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Insulin sensitivity is preserved in mice made obese by feeding a high starch diet

Version 3 2024-06-19, 16:32
Version 2 2024-06-05, 11:53
Version 1 2023-02-13, 00:59
journal contribution
posted on 2024-06-19, 16:32 authored by AE Brandon, L Small, TV Nguyen, E Suryana, H Gong, C Yassmin, SE Hancock, T Pulpitel, S Stonehouse, L Prescott, MA Kebede, B Yau, LE Quek, Greg KowalskiGreg Kowalski, Clinton BruceClinton Bruce, N Turner, GJ Cooney
Obesity is generally associated with insulin resistance in liver and muscle and increased risk of developing type 2 diabetes, however there is a population of obese people that remain insulin sensitive. Similarly, recent work suggests that mice fed high carbohydrate diets can become obese without apparent glucose intolerance. To investigate this phenomenon further, we fed mice either a high fat (Hi-F) or high starch (Hi-ST) diet and measured adiposity, glucose tolerance, insulin sensitivity, and tissue lipids compared to control mice fed a standard laboratory chow. Both Hi-ST and Hi-F mice accumulated a similar amount of fat and tissue triglyceride compared to chow-fed mice. However, while Hi-F diet mice developed glucose intolerance as well as liver and muscle insulin resistance (assessed via euglycaemic/hyperinsulinaemic clamp), obese Hi-ST mice maintained glucose tolerance and insulin action similar to lean, chow-fed controls. This preservation of insulin action despite obesity in Hi-ST mice was associated with differences in de novo lipogenesis and levels of C22:0 ceramide in liver and C18:0 ceramide in muscle. This indicates that dietary manipulation can influence insulin action independently of the level of adiposity and that the presence of specific ceramide species correlates with these differences.

History

Journal

eLife

Volume

11

Article number

ARTN e79250

Pagination

e79250-

Location

England

ISSN

2050-084X

eISSN

2050-084X

Language

English

Publication classification

C1 Refereed article in a scholarly journal

Publisher

eLIFE SCIENCES PUBL LTD