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Diabetes Mellitus: Type 2 and Gestational01:22

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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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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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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...
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Semi-Automated Analysis of Peak Amplitude and Latency for Auditory Brainstem Response Waveforms Using R
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Type-2 diabetes mellitus and auditory brainstem response.

Sheelu S Siddiqi1, Rahul Gupta2, Mohd Aslam3

  • 1Rajiv Gandhi Centre for Diabetes and Endocrinology, Faculty of Medicine, J.N. Medical College, AMU, Aligarh, India.

Indian Journal of Endocrinology and Metabolism
|January 2, 2014
PubMed
Summary

Brainstem auditory evoked potentials (BAEP) reveal central neuropathy in long-standing Type-2 diabetes. Delays in wave latencies indicate brainstem and midbrain defects, particularly in patients with diabetic neuropathy.

Keywords:
Auditory brainstem responsebrainstem evoked response audiometrytype-2 diabetes mellitus

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Area of Science:

  • Neuroscience
  • Endocrinology
  • Audiology

Background:

  • Diabetes mellitus (DM) causes widespread pathophysiological changes.
  • Evoked potential techniques, like brainstem auditory response, can detect damage in the acoustic nerve and central nervous system pathways.
  • Auditory evoked potentials offer a non-invasive method to assess neural function.

Purpose of the Study:

  • To detect central neuropathy in Type-2 diabetes patients using auditory evoked potentials.
  • To quantify auditory brain response characteristics in long-standing diabetes.
  • To evaluate the utility of auditory evoked potentials in identifying the type, site, and nature of lesions in the auditory pathway.

Main Methods:

  • Brainstem Evoked Response Audiometry (BERA) was performed on 25 Type-2 diabetes patients (duration > 5 years, age > 30) and 25 healthy controls.
  • BERA was conducted at 70, 80, and 90 dB.
  • Wave latency patterns and interpeak latencies were analyzed and compared between groups.

Main Results:

  • Type-2 DM patients showed significantly delayed wave-III and wave-V latencies and interpeak latencies (I-III, I-V) compared to controls (P < 0.001).
  • Delays were observed at 70, 80, and 90 dB, indicating brainstem and midbrain pathway dysfunction.
  • Abnormal BERA results were found in 92% of diabetic patients with neuropathy and 50% of those without neuropathy.

Conclusions:

  • Delayed latencies in BERA confirm brainstem and midbrain defects in long-standing Type-2 diabetes.
  • Auditory evoked potentials are valuable in detecting central neuropathy in diabetic patients.
  • The severity of BERA abnormalities correlates with the presence of diabetic neuropathy.