ReviewDiabetologia2015
The new biology of diabetes.
Review in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 57 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
57 citing papers in PubMed, 90 citations in OpenAlex.
- The complex interplay between diabetes mellitus and pancreatic carcinogenesis: deciphering multifactorial mechanisms and identifying emerging therapeutic vulnerabilities.Cell & bioscience · 2025Review
- Review
- Identification and Functional Analysis of Key microRNAs in the Early Extrauterine Environmental Adaptation of Piglets.International journal of molecular sciences · 2025Article
- Review
- Association of serum trimethylamine N-oxide levels and bone mineral density in type 2 diabetes mellitus.Endocrine · 2024Article
- Genes That Extend Lifespan May Do So by Mitigating the Increased Risk of Death Posed by Having Hypertension.American journal of hypertension · 2023Article
- Reversing pancreatic β-cell dedifferentiation in the treatment of type 2 diabetes.Experimental & molecular medicine · 2023Review
- Article
- Article
- Immature ginger reduces triglyceride accumulation by downregulating Acyl CoA carboxylase and phosphoenolpyruvate carboxykinase-1 genes in 3T3-L1 adipocytes.Food & nutrition research · 2023Article
- Article
- Phytochemicals targeting NAFLD through modulating the dual function of forkhead box O1 (FOXO1) transcription factor signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2022Review
- Simiao Wan and its ingredients alleviate type 2 diabetes mellitusFrontiers in nutrition · 2022Article
- Data assimilation on mechanistic models of glucose metabolism predicts glycemic states in adolescents following bariatric surgery.Frontiers in physiology · 2022Article
- Botanical Interventions to Improve Glucose Control and Options for Diabetes Therapy.SN comprehensive clinical medicine · 2021Article
- Role of FoxO transcription factors in aging and age-related metabolic and neurodegenerative diseases.Cell & bioscience · 2021Review
- Adropin and insulin resistance: Integration of endocrine, circadian, and stress signals regulating glucose metabolism.Obesity (Silver Spring, Md.) · 2021Article
- Genetic deficiency or pharmacological inhibition of soluble epoxide hydrolase ameliorates high fat diet-induced pancreatic β-cell dysfunction and loss.Free radical biology & medicine · 2021Article
- Functional Role of miR-155 in the Pathogenesis of Diabetes Mellitus and Its Complications.Non-coding RNA · 2021Review
- Gene expression studies in Depression development and treatment: an overview of the underlying molecular mechanisms and biological processes to identify biomarkers.Translational psychiatry · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Until recently, type 2 diabetes was seen as a disease caused by an impaired ability of insulin to promote the uptake and utilisation of glucose. Work on forkhead box protein O (FOXO) transcription factors revealed new aspects of insulin action that have led us to articulate a liver- and beta cell-centric narrative of diabetes pathophysiology and treatment. FOXO integrate a surprisingly diverse subset of biological functions to promote metabolic flexibility. In the liver, they controls the glucokinase/glucose-6-phosphatase switch and bile acid pool composition, directing carbons to glucose or lipid utilisation, thus providing a unifying mechanism for the two abnormalities of the diabetic liver: excessive glucose production and increased lipid synthesis and secretion. Moreover, FOXO are necessary to maintain beta cell differentiation, and diabetes development is associated with a gradual loss of FOXO function that brings about beta cell dedifferentiation. We proposed that dedifferentiation is the main cause of beta cell failure and conversion into non-beta endocrine cells, and that treatment should restore beta cell differentiation. Our studies investigating these proposals have revealed new dimensions to the pathophysiology of diabetes that can be leveraged to design new therapies.
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.