Metabolic Implications of Dietary Trans-Fatty Acids

Obesity (Silver Spring). 2009 Jun;17(6):1200-7. doi: 10.1038/oby.2008.662. Epub 2009 Feb 19.

Abstract

Dietary trans-fatty acids are associated with increased risk of cardiovascular disease and have been implicated in the incidence of obesity and type 2 diabetes mellitus (T2DM). It is established that high-fat saturated diets, relative to low-fat diets, induce adiposity and whole-body insulin resistance. Here, we test the hypothesis that markers of an obese, prediabetic state (fatty liver, visceral fat accumulation, insulin resistance) are also worsened with provision of a low-fat diet containing elaidic acid (18:1t), the predominant trans-fatty acid isomer found in the human food supply. Male 8-week-old Sprague-Dawley rats were fed a 10% trans-fatty acid enriched (LF-trans) diet for 8 weeks. At baseline, 3 and 6 weeks, in vivo magnetic resonance spectroscopy (1H-MR) assessed intramyocellular lipid (IMCL) and intrahepatic lipid (IHL) content. Euglycemic-hyperinsulinemic clamps (week 8) determined whole-body and tissue-specific insulin sensitivity followed by high-resolution ex vivo 1H-NMR to assess tissue biochemistry. Rats fed the LF-trans diet were in positive energy balance, largely explained by increased energy intake, and showed significantly increased visceral fat and liver lipid accumulation relative to the low-fat control diet. Net glycogen synthesis was also increased in the LF-trans group. A reduction in glucose disposal, independent of IMCL accumulation was observed in rats fed the LF-trans diet, whereas in rats fed a 45% saturated fat (HF-sat) diet, impaired glucose disposal corresponded to increased IMCLTA. Neither diet induced an increase in IMCLsoleus. These findings imply that trans-fatty acids may alter nutrient handling in liver, adipose tissue, and skeletal muscle and that the mechanism by which trans-fatty acids induce insulin resistance differs from diets enriched with saturated fats.

MeSH terms

  • Adiposity*
  • Animals
  • Blood Glucose / metabolism
  • Diet, Fat-Restricted*
  • Energy Intake
  • Energy Metabolism
  • Glucose Clamp Technique
  • Glycogen / metabolism
  • Hyperphagia / etiology
  • Hyperphagia / metabolism
  • Hyperphagia / physiopathology
  • Insulin / blood
  • Insulin Resistance*
  • Intra-Abdominal Fat / metabolism
  • Liver / metabolism
  • Magnetic Resonance Spectroscopy
  • Male
  • Metabolic Syndrome / etiology*
  • Metabolic Syndrome / metabolism
  • Metabolic Syndrome / physiopathology
  • Muscle, Skeletal / metabolism
  • Obesity / etiology*
  • Obesity / metabolism
  • Obesity / physiopathology
  • Oleic Acid / administration & dosage
  • Oleic Acid / adverse effects
  • Oleic Acid / metabolism*
  • Oleic Acids
  • Prediabetic State / etiology*
  • Prediabetic State / metabolism
  • Prediabetic State / physiopathology
  • Rats
  • Rats, Sprague-Dawley
  • Time Factors
  • Trans Fatty Acids / administration & dosage
  • Trans Fatty Acids / adverse effects
  • Trans Fatty Acids / metabolism*

Substances

  • Blood Glucose
  • Insulin
  • Oleic Acids
  • Trans Fatty Acids
  • Oleic Acid
  • elaidic acid
  • Glycogen