ReviewDiabetologia2021
Brain control of blood glucose levels: implications for the pathogenesis of type 2 diabetes.
Review in Diabetologia, 2021. 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 31 papers, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Orexinergic pathway as a potential therapeutic candidate for the modulation of glucose homeostasis.Frontiers in physiology · 2025Pooled it
- Hormonal adaptations to weight loss: Responses to an oral glucose load 4 weeks after obesity surgery and low-energy diet.Diabetes, obesity & metabolism · 2025Trial
- Sex differences in glucose-regulating neurohormonal pathways-potential impact for type 2 diabetes development.Journal of the Endocrine Society · 2026Article
- Trans-ethnic estimation and implications of genetic impact on continuous glycemic profiles.Cell discovery · 2026Article
- Glucose-dependent dynamics of glucagon, cortisol and adrenocorticotropic hormone before and after gastric bypass.Journal of the Endocrine Society · 2026Article
- Immunometabolism in obesity: Understanding the beneficial and detrimental roles of inflammation.PLoS biology · 2026Article
- Is Hypothalamic Dysfunction a Cause of Type II Diabetes Mellitus?Neuroendocrinology · 2026Review
- Therapeutic Trends in Diabetes Management: A Review on Oral Hypoglycemic Agents (OHAs) Utilization in Tertiary Care.Cardiovascular & hematological disorders drug targets · 2026Review
- Low-dose metformin requires brain Rap1 for its antidiabetic action.Science advances · 2025Article
- Targeting the RAGE-RIPK1 binding site attenuates diabetes-associated cognitive deficits.Journal of neuroinflammation · 2025Article
- Synthesis, characterization, andRSC advances · 2025Article
- Scaffold-free endocrine tissue engineering: role of islet organization and implications in type 1 diabetes.BMC endocrine disorders · 2025Review
- Fueling Brain Inhibition: Integrating GABAergic Neurotransmission and Energy Metabolism.Neurochemical research · 2025Review
- Relations between neurometabolism and clinical biomarkers in patients with metabolic disease.Frontiers in neuroscience · 2025Article
- Review
- (Pro)renin receptor signaling in hypothalamic tyrosine hydroxylase neurons is required for obesity-associated glucose metabolic impairment.JCI insight · 2024Article
- Nasal lymphatic obstruction of CSF drainage as a possible cause of Alzheimer's disease and dementia.Frontiers in aging neuroscience · 2024Article
- Paracrine signalling by pancreatic δ cells determines the glycaemic set point in mice.Nature metabolism · 2024Article
- Targeting the Epigenetic Marks in Type 2 Diabetes Mellitus: Will Epigenetic Therapy Be a Valuable Adjunct to Pharmacotherapy?Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Cognition from the Body-Brain Partnership: Exaptation of Memory.Annual review of neuroscience · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Despite a rapidly growing literature, the role played by the brain in both normal glucose homeostasis and in type 2 diabetes pathogenesis remains poorly understood. In this review, we introduce a framework for understanding the brain's essential role in these processes based on evidence that the brain, like the pancreas, is equipped to sense and respond to changes in the circulating glucose level. Further, we review evidence that glucose sensing by the brain plays a fundamental role in establishing the defended level of blood glucose, and that defects in this control system contribute to type 2 diabetes pathogenesis. We also consider the possibility that the close association between obesity and type 2 diabetes arises from a shared defect in the highly integrated neurocircuitry governing energy homeostasis and glucose homeostasis. Thus, whereas obesity is characterised by an increase in the defended level of the body's fuel stores (e.g. adipose mass), type 2 diabetes is characterised by an increase in the defended level of the body's available fuel (e.g. circulating glucose), with the underlying pathogenesis in each case involving impaired sensing of (or responsiveness to) relevant humoral negative feedback signals. This perspective is strengthened by growing preclinical evidence that in type 2 diabetes the defended level of blood glucose can be restored to normal by therapies that restore the brain's ability to properly sense the circulating glucose level. Graphical abstract.
Indexed as
Identifiers
What Socratic 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 Socratic graph.