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Related Concept Videos

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 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...
Bone Disorders01:29

Bone Disorders

Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
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 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 Mellitus III: Clinical Manifestations and Diagnosis01:25

Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis

Type 2 diabetes mellitus develops gradually and is often asymptomatic in early stages.Clinical ManifestationsWhen symptoms appear, they include fatigue, blurred vision, pruritus, delayed wound healing, and recurrent infections, particularly candidal infections. Peripheral neuropathy may present as numbness or tingling in the extremities. Classic hyperglycemia symptoms—polyuria, polydipsia, and polyphagia—are less common. Most patients are overweight and frequently have associated hypertension...

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A Simple Critical-sized Femoral Defect Model in Mice
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Bone fragility in type 2 diabetes mellitus.

Toru Yamaguchi1

  • 1Toru Yamaguchi, Internal Medicine 1, Shimane University Faculty of Medicine, Shimane 693-8501, Japan.

World Journal of Orthopedics
|April 5, 2012
PubMed
Summary

Type 2 diabetes mellitus (T2DM) increases fracture risk in elderly patients, independent of bone mineral density. Bone quality, not mass, is key, necessitating new markers like pentosidine for assessing fragility.

Keywords:
Fracture riskOsteocalcinOsteoporosisType 2 diabetes mellitusWnt signaling

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07:56

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Method and Instrumented Fixture for Femoral Fracture Testing in a Sideways Fall-on-the-Hip Position
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Published on: August 17, 2017

Area of Science:

  • Endocrinology
  • Metabolic Bone Disease
  • Geriatrics

Background:

  • Osteoporosis and type 2 diabetes mellitus (T2DM) are increasing in aging populations.
  • Both conditions lead to fractures and vascular complications, respectively.
  • Emerging evidence suggests a link between bone and glucose/fat metabolism.

Purpose of the Study:

  • To explore the relationship between T2DM and bone fragility.
  • To identify potential surrogate markers for fracture risk in T2DM patients.
  • To address the limitations of bone mineral density (BMD) in assessing T2DM-related fractures.

Main Methods:

  • Review of animal studies on osteocalcin and Wnt signaling.
  • Analysis of meta-analyses of human clinical studies on T2DM and fracture risk.
  • Evaluation of potential surrogate markers such as pentosidine and insulin-like growth factor-I.

Main Results:

  • T2DM patients exhibit a 1.4-1.7 fold increased hip fracture risk, with normal BMD.
  • Vertebral fracture risk is also elevated in T2DM patients.
  • Bone fragility in T2DM appears linked to bone quality deterioration, not reduced bone mass.

Conclusions:

  • BMD is insufficient for assessing fracture risk in T2DM patients.
  • Bone quality, rather than bone mass, is crucial for T2DM-related fragility.
  • Pentosidine and IGF-I are potential markers needing further prospective validation.