ArticleThe Journal of biological chemistry2016
The Amplifying Pathway of the β-Cell Contributes to Diet-induced Obesity.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 19 citations in OpenAlex.
- Hyperinsulinaemia as a cause of obesity and cardiometabolic diseases.Nature reviews. Endocrinology · 2026Review
- NADPH Dynamics: Linking Insulin Resistance and β-Cells Ferroptosis in Diabetes Mellitus.International journal of molecular sciences · 2023Review
- Epigenetic activation of secretory phenotypes in senescence by the FOXQ1-SIRT4-GDH signaling.Cell death & disease · 2023Article
- Deletion of ABCB10 in beta-cells protects from high-fat diet induced insulin resistance.Molecular metabolism · 2022Article
- The Pancreatic ß-cell Response to Secretory Demands and Adaption to Stress.Endocrinology · 2021Review
- BACE2 suppression in mice aggravates the adverse metabolic consequences of an obesogenic diet.Molecular metabolism · 2021Article
- Hyperinsulinemia in Obesity, Inflammation, and Cancer.Diabetes & metabolism journal · 2021Review
- Changes of Serum Adiponectin and Glycated Albumin Levels in Gestational Diabetes Mellitus Patients and Their Relationship with Insulin Resistance.Iranian journal of public health · 2020Article
- AMPK Profiling in Rodent and Human Pancreatic Beta-Cells under Nutrient-Rich Metabolic Stress.International journal of molecular sciences · 2020Article
- High-fat-diet-induced remission of diabetes in a subset of KDiabetes, obesity & metabolism · 2018Article
- Reducing insulin via conditional partial gene ablation in adults reverses diet-induced weight gain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Mechanisms of the amplifying pathway of insulin secretion in the β cell.Pharmacology & therapeutics · 2017Review
- The Glutamate Dehydrogenase Pathway and Its Roles in Cell and Tissue Biology in Health and Disease.Biology · 2017Review
- Insulin promoter-driven Gaussia luciferase-based insulin secretion biosensor assay for discovery of β-cell glucose-sensing pathways.ACS sensors · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Efficient energy storage in adipose tissues requires optimal function of the insulin-producing β-cell, whereas its dysfunction promotes diabetes. The associated paradox related to β-cell efficiency is that excessive accumulation of fat in adipose tissue predisposes for type 2 diabetes. Insulin exocytosis is regulated by intracellular metabolic signal transduction, with glutamate dehydrogenase playing a key role in the amplification of the secretory response. Here, we used mice with β-cell-selective glutamate dehydrogenase deletion (βGlud1(-/-)), lacking an amplifying pathway of insulin secretion. As opposed to control mice, βGlud1(-/-) animals fed a high calorie diet maintained glucose tolerance and did not develop diet-induced obesity. Islets of βGlud1(-/-) mice did not increase their secretory response upon high calorie feeding, as did islets of control mice. Inhibited adipose tissue expansion observed in knock-out mice correlated with lower expression of genes responsible for adipogenesis. Rather than being efficiently stored, lipids were consumed at a higher rate in βGlud1(-/-) mice compared with controls, in particular during food intake periods. These results show that reduced β-cell function prior to high calorie feeding prevented diet-induced obesity.
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.