Functional outcomes of molasses and molasses extract on body composition and glucose tolerance

Submission note: A thesis submitted in total fulfilment of the requirements for the degree of Doctor of Philosophy to the School of Psychological Science, Faculty of Science, Technology and Engineering, La Trobe University, Bundoora, Victoria.

The public version of this thesis does not contain all material submitted for examination.

Aim: This thesis investigated long-term administration of molasses extract (ME) (Experiment One) and molasses (Experiment Two) on body composition and glucose tolerance in C57BL-6J mice fed a high-fat diet (HFD, fat content = 22 per cent). Molasses was also investigated (Experiment Three) on body composition and glucose tolerance in C57BL-6J mice with established obesity fed a HFD. In experiments two and three, molasses was obtained from several different sources in order to determine the influence of compositional variations within molasses on physiological and functional outcomes. Method and Results: In the first experiment, mice were fed a HFD with 0 (control), 16 or 32 per cent ME (ME16, ME32) for 18-weeks. ME fed mice had reduced body weight, body fat, epididymal fat and liver weights. Concomitantly, ME-induced increases in energy expenditure (Indirect Calorimetry) and metabolism determined by the up-regulation of hepatic peroxisome proliferatoractivated receptor gamma coactivator-1 alpha (PGC-1α) and peroxisome proliferator-activated receptor alpha (PPARα) mRNA expression, and reduced digestive efficiency (Bomb Calorimetry). ME32 induced down-regulation of inflammatory gene, monocyte chemoattractant protein (MCP-1) and upregulated uncoupling protein 2 (UCP2), possibly a result of reduced hepatic oxidative stress. ME32 also resulted in improved glucose tolerance (Glucose Tolerance Test, GTT) and insulin sensitivity (Insulin Tolerance Test, ITT). In the second experiment, mice were fed a HFD with 0 (control) or 10 per cent molasses (obtained from 4 different sources) for 13-weeks. Molasses induced reductions in body weight and body fat (Dual Energy X-Ray Absorptiometry, DEXA) and epididymal fat weights while kidney weight was increased. Molasses-treated mice had increased faecal energy output and reduced digestive efficiency (Bomb Calorimetry). There was no change in blood glucose (GTT) between molasses-fed and control-fed mice. In the third experiment, mice with established obesity were fed the HFD supplemented with 0 (control) or 10 per cent molasses (obtained from 6 different sources) for 16-weeks. In the main, obese mice treated with molasses had greater antioxidant activity in liver (Oxygen Radical Absorbance Capacity, ORAC) compared with controls. Obese molasses-fed mice showed no change in body composition or in hepatic gene analysis associated with energy expenditure and metabolism (PGC-1α and PPARα), lipolysis (hormone sensitive lipase, HSL), inflammation (MCP-1) or an adaptive response to oxidative stress (UCP2). Glucose tolerance (GTT) was not significantly different between molasses-fed and control-fed mice. Obese molasses-fed mice had increased energy output and reduced digestive efficiency (~ 1.5 per cent) (Bomb Calorimetry). Furthermore, there were no functional or outcome differences between the molasses samples investigated in experiments two and three. Conclusion: The addition of molasses and or its extract attenuated body weight gain caused by consumption of a HFD. Furthermore, the addition of ME to the HFD improved glucose tolerance, markers of inflammation, lipid oxidation and energy expenditure. On the other hand, molasses did not reverse the negative effects associated with obesity. Therefore, the polyphenols derived from sugarcane may be an alternative supplement for the prevention of obesity.