Kobaek-Larsen Morten, Maschek Sina, Kolstrup Stefanie Hansborg, Højlund Kurt, Nielsen Dennis Sandris, Hansen Axel Kornerup, Christensen Lars Porskjær
Department of Clinical Research, University of Southern Denmark, Odense M, Denmark.
Department of Food Science, University of Copenhagen, Frederiksberg C, Denmark.
Clin Transl Sci. 2024 Dec;17(12):e70090. doi: 10.1111/cts.70090.
Type 2 diabetes (T2D) pathophysiology involves insulin resistance (IR) and inadequate insulin secretion. Current T2D management includes dietary adjustments and/or oral medications such as thiazolidinediones (TZDs). Carrots have shown to contain bioactive acetylenic oxylipins that are partial agonists of the peroxisome proliferator-activated receptor γ (Pparg) that mimic the antidiabetic effect of TZDs without any adverse effects. TZDs exert hypoglycemic effects through activation of Pparg and through the regulation of the gut microbiota (GM) producing short-chain fatty acids (SCFAs), which impact glucose and energy homeostasis, promote intestinal gluconeogenesis, and influence insulin signaling pathways. This study investigated the metabolic effects of carrot intake in a T2D mouse model, elucidating underlying mechanisms. Mice were fed a low-fat diet (LFD), high-fat diet (HFD), or adjusted HFD supplemented with 10% carrot powder for 16 weeks. Oral glucose tolerance tests were conducted at weeks 0 and 16. Fecal, cecum, and colon samples, as well as tissue samples, were collected at week 16 during the autopsy. Results showed improved oral glucose tolerance in the HFD carrot group compared to HFD alone after 16 weeks. GM analysis demonstrated increased diversity and compositional changes in the cecum of mice fed HFD with carrot relative to HFD. These findings suggest the potential effect of carrots in T2D management, possibly through modulation of GM. Gene expression analysis revealed no significant alterations in adipose or muscle tissue between diet groups. Further research into carrot-derived bioactive compounds and their mechanisms of action is warranted for developing effective dietary strategies against T2D.
2型糖尿病（T2D）的病理生理学涉及胰岛素抵抗（IR）和胰岛素分泌不足。目前T2D的管理包括饮食调整和/或口服药物，如噻唑烷二酮（TZDs）。胡萝卜已被证明含有生物活性炔基氧化脂质，它们是过氧化物酶体增殖物激活受体γ（Pparg）的部分激动剂，可模拟TZDs的抗糖尿病作用且无任何不良反应。TZDs通过激活Pparg和调节产生短链脂肪酸（SCFAs）的肠道微生物群（GM）发挥降糖作用，SCFAs会影响葡萄糖和能量稳态，促进肠道糖异生，并影响胰岛素信号通路。本研究调查了在T2D小鼠模型中摄入胡萝卜的代谢效应，阐明其潜在机制。给小鼠喂食低脂饮食（LFD）、高脂饮食（HFD）或添加10%胡萝卜粉的调整后HFD，持续16周。在第0周和第16周进行口服葡萄糖耐量试验。在尸检时于第16周收集粪便、盲肠和结肠样本以及组织样本。结果显示，16周后，与单独的HFD组相比，HFD胡萝卜组的口服葡萄糖耐量有所改善。GM分析表明，与HFD相比，喂食含胡萝卜HFD的小鼠盲肠中多样性增加且组成发生变化。这些发现表明胡萝卜在T2D管理中可能具有潜在作用，可能是通过调节GM。基因表达分析显示饮食组之间脂肪或肌肉组织无显著变化。有必要对胡萝卜衍生的生物活性化合物及其作用机制进行进一步研究，以制定有效的抗T2D饮食策略。
