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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.
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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...
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Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
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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...
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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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Bone damage in type 2 diabetes mellitus.

V Carnevale1, E Romagnoli2, L D'Erasmo3

  • 1Unit of Internal Medicine, "Casa Sollievo della Sofferenza" Hospital, IRCCS, Viale dei Cappuccini snc, 71013 San Giovanni Rotondo, FG, Italy.

Nutrition, Metabolism, and Cardiovascular Diseases : NMCD
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Summary

Patients with type 2 diabetes mellitus (T2DM) experience high fracture rates due to poor bone quality, not low bone density. Understanding these mechanisms is crucial for managing T2DM-related bone fragility.

Keywords:
Bone mineral densityBone qualityClinical risk factorsFracturesType 2 diabetes mellitus

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Area of Science:

  • Endocrinology
  • Orthopedics
  • Gerontology

Background:

  • Type 2 Diabetes Mellitus (T2DM) is associated with increased fracture incidence despite normal or elevated bone mineral density (BMD).
  • Altered bone quality, rather than density, is implicated in T2DM-related bone fragility.
  • Current fracture risk assessment tools may have limited predictive capacity in T2DM patients.

Purpose of the Study:

  • To review the mechanisms contributing to bone fragility in patients with T2DM.
  • To highlight the challenges in assessing fracture risk in this population.
  • To emphasize the importance of bone quality over bone density in T2DM.

Main Methods:

  • Literature review of studies investigating bone quality and fracture risk in T2DM.
  • Analysis of factors influencing bone fragility, including advanced glycation end-products, cellular differentiation, and bone turnover.
  • Evaluation of the role of disease duration, severity, metabolic control, and T2DM therapies.

Main Results:

  • Increased skeletal advanced glycation end-products lead to collagen deterioration.
  • Altered osteogenic cell differentiation and impaired bone turnover contribute to poor bone quality.
  • Disease duration, severity, metabolic control, and fall predictors significantly impact fracture risk in T2DM.

Conclusions:

  • Bone fragility in T2DM is multifactorial, involving impaired bone quality due to glycation, cellular changes, and altered micro-architecture.
  • Fracture risk assessment in T2DM is challenging due to the limitations of BMD and standard risk algorithms.
  • Further research is needed to develop accurate fracture risk prediction models for T2DM patients.