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Open research questions in Pancreatic function and diabetes

120 unresolved questions extracted from the limitations and future-work sections of 375 Pancreatic function and diabetes papers in our library. Each links back to the study that raised it.

What the literature leaves open

  • Investigate the role of CA in diabetic complications, - Examine the relationship between CA and ciliogenesis in diabetes

    The roles of centrosome amplification in diabetes-associated diseases · 2026 · DOI

  • The pathogenesis mechanisms of many diabetes-associated diseases are not well understood. The existing experimental data on centrosome amplification and diabetes-associated diseases are limited.

    The roles of centrosome amplification in diabetes-associated diseases · 2026 · DOI

  • Disease-associated transcriptional changes alone cannot distinguish likely regulatory drivers from secondary stress markers. Many single-cell studies remain mainly descriptive and do not show whether a candidate gene is predicted to perturb a wider beta-cell regulatory network.

    Single-cell virtual knockout network perturbation prioritizes candidate regulators of beta-cell functional failure in type 2 diabetes · 2026 · DOI

  • Further studies are needed to investigate the role of PFKFB3 in human beta cells - Research on the mechanisms of PFKFB3 regulation and its potential as a therapeutic target for diabetes - Investigation of the relationship between PFKFB3 and other regulators of glycolysis

    Metabolic adaptation to acute metabolic stress via PFKFB3 upregulation in rodent beta cells · 2025 · DOI

  • The pathogenesis and progression mechanisms of type 2 diabetes remain largely unknown. The regulatory effects of other components in the pancreatic islets' microenvironment have been neglected.

    Identification of a pancreatic stellate cell gene signature and lncRNA interactions associated with type 2 diabetes progression · 2025 · DOI

  • Pregnancy requires maternal pancreatic {beta}-cells adaptations to increased insulin demand, yet the embryo-derived signals contributing to this response remain poorly defined.

    Preimplantation factor (PIF) links embryo-derived signaling to maternal pancreatic β-cell adaptation through an ERα-dependent pathway · 2026 · DOI

  • Primary cilia are sensory organelles that act as signaling hubs, for pathways controlling cell differentiation, proliferation, and function, yet their contribution to -cell biology remains poorly defined.

    Primary cilia coordinate c-KIT signaling induced proliferation in alpha cells · 2026 · DOI

  • The mechanisms underlying hyperglucagonemia remain poorly understood, but expansion of pancreatic -cell mass is thought to play an important role.

    Primary cilia coordinate c-KIT signaling induced proliferation in alpha cells · 2026 · DOI

  • Essential roles for the PDX1 transcription factor in pancreatic development and β-cell function are well-known, yet the structure-function relationships of domains within its C-terminus remain incompletely defined.

    Conserved C-terminal residues adjacent to the canonical PDX1 homeodomain are required for chromatin occupancy and pancreas development · 2026 · DOI

  • Although the precise mechanisms remain incompletely understood, recent evidence suggests that DMR may induce significant genetic, enteroendocrine, and gut microbiota changes involving pathways associated with glucose uptake, intestinal differentiation, and metabolic signaling.

    New avenues in metabolic disease treatment: duodenal mucosal resurfacing and gene therapy · 2026 · DOI

  • The contribution of stressed β-cells to ECM degradation during T1D remains unclear.

    Stressed β-cells contribute to loss of peri-islet extracellular matrix in type 1 diabetes · 2025 · DOI

  • Introduction Pancreatic beta cells undergo metabolic remodeling in response to metabolic overload, but the functional significance of this remains unclear.

    Metabolic adaptation to acute metabolic stress via PFKFB3 upregulation in rodent beta cells · 2025 · DOI

  • Background Type 2 diabetes (T2D) has become a significant global health threat, yet its precise causes and mechanisms remain unclear.

    Identification of a pancreatic stellate cell gene signature and lncRNA interactions associated with type 2 diabetes progression · 2025 · DOI

  • Polygonatum sibiricum polysaccharides (PSP) have demonstrated potential anti-diabetic effects; however, their precise mechanism, particularly through the AMPK-SIRT1 pathway, remains unclear.

    Polygonatum sibiricum polysaccharides enhance pancreatic β-cell function in diabetic zebrafish by mitigating mitochondrial oxidative damage via the AMPK-SIRT1 pathway · 2025 · DOI

  • While the insulin-like growth factor 2 (IGF2) gene is known to be involved in various physiological processes, its precise role in lipid metabolism is still not well understood.

    Paradoxical regulation of IGF2 in promoting lipid metabolism in adipose tissues · 2025 · DOI

  • The embryonic time point at which adult pancreatic multipotent progenitor cells emerge has not been established.

    Pancreatic stem cells originate during the pancreatic progenitor developmental stage · 2025 · DOI

  • The activation of cyclin-dependent kinase 5 (Cdk5) is involved in the development of diabetes; however, its specific mechanism has not been fully elucidated.

    Cdk5 mediates impaired autophagy by regulating NGF/Sirt1 axis to cause diabetic islet β cell damage · 2025 · DOI

  • Recent studies have highlighted the glucagon-like peptide-1 receptor (GLP1R) as a critical regulator of immune homeostasis, yet its role in HSC engraftment remains unexplored.

    Glucagon-like peptide-1 receptor signaling deficiency exacerbates hematopoietic stem cell graft rejection in mice · 2025 · DOI

  • Although animal models are essential for understanding pancreatic development and disease, they are limited by their low throughput and major species-specific molecular and physiological differences.

    Generation of human iPSC-derived pancreatic organoids to study pancreas development and disease · 2025 · DOI

  • The underlying mechanisms driving β-cell dedifferentiation remain elusive due to the intricate interplay of genetic factors and cellular stress.

    Loss of β-cell identity and dedifferentiation, not an irreversible process? · 2024 · DOI

  • However, the specific markers of mature β-cell populations and postnatal pancreatic progenitors capable of increasing self-reproduction in these conditions remain to be elucidated.

    Development, regeneration, and physiological expansion of functional β-cells: Cellular sources and regulators · 2024 · DOI

  • We believe that this amenable and simplified protocol can provide a stable source of SC-delta cells from efficient differentiation, facilitating further investigation of the physiological role of delta cells as well as refinement of islet cell therapeutic strategies.

    A differentiation protocol for generating pancreatic delta cells from human pluripotent stem cells · 2024 · DOI

  • However, current research on the hypoglycemic activity of P-AKK is limited to the metabolic level, neglecting systematic exploration at the pathological level.

    Molecular Mechanism of Pasteurized Akkermansia muciniphila in Alleviating Type 2 Diabetes Symptoms · 2024 · DOI

  • Consequently, its material basis and mechanism of action for hypoglycemia remain unclear.

    Molecular Mechanism of Pasteurized Akkermansia muciniphila in Alleviating Type 2 Diabetes Symptoms · 2024 · DOI

  • The current method lacks glucagon regulation. The mRNA is a relatively weak actuator to control glucose levels. The study is entirely computational/simulation-based and did not involve human participants or animal experiments.

    PID-controller enhanced artificial β-cells · 2026 · DOI

Most-cited papers in Pancreatic function and diabetes

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120 open questions have been extracted from the limitations and future-work passages of 375 Pancreatic function and diabetes papers in our library. Each one below links back to the study that raised it, so you can read the original claim in context.

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