Division of Endocrinology, Boston Children's Hospital, Boston, Massachusetts, USA.
Harvard Medical School, Boston, Massachusetts, USA.
Obesity (Silver Spring). 2024 Nov;32(11):2135-2148. doi: 10.1002/oby.24135. Epub 2024 Oct 15.
We have previously shown that early intestinal adaptation precedes and relates to metabolic improvement in humans after Roux-en-Y gastric bypass surgery (RYGB). We hypothesized that intestinal adaptation would persist at the 1-year postoperative time point and that gene expression (GE) signatures would relate to type 2 diabetes remission, providing insight into potential mechanisms for intestinally mediated metabolic improvement after RYGB.
We determined GE by RNA sequencing in jejunum (Roux limb [RL]) collected from 28 patients before and 12 months after RYGB.
Global GE from paired baseline and 1-year jejunal samples did not separate according to clinical phenotype (type 2 diabetes remission, sustained weight loss). In general, GE was consistent with persistent RL remodeling, and microvilli were elongated by 39%. Remodeling was not attenuated in patients with lack of diabetes remission or with weight regain. Patients with diabetes remission demonstrated greater jejunal activation of lipogenesis-related pathways driven by RXR, LXR, and SREBP.
RL adaptation is a key feature of RYGB in all patients, likely reflecting the dramatic alterations to gastrointestinal anatomy, but jejunal lipogenesis appears to be more strongly activated in those patients with diabetes remission. Further study is needed to understand whether these pathways may drive metabolic remission after RYGB.
我们之前的研究表明,在 Roux-en-Y 胃旁路手术(RYGB)后,人类早期肠道适应先于并与代谢改善相关。我们假设肠道适应将在术后 1 年的时间点持续存在,并且基因表达(GE)特征与 2 型糖尿病缓解相关,这为 RYGB 后肠道介导的代谢改善的潜在机制提供了深入了解。
我们通过 RNA 测序确定了来自 28 例患者术前和 RYGB 术后 12 个月的空肠(Roux 袢[RL])中的 GE。
根据临床表型(2 型糖尿病缓解,持续体重减轻),配对基线和 1 年空肠样本的整体 GE 并未分离。一般来说,GE 与 RL 持续重塑一致,微绒毛伸长了 39%。在糖尿病缓解缺乏或体重增加的患者中,重塑并未减弱。糖尿病缓解患者的 RXR、LXR 和 SREBP 驱动的脂生成相关途径的空肠激活更大。
RL 适应是所有患者 RYGB 的一个关键特征,可能反映了胃肠道解剖结构的剧烈改变,但在糖尿病缓解患者中,空肠脂生成似乎更强烈地激活。需要进一步研究以了解这些途径是否可能在 RYGB 后驱动代谢缓解。