Oral Presentation Australian and New Zealand Obesity Society Annual Scientific Conference 2026

A palatable high carbohydrate diet rapidly improves glucose tolerance in high-fat diet fed mice without changes in adiposity. (147734)

Lewin Small 1 2 , Jinfeng (Sophia) Lin 3 4 , Carsten Schmitz-Peiffer 2 3 , Sarah E Hancock 1 , Nigel Turner 1 , Gregory J Cooney 3 4 , Amanda E Brandon 3
  1. Victor Chang Cardiac Research Institute , Sydney, NSW
  2. School of Life and Environmental Science, The University of Sydney, Sydney, NSW, Australia
  3. Charles Perkins Centre, The University of Sydney, Sydney, NSW, Australia
  4. School of Medical Sciences, The University of Sydney, Sydney, NSW, Australia

Feeding mice a high fat, low carbohydrate (Hi-F) diet results in obesity and glucose intolerance. Switching from a Hi-F back to a chow has been shown to reverse the diet-induced glucose intolerance within a week. However, this improvement was associated with a decrease in food intake, body fat content and tissue lipid levels [1]. This makes it difficult to conclude whether a change of diet or loss of fat leads to improved glucose homeostasis. We have shown that feeding a palatable high-starch (Hi-ST) diet produced obesity while maintaining glucose tolerance. We have used this model to investigate whether switching diet composition between Hi-F and Hi-ST can alter glucose tolerance without changing body composition.

 

Mice were fed either chow, Hi-F or Hi-ST diet for 12 weeks. After this initial feeding period, mice in the Hi-F group were switched from Hi-ST and Hi-ST switched Hi-F for 7 days. Body composition, food intake and glucose tolerance were assessed before and after switch.

 

Energy intake and fat mass were similarly increased in the Hi-F and Hi-ST mice compared to chow and this did not change after the 7-day switch. Prior to the switch, Hi-F mice were glucose intolerant, while H-ST were similar to chow controls. After only 7 days of diet switch, the Hi-STàHi-F became glucose intolerant, while the Hi-FàHi-ST had glucose tolerance similar to chow controls. This improvement was not associated with changes in total liver triglyceride levels, but there was an enrichment in 16C lipid species, likely a result of increased levels of enzymes involved in de novo lipogenesis.

 

Collectively these findings suggest that variations in glucose homeostasis in mice are largely independent of whole-body adiposity level and more closely associated with the ratio of macronutrients in a diet.

  1. Kowalski, G.M., et al., Reversing diet-induced metabolic dysregulation by diet switching leads to altered hepatic de novo lipogenesis and glycerolipid synthesis. Sci Rep, 2016. 6: p. 27541.