ArticleObesity (Silver Spring, Md.)2024
Gastric bypass elicits persistent gut adaptation and unique diabetes remission-related metabolic gene regulation.
Article in Obesity (Silver Spring, Md.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02710370 (Intestinal Metabolic Reprogramming as a Key Mechanism of Gastric Bypass in Humans), which is not on this map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Intestinal Metabolic Reprogramming as a Key Mechanism of Gastric Bypass in Humans
Who cites it
1 citing paper in PubMed.
- Roux-en-Y Gastric Bypass is Associated With Increased Intestinal Glucose Uptake in Humans.Journal of the Endocrine Society · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
objectiveWe 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.
methodsWe determined GE by RNA sequencing in jejunum (Roux limb [RL]) collected from 28 patients before and 12 months after RYGB.
resultsGlobal 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.
conclusionsRL 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.
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