Related Experiment Video

Updated: May 11, 2026

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
10:03

A Zebrafish Model of Diabetes Mellitus and Metabolic Memory

Published on: February 28, 2013

Glycemic memories and the epigenetic component of diabetic nephropathy

Samuel T Keating1, Assam El-Osta

  • 1Epigenetics in Human Health and Disease Laboratory, Baker IDI Heart and Diabetes Institute, The Alfred Medical Research and Education Precinct, Melbourne, Victoria, 3004, Australia.

Current Diabetes Reports
|May 4, 2013
PubMed

Insights

Epigenetic changes in chromatin modifications are linked to chronic diabetes complications like diabetic nephropathy. Understanding these persistent, glucose-driven gene expression changes offers new therapeutic avenues.

Area of Science:

  • Molecular Biology
  • Endocrinology
  • Nephrology

Background:

  • Chronic diabetes complications, including diabetic nephropathy, are linked to epigenetic chromatin modifications.
  • Hyperglycemia causes prolonged organ damage, particularly in the kidneys, despite early treatment.

Purpose of the Study:

  • To investigate the role of epigenetic mechanisms in persistent gene expression changes in renal cells due to hyperglycemia.
  • To understand the molecular determinants of metabolic memory in the context of diabetic nephropathy.

Main Methods:

  • Review of experimental observations and clinical trial data.
  • Analysis of studies implicating epigenetic changes in deregulated gene expression in diabetic nephropathy.
  • Examination of evidence from animal models and cell cultures on glucose-driven gene expression changes.

Main Results:

  • Emerging evidence supports deregulation of epigenetic chromatin modifications in diabetes complications.
  • Persistent, glucose-driven changes in vascular endothelial gene expression observed in experimental models.
  • Molecular determinants of metabolic memory in renal cells remain largely unknown.

Conclusions:

  • Epigenetic mechanisms are crucial for understanding persistent transcriptional changes in renal cells caused by hyperglycemia.
  • Exploring these epigenetic pathways offers novel therapeutic potential for treating diabetic nephropathy.
  • Further research is needed to elucidate the precise molecular mechanisms involved.

More Related Videos

Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid06:21

Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid

Published on: April 7, 2023

Related Concept Videos

Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...
Diabetic Neuropathy01:22

Diabetic Neuropathy

DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Type I Diabetes III: Clinical Manifestations01:19

Type I Diabetes III: Clinical Manifestations

Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...