内科学
内分泌学
胰岛素抵抗
胰岛素
脂肪生成
神经酰胺
人口
肥胖
生物
甘油三酯
2型糖尿病
糖尿病
葡萄糖钳夹技术
糖耐量试验
脂肪组织
胰岛素敏感性
医学
胆固醇
生物化学
细胞凋亡
环境卫生
作者
Amanda E. Brandon,Lewin Small,Tuong-Vi Nguyen,Eurwin Suryana,Henry Gong,Christian Yassmin,Sarah Hancock,Tamara Pulpitel,Sophie Stonehouse,Leteisha Prescott,Melkam A. Kebede,Belinda Yau,Lake‐Ee Quek,Greg M. Kowalski,Clinton R. Bruce,Nigel Turner,Gregory J. Cooney
标识
DOI:10.1101/2022.05.25.493410
摘要
Abstract 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 euglycemic/hyperinsulinemic 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 correlate with these differences.
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