High-fat diet induced obesity and the effect of fructooligosaccharides on cardiac protein expression

ABSTRACT

Hypothesis: Obesity alters cardiac protein expression. Fructooligosaccharide modulates this effect. Design and Methodology: Rats fed AIN-93G chow were subsequently fed high-fat AIN-93G. The top 40% weight-gain category were allocated into control (CON), highfat (HF) and high-fat with fructooligosaccharide (HF-FOS) groups; n=10. Body weights were monitored. After 12 weeks, left ventricles were cryopreserved. Serum was stored for glucose and insulin estimations. Tissues were analysed by mass spectrometry using an Orbitrap with a nanospray source and EASY-nLC nano-LC system(ThermoFisher, San Jose, CA). Spectra were analysed with Sequest and fold changes with Scaffold Q+ (Proteome Software Inc., Portland, OR). T-Tests detected differentially expressed proteins (CON vs HF and HF vs HF-FOS) and mean (±SE) differences in body weights, glucose and insulin. The Database for Annotation, Visualization and Integrated Discovery and the Kyoto Encyclopedia of Genes and Genomes revealed pathways containing overrepresented proteins. Hematoxylin and eosin sections were graded for hypertrophy and chi-squared analyses sought differences. A p-value of <0.05 was considered significant with Benjamini­Hochberg corrections where applicable. Results: HF rats (549.4±17.1g) were significantly (p<0.05) heavier than CON (513.6±14.8g). Twenty-three proteins involved in mitochondrial function and lipid metabolism were differentially expressed (p<0.001) between the CON and HF. One hundred and thirty-two proteins involved in contractility, lipid/carbohydrate metabolism and signaling were differentially expressed (p<0.001) between HF and HF-FOS. HF cardiomyocytes were significantly (p<0.001) more hypertrophic than CON. Conclusion: High-fat feeding is associated with subclinical deviations in the cardiac proteome. Coupled to cellular hypertrophy this may influence myocardial compliance. Fructooligosaccharides modulates protein expression.