Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Diabetes Insipidus II: Pathophysiology01:22

Diabetes Insipidus II: Pathophysiology

Normally, water balance is maintained through three interconnected mechanisms: the hypothalamic thirst center, the synthesis and release of antidiuretic hormone (ADH, or vasopressin), and the kidneys' responsiveness to this hormone. ADH is synthesized in the hypothalamus, released from the posterior pituitary, and acts on the distal nephron, allowing water reabsorption and concentrated urine production.Diabetes Insipidus and Its TypesIn diabetes insipidus (DI), this regulatory system is...
Diabetes Insipidus I: Introduction01:29

Diabetes Insipidus I: Introduction

Definition Diabetes insipidus is a disorder marked by the production of large amounts of dilute urine because of impaired vasopressin production, release, or kidney response. The lack of effective vasopressin action limits water reabsorption in the renal collecting ducts, which leads to excessive urinary water loss and intense thirst.Clinical PresentationIndividuals with diabetes insipidus report persistent thirst and very high urine output. In severe cases, fluid intake can reach up to 20...
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...
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.
Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Glucagon-like peptide-1 receptor agonists and major limb events in adults with type 2 diabetes and peripheral artery disease: a systematic review and meta-analysis of RCTs and cohort studies.

Cardiovascular diabetology·2026
Same author

Late-onset hypogonadism and lower limb vascular complications in men with type 2 diabetes: an observational study in a tertiary care centre.

Journal of endocrinological investigation·2026
Same author

HbA1c variability as an independent risk factor for diabetic retinopathy: results from a screening program.

Acta diabetologica·2026
Same author

Polygenic risk in early-onset coronary artery disease with low prevalence of traditional cardiovascular risk factors.

Journal of cardiovascular medicine (Hagerstown, Md.)·2026
Same author

Angiogenic T cells and cognitive function in older adults with type 2 diabetes treated with GLP-1 receptor agonists.

Aging clinical and experimental research·2026
Same author

Dyslipidemias associated with endocrine disorders: a position statement of the working group of the nutrition hormones and metabolism club of the italian society of endocrinology (SIE).

Journal of endocrinological investigation·2026

Related Experiment Video

Updated: May 19, 2026

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
08:32

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain

Published on: January 4, 2018

Subclinical diabetes insipidus.

Antonio Bellastella1, Antonio Bizzarro, Caterina Colella

  • 1Department of Cardiothoracic and Respiratory Sciences, Second University of Naples, Via Leonardo Bianchi, Monaldi Hospital, 80131 Naples, Italy.

Best Practice & Research. Clinical Endocrinology & Metabolism
|August 7, 2012
PubMed
Summary

Subclinical central diabetes insipidus (CDI) can stem from various conditions affecting the brain. Autoimmune causes are common, and understanding the 4 stages of autoimmune CDI is key for treatment.

More Related Videos

Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid
06:21

Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid

Published on: April 7, 2023

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test
06:59

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test

Published on: November 13, 2016

Related Experiment Videos

Last Updated: May 19, 2026

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
08:32

Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain

Published on: January 4, 2018

Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid
06:21

Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid

Published on: April 7, 2023

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test
06:59

Characterization of Metabolic Status in Nonhuman Primates with the Intravenous Glucose Tolerance Test

Published on: November 13, 2016

Area of Science:

  • Neuroendocrinology
  • Immunology

Background:

  • Subclinical central diabetes insipidus (CDI) arises from dysfunction of the hypothalamus-infundibulum-post hypophysis axis.
  • Autoimmune pathogenesis is a frequent cause of subclinical CDI, alongside other conditions like brain injury, infections, and tumors.

Purpose of the Study:

  • To describe the natural history and staging of autoimmune central diabetes insipidus.
  • To highlight the importance of staging for therapeutic strategies in subclinical CDI.

Main Methods:

  • Characterization of autoimmune CDI based on antibodies to vasopressin-secreting cells (AVPcAb).
  • Correlation of AVPcAb behavior, posterior pituitary function, and MRI findings of the hypothalamic-hypophyseal region.
  • Evaluation of 4 distinct functional stages in the natural history of autoimmune CDI.

Main Results:

  • Autoimmune CDI progresses through 4 identifiable functional stages.
  • Staging integrates antibody presence, pituitary function, and imaging characteristics.
  • Certain stages of subclinical CDI may be reversible with timely intervention.

Conclusions:

  • The 4-stage model provides a framework for understanding autoimmune CDI progression.
  • Accurate staging is critical for guiding therapeutic interventions.
  • Further research is needed to validate and optimize medical treatments for halting CDI progression.