

Conjugated linoleic acid (CLA) includes linoleic acid isomers having conjugated double bonds. Trans-10, cis-12-CLA has been shown in animal work enhance insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) The objective of the present study was to determine if ALA will prevent the development of fatty liver and IR induced by CLA. A small amount of ALA (0.3g/100g diet) prevented the CLA induced IR and significantly decreased the fasting plasma glucose concentration. It also significantly reduced the development of fatty liver; however, it was not a complete prevention. Dietary flax oil increased the hepatic concentration of n-6 PUFA (linoleic acid, arachidonic acid and docosapentaenoic acid) and n-3 PUFA (ALA, EPA and DHA) and decreased the n-6:n-3 PUFA ratio by 71%. The underlying mechanism(s) by which CLA increased and ALA reduced the plasma insulin concentrations are not known.

ABSTRACT:

Insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) are found in 35 and 30% of US adults, respectively. Trans-10, cis12-conjugated linoleic acid (CLA) has been found to cause both these disorders in several animal models. We hypothesised that IR and NAFLD caused by CLA result from n-3 fatty acid deficiency. Pathogen-free C57BL/6N female mice (aged 8 weeks; n 10) were fed either a control diet or diets containing trans-10, cis-12-CLA (0.5%) or CLA + flaxseed oil (FSO) (0.5%) for 8 weeks. Weights of livers, concentration of circulating insulin, values of homeostatic model 1 (HOMA1) for IR and HOMA1 forb cell function were higher by 160, 636, 985 and 968% in the CLA group compared with those in the control group. FSO decreased fasting glucose by 20% and liver weights by 37% compared with those in the CLA group; it maintained circulating insulin, HOMA1-IR and HOMA1 forb cell function at levels found in the control group. CLA supplementation decreased n-6 and n-3 wt% concentrations of liver lipids by 57 and 73% and increased the n-6:n-3 ratio by 58% compared with corresponding values in the control group. FSO increased n-6 and n-3 PUFA in liver lipids by 33 and 342% and decreased the n-6:n-3 ratio by 70% compared with corresponding values in the CLA group. The present results suggest that some adverse effects of CLA may be due to n-3 PUFA deficiency and that these can be corrected by a concomitant increase in the intake of alpha-linolenic acid (ALA), 18:3n-3. (Author’s abstract)