ArticlePloS one2014
Role of endogenous GLP-1 and GIP in beta cell compensatory responses to insulin resistance and cellular stress.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed.
- Peptide YY in Type 2 Diabetes: A Complementary Gut Hormone with Therapeutic Potential Beyond GLP-1.Nutrients · 2025Review
- High-resolution imaging atlas reveals the context-dependent role of pancreatic sympathetic innervation in diabetic mice.Acta biochimica et biophysica Sinica · 2025Article
- Research Progress on Peptide Drugs for Type 2 Diabetes and the Possibility of Oral Administration.Pharmaceutics · 2024Review
- A review of an investigational drug retatrutide, a novel triple agonist agent for the treatment of obesity.European journal of clinical pharmacology · 2024Review
- Sex-based impact of pancreatic islet stressors in GluCreERT2/Rosa26-eYFP mice.The Journal of endocrinology · 2023Article
- Treatment with the dual-incretin agonist DA-CH5 demonstrates potent therapeutic effect in a rat model of Wolfram Syndrome.Frontiers in endocrinology · 2023Article
- Roles of glucose-dependent insulinotropic polypeptide in diet-induced obesity.Journal of diabetes investigation · 2022Review
- Article
- Effects of first-line diabetes therapy with biguanides, sulphonylurea and thiazolidinediones on the differentiation, proliferation and apoptosis of islet cell populations.Journal of endocrinological investigation · 2022Article
- Alpha-cell paracrine signaling in the regulation of beta-cell insulin secretion.Frontiers in endocrinology · 2022Review
- Mechanisms of Beta-Cell Apoptosis in Type 2 Diabetes-Prone Situations and Potential Protection by GLP-1-Based Therapies.International journal of molecular sciences · 2021Review
- Glucagon's Metabolic Action in Health and Disease.Comprehensive Physiology · 2021Article
- Proglucagon-Derived Peptides as Therapeutics.Frontiers in endocrinology · 2021Review
- Article
- Antidiabetic drug therapy alleviates type 1 diabetes in mice by promoting pancreatic α-cell transdifferentiation.Biochemical pharmacology · 2020Article
- Alpha cell regulation of beta cell function.Diabetologia · 2020Review
- Article
- Glucagon-like peptide 1 (GLP-1).Molecular metabolism · 2019 · on this mapReview
- Gut-Proglucagon-Derived Peptides Are Essential for Regulating Glucose Homeostasis in Mice.Cell metabolism · 2019Article
- Complement 1q-like-3 protein inhibits insulin secretion from pancreatic β-cells via the cell adhesion G protein-coupled receptor BAI3.The Journal of biological chemistry · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Role of GLP-1 and GIP in beta cell compensatory responses to beta cell attack and insulin resistance were examined in C57BL/6 mice lacking functional receptors for GLP-1 and GIP. Mice were treated with multiple low dose streptozotocin or hydrocortisone. Islet parameters were assessed by immunohistochemistry and hormone measurements were determined by specific enzyme linked immunoassays. Wild-type streptozotocin controls exhibited severe diabetes, irregularly shaped islets with lymphocytic infiltration, decreased Ki67/TUNEL ratio with decreased beta cell and increased alpha cell areas. GLP-1 and GIP were co-expressed with glucagon and numbers of alpha cells mainly expressing GLP-1 were increased. In contrast, hydrocortisone treatment and induction of insulin resistance increased islet numbers and area, with enhanced beta cell replication, elevated mass of beta and alpha cells, together with co-expression of GLP-1 and GIP with glucagon in islets. The metabolic responses to streptozotocin in GLP-1RKO and GIPRKO mice were broadly similar to C57BL/6 controls, although decreases in islet numbers and size were more severe. In contrast, both groups of mice lacking functional incretin receptors displayed substantially impaired islet adaptations to insulin resistance induced by hydrocortisone, including marked curtailment of expansion of islet area, beta cell mass and islet number. Our observations cannot be explained by simple changes in circulating incretin concentrations, suggesting that intra-islet GLP-1 and GIP make a significant contribution to islet adaptation, particularly expansion of beta cell mass and compensatory islet compensation to hydrocortisone and insulin resistance.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.