Mechanisms of diabetes improvement following bariatric/metabolic surgery
Open accessAbstract
More than 20 years ago, Pories et al. published a seminal article, "Who Would Have Thought It? An Operation Proves to Be the Most Effective Therapy for Adult-Onset Diabetes Mellitus." This was based on their observation that bariatric surgery rapidly normalized blood glucose levels in obese people with type 2 diabetes mellitus (T2DM), and 10 years later, almost 90% remained diabetes free. Pories et al. suggested that caloric restriction played a key role and that the relative contributions of proximal intestinal nutrient exclusion, rapid distal gut nutrient delivery, and the role of gut hormones required further investigation. These findings of T2DM improvement/remission after bariatric surgery have been widely replicated, together with the observation that bariatric surgery prevents or delays incident T2DM. Over the ensuing two decades, important glucoregulatory roles of the gastrointestinal (GI) tract have been firmly established. However, the physiological and molecular mechanisms underlying the beneficial glycemic effects of bariatric surgery remain incompletely understood. In addition to the mechanisms proposed by Pories et al., changes in bile acid metabolism, GI tract nutrient sensing and glucose utilization, incretins, possible anti-incretin(s), and the intestinal microbiome are implicated. These changes, acting through peripheral and/or central pathways, lead to reduced hepatic glucose production, increased tissue glucose uptake, improved insulin sensitivity, and enhanced β-cell function. A constellation of factors, rather than a single overarching mechanism, likely mediate postoperative glycemic improvement, with the contributing factors varying according to the surgical procedure. Thus, different bariatric/metabolic procedures provide us with experimental tools to probe GI tract physiology. Embracing this approach through the application of detailed phenotyping, genomics, metabolomics, and gut microbiome studies will enhance our understanding of metabolic regulation and help identify novel therapeutic targets.
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Acute caloric restriction and the immediate dramatic increase in GLP-1 after surgery largely contribute to the improvement in glycemia seen within days.
“the acute caloric restriction and the immediate dramatic increase in the levels of the gut peptide glucagon-like peptide (GLP)-1 after surgery largely contribute to the immense improvement in glycemia seen within days of the procedure [39, 47]”
From Bariatric surgery: remission of inflammation, cardiometabolic benefits, and common adverse effects (2020) · cites this paper as [47]
Modifications in gut hormones, neural signaling, appetite suppression, and weight loss result in improved glucose homeostasis and amelioration or resolution of diabetes.
“Modifications in the gut hormones coupled with appropriate alterations in neural signaling and appetite suppression, and the associated impressive weight loss following bariatric procedures result in improved glucose homeostasis and amelioration or complete resolution of diabetes [47].”
From Bariatric surgery: remission of inflammation, cardiometabolic benefits, and common adverse effects (2020) · cites this paper as [47]
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- Authors
- Batterham, R. L., & Cummings, D. E.
- Affiliations
- University College Hospital (GB)
- University of Washington (US)
- Corresponding author
- Batterham, Rachel L.
- ORCID
- Batterham, Rachel L.
- Venue
- Diabetes Care
- Publisher
- American Diabetes Association
- Published
- 2016-05-13
- Volume
- 39
- Issue
- 6
- Pages
- 893-901
- ISSN
- 0149-5992 (ISSN-L)
- 1935-5548
- PMC
- PMC5864134
- OpenAlex
- W2399832243
- Cited by
- 376
- References
- 65
- Citations by year
- 2026: 22 · 2025: 24 · 2024: 24 · 2023: 33 · 2022: 23 · 2021: 54 · 2020: 51 · 2019: 54 · 2018: 38 · 2017: 41 · 2016: 10 · 2014: 1
- FWCI
- 52.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes Care (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Rosetrees Trust
- Stoneygate Trust
- National Institute of Diabetes and Digestive and Kidney Diseases (RO1-DK-103842, RO1-DK-084324, RO1-DK-089528, U34-DK-107917)
- Topics
- Health Sciences › Medicine › Surgery › Bariatric Surgery and Outcomes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Keywords
- bariatric surgery, metabolic surgery, type 2 diabetes, diabetes remission, glucose homeostasis, gastrointestinal hormones, incretins, bile acid metabolism, gut microbiota, insulin sensitivity, beta-cell function, hepatic glucose production, caloric restriction, obesity
- MeSH terms
- Blood Glucose, Diabetes Mellitus, Type 2, Energy Metabolism, Gastrointestinal Hormones, Glucose, Humans, Insulin Resistance, Obesity, Remission Induction, Signal Transduction, Weight Loss, Caloric Restriction, Gastrointestinal Tract, Bariatric Surgery, Incretins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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