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Related Concept Videos

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 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 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...
Type II Diabetes II: Pathophysiology01:24

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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.
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

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The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are co-secreted in...
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...

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Related Experiment Video

Updated: May 16, 2026

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
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Depressive symptoms, insulin sensitivity and insulin secretion in the RISC cohort study.

M Bot1, F Pouwer, P De Jonge

  • 1CoRPS-Center of Research on Psychology in Somatic diseases, Department of Medical Psychology and Neuropsychology, Tilburg University, Tilburg, The Netherlands.

Diabetes & Metabolism
|November 28, 2012
PubMed
Summary

Depressive symptoms were not linked to insulin sensitivity in adults. However, depression showed a weak association with certain insulin secretion parameters, suggesting further research is needed.

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Area of Science:

  • Metabolic Health
  • Psychiatry
  • Cardiovascular Disease Risk

Background:

  • Depressive symptoms are increasingly recognized as a potential risk factor for metabolic dysfunction.
  • Understanding the relationship between depression and glucose metabolism is crucial for public health.
  • Previous research has yielded mixed results on the association between depression and insulin dynamics.

Purpose of the Study:

  • To investigate the association between depressive symptoms and measures of insulin sensitivity and insulin secretion.
  • To examine these relationships in a cohort of non-diabetic adults aged 30-64 years.

Main Methods:

  • Utilized data from the Relationship between Insulin Sensitivity and Cardiovascular Disease Risk (RISC) study.
  • Assessed depressive symptoms using the Center for Epidemiologic Studies Depression Scale (CES-D) score ≥ 16.
  • Measured insulin sensitivity via the oral glucose insulin sensitivity (OGIS) index and insulin secretion using three model-based parameters.

Main Results:

  • 16% of participants (162/1027) reported significant depressive symptoms.
  • No significant association was found between depressive symptoms and insulin sensitivity (OGIS).
  • Depressive symptoms were linked to reduced beta-cell rate sensitivity and, in unadjusted models, a decreased potentiation factor ratio.

Conclusions:

  • Depressive symptoms were not associated with insulin sensitivity in non-diabetic individuals.
  • A weak association was observed between depressive symptoms and specific parameters of insulin secretion.
  • Further prospective studies are warranted to elucidate the temporal relationship between depression and insulin secretion.