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Related Concept Videos

Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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...
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 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...
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Psychoneuroimmunology: Diabetes and Cancer

Chronic stress has been linked to both the onset and progression of serious health conditions, including Type 2 diabetes and cancer. Type 2 diabetes, a widespread chronic illness, is closely associated with obesity and insulin resistance, both of which often worsen under stress. Studies indicate that men experiencing high levels of chronic stress face a 45% higher risk of developing diabetes compared to those with minimal stress. Stress triggers physiological responses that elevate blood...

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Related Experiment Video

Updated: Jun 26, 2026

A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging
09:37

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The risk allele load accelerates the age-dependent decline in beta cell function.

A Haupt1, H Staiger, S A Schäfer

  • 1Medical Clinic, Department of Internal Medicine IV (Diabetology, Endocrinology, Nephrology, Angiology, and Clinical Chemistry), Eberhard Karls University, Otfried-Müller-Strasse 10, 72076, Tübingen, Germany.

Diabetologia
|January 28, 2009
PubMed
Summary

Genetic risk alleles for type 2 diabetes accelerate age-related decline in beta cell function, particularly in obese individuals. Higher allele loads correlate with reduced insulin secretion and impaired proinsulin conversion over time.

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Area of Science:

  • Genetics
  • Endocrinology
  • Metabolic Diseases

Background:

  • Genome-wide association studies have identified several novel type 2 diabetes risk loci.
  • TCF7L2, HHEX, SLC30A8, and CDKAL1 are among these loci and are suspected to influence beta cell function.

Purpose of the Study:

  • To investigate the impact of risk alleles in TCF7L2, HHEX, SLC30A8, and CDKAL1 on the age-dependent decline of insulin secretion.
  • To assess how genetic predisposition interacts with aging to affect beta cell function.

Main Methods:

  • Genotyping of specific single nucleotide polymorphisms (SNPs) in 1,412 non-diabetic individuals.
  • Stratification of participants based on the number of risk alleles (low, median, high allele load).
  • Assessment of insulin secretion and proinsulin conversion during an oral glucose tolerance test (OGTT).

Main Results:

  • Participants with higher risk allele loads (median and high) exhibited significantly lower insulin secretion and proinsulin conversion compared to those with low allele loads.
  • Age was negatively associated with insulin secretion and proinsulin conversion in the entire cohort.
  • The age-dependent decline in insulin secretion was more pronounced in individuals with higher risk allele loads, especially in obese participants.
  • Proinsulin conversion decreased with age in individuals with higher allele loads, but not in those with low allele loads.

Conclusions:

  • The cumulative load of type 2 diabetes risk alleles significantly accelerates the age-related decline in beta cell function.
  • This accelerated decline in beta cell function may be particularly relevant for obese individuals.
  • Genetic factors play a crucial role in the progressive loss of pancreatic beta cell function with age.