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High glucose

High glucose has been studied in 7 papers since 2018: 1 observational study in people, 2 in animals, 3 in cells, 1 review. The newest paper, Apr 1, 2025: “High glucose induces FABP3-mediated membrane rigidity via downregulation of SIRT1”.

Intervention

7 papers study it32 findingsUpdated

Research on it is growing 25% slower than aging research as a whole: 23 papers in the latest year counted

See all 7

1 of its findings points the other way.

C, W, M, H: cells, worms or flies, mice, humans. Dark: independent labs found the same change there. Light: one lab or one study. Outline: nothing yet.

Labs are independent when their papers share no last author and no institution.

Against: findings that point the other way from most findings on the same outcome.

  • 14 independent labs in 8 countries
  • 1 finding against
  • Funders: Italian Government Ministry of Health and others
  • Humans1
  • Animals2
  • Cells3

What did studies of High glucose find?

23

Studies of High glucose measured 23 outcomes; the most studied are cellular senescence (9 studies), apoptosis (2) and oxidative stress and ROS signaling (1).

Cellular senescence

upin human cells5upin cells1no changein human cells1upin mouse cells1+1

9 studies

  1. High glucose increases cellular senescence in human cells (cultured human limbal niche cells).

    “In vitro, hyperglycemia reduced LNCs proliferation, induced oxidative stress and senescence, and decreased the expression of SCF, PDGFRβ, and PAX6.”

    Cellscultured human limbal niche cells

    SIRT1 alleviates hyperglycemia-induced oxidative stress and dysfunction of limbal niche cells by deacetylating FOXO1

    Free radical biology & medicine

  2. High glucose showed no clear effect on cellular senescence in human cells (passage 6 (P6) hAD-MSCs).

    “while the extent of senescence did not change significantly under stress conditions.”

    Cellspassage 6 (P6) hAD-MSCs

    Effects of high glucose and severe hypoxia on the biological behavior of mesenchymal stem cells at various passages

    World journal of stem cells

  3. High glucose increases cellular senescence in primary HUVECs and cell lines.

    “exposing primary HUVECs and cell lines to high glucose resulted in an increase in the synthesis of these senescence indicators”

    Cellsin primary HUVECs and cell lineshigh glucose culture

    High Glucose Promotes and Aggravates the Senescence and Dysfunction of Vascular Endothelial Cells in Women with Hyperglycemia in Pregnancy

    Biomolecules

  4. High glucose induces cellular senescence in human cells (p21-dependent senescence in primary human RPTECs).

    “high glucose induces p21-dependent RPTEC senescence, whereas dapagliflozin prevents it”

    Cellsp21-dependent senescence in primary human RPTECs

    Dapagliflozin Prevents High-Glucose-Induced Cellular Senescence in Renal Tubular Epithelial Cells

    International journal of molecular sciences

  5. High glucose increases cellular senescence in human cells.

    “HG stimulation of HuREC increased the expression of miR-34a and induced cellular senescence.”

    Cells25 mM

    MicroRNA-34a (miR-34a) Mediates Retinal Endothelial Cell Premature Senescence through Mitochondrial Dysfunction and Loss of Antioxidant Activities

    Antioxidants (Basel, Switzerland)

  6. High glucose induces cellular senescence in proximal tubular epithelial cells.

    “We found that HG induced cell senescence in PTECs”

    Cellsin proximal tubular epithelial cellsproximal tubular epithelial cell

    The Interaction of miR-378i-Skp2 Regulates Cell Senescence in Diabetic Nephropathy

    Journal of clinical medicine

  7. High glucose increases cellular senescence in mouse cells (wild-type MSCs in high glucose medium).

    “in association with increased cell death by apoptosis and acquisition of the senescent phenotype”

    Cellswild-type MSCs in high glucose mediumkidney

    Aging phenotype(s) in kidneys of diabetic mice are p66ShcA dependent

    American journal of physiology. Renal physiology

  8. High glucose induces cellular senescence in cell types linked with obesity and diabetes.

    “accelerating ageing through induction of premature cell senescence mediated by high glucose levels and oxidised low-density lipoproteins”

    Reviewin cell types linked with obesity and diabetes

    Obesity and type-2 diabetes as inducers of premature cellular senescence and ageing

    Biogerontology

  9. High glucose increases cellular senescence in human cells.

    “This in turn accelerates endothelial senescence and induces functional abnormalities.”

    Cellsendothelial cell

    Protective role of SIRT1 in diabetic vascular dysfunction

    Arteriosclerosis, thrombosis, and vascular biology

More on Cellular senescence

Apoptosis

upin human cells1upin mouse cells1

2 studies

  1. High glucose induces apoptosis in human cells (passage 6 (P6) hAD-MSCs).

    “Cells at P6 showed decreased proliferation and increased apoptosis under conditions of high glucose and hypoxia compared to control”

    Cellspassage 6 (P6) hAD-MSCs

    Effects of high glucose and severe hypoxia on the biological behavior of mesenchymal stem cells at various passages

    World journal of stem cells

  2. High glucose increases apoptosis in mouse cells (wild-type MSCs in high glucose medium).

    “in association with increased cell death by apoptosis and acquisition of the senescent phenotype”

    Cellswild-type MSCs in high glucose mediumkidney

    Aging phenotype(s) in kidneys of diabetic mice are p66ShcA dependent

    American journal of physiology. Renal physiology

More on Apoptosis

Oxidative stress and ROS signaling

upin human cells1

1 study

  1. High glucose increases oxidative stress and ROS signaling in human cells (cultured human limbal niche cells).

    “In vitro, hyperglycemia reduced LNCs proliferation, induced oxidative stress and senescence, and decreased the expression of SCF, PDGFRβ, and PAX6.”

    Cellscultured human limbal niche cells

    SIRT1 alleviates hyperglycemia-induced oxidative stress and dysfunction of limbal niche cells by deacetylating FOXO1

    Free radical biology & medicine

More on Oxidative stress and ROS signaling

Limbal niche cell proliferation

downin human cells1

1 study

  1. High glucose decreases limbal niche cell proliferation in human cells (cultured human limbal niche cells).

    “In vitro, hyperglycemia reduced LNCs proliferation, induced oxidative stress and senescence, and decreased the expression of SCF, PDGFRβ, and PAX6.”

    Cellscultured human limbal niche cells

    SIRT1 alleviates hyperglycemia-induced oxidative stress and dysfunction of limbal niche cells by deacetylating FOXO1

    Free radical biology & medicine

ANXA2

downin human cells1

1 study

  1. High glucose decreases ANXA2 in periodontal ligament cells.

    “We observed that ANXA2 expression was down-regulated in Periodontal ligament cells (PDLCs) under high glucose conditions.”

    Cellsin periodontal ligament cells

    ANXA2 regulates mitochondrial function and cellular senescence of PDLCs via AKT/eNOS signaling pathway under high glucose conditions

    Scientific reports

More on ANXA2

FABP3

upin mouse cells1

1 study

  1. High glucose increases FABP3 in cultured myotubes.

    “In cultured myotubes, high glucose elevated the mRNA and protein levels of FABP3”

    Cellsin cultured myotubes

    High glucose induces FABP3-mediated membrane rigidity via downregulation of SIRT1

    Biochimica et biophysica acta. General subjects

More on FABP3

NAD+

downin mice1

1 study

  1. High glucose decreases NAD+ in mice (dietary HG intake in young mice).

    “In vivo, HG intake in young mice depleted MSC NAD+”

    Animalsdietary HG intake in young micebone marrow MSCs

    Excess glucose alone depress young mesenchymal stromal/stem cell osteogenesis and mitochondria activity within hours/days via NAD⁺/SIRT1 axis

    Journal of biomedical science

More on NAD+

adipogenesis

upin cells1

1 study

  1. High glucose increases adipogenesis in vitro, without differentiation induction.

    “in vitro HG alone without differentiation induction decreased both MSC mitochondrial activity and osteogenesis while enhancing adipogenesis by 8 h' time”

    Cellsin vitro, without differentiation induction8 h

    Excess glucose alone depress young mesenchymal stromal/stem cell osteogenesis and mitochondria activity within hours/days via NAD⁺/SIRT1 axis

    Journal of biomedical science

mitochondrial activity

downin cells1

1 study

  1. High glucose decreases mitochondrial activity in vitro, without differentiation induction.

    “in vitro HG alone without differentiation induction decreased both MSC mitochondrial activity and osteogenesis while enhancing adipogenesis by 8 h' time”

    Cellsin vitro, without differentiation induction

    Excess glucose alone depress young mesenchymal stromal/stem cell osteogenesis and mitochondria activity within hours/days via NAD⁺/SIRT1 axis

    Journal of biomedical science

osteogenic differentiation

downin cells1

1 study

  1. High glucose decreases osteogenic differentiation in vitro, without differentiation induction.

    “in vitro HG alone without differentiation induction decreased both MSC mitochondrial activity and osteogenesis while enhancing adipogenesis by 8 h' time”

    Cellsin vitro, without differentiation induction

    Excess glucose alone depress young mesenchymal stromal/stem cell osteogenesis and mitochondria activity within hours/days via NAD⁺/SIRT1 axis

    Journal of biomedical science

All 23

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