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

Diabetic Ketoacidosis ll: Pathophysiology01:22

Diabetic Ketoacidosis ll: Pathophysiology

Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...
Diabetic Ketoacidosis l: Introduction01:25

Diabetic Ketoacidosis l: Introduction

DefinitionDiabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus, characterized by a triad of hyperglycemia (blood glucose >250 mg/dL), ketonemia or ketonuria, and metabolic acidosis (arterial pH <7.30 and serum bicarbonate <18 mEq/L). It results from insulin deficiency combined with elevated levels of counterregulatory hormones—glucagon, catecholamines, cortisol, and growth hormone—leading to increased lipolysis, hepatic ketone production, and...
Hypoglycemia01:26

Hypoglycemia

Hypoglycemia is a blood glucose level below 70 mg/dL. It commonly occurs in individuals using insulin or insulin-secreting drugs, but may also arise in non-diabetic conditions. People with type 1 diabetes are at the highest risk because they depend on exogenous insulin. People with type 2 diabetes are also at risk, especially when treated with insulin or medications such as sulfonylureas, which increase insulin release regardless of blood glucose levels. It develops when insulin levels exceed...
Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment primarily uses...
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
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...

You might also read

Related Articles

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

Sort by
Same author

Sources of Environmental Exposure to the Naturally Occurring Anabolic Steroid Ecdysterone in Horses.

Animals : an open access journal from MDPI·2025
Same author

Effect of pergolide treatment on insulin dysregulation in horses and ponies with pituitary pars intermedia dysfunction.

Equine veterinary journal·2025
Same author

Distribution and sequence analysis of the melanocortin 2 receptor in horses and ponies.

Domestic animal endocrinology·2024
Same author

Effect of short-term dopamine reduction on insulin sensitivity and post-prandial insulin and glucose responses in Standardbred horses.

Domestic animal endocrinology·2024
Same author

Physiological and metabolic effects of short-term dopamine reduction in healthy horses using a tyrosine hydroxylase inhibitor (alpha-methyl-para-tyrosine).

Domestic animal endocrinology·2024
Same author

Posture and postural dysfunction in dogs: Implications for veterinary physiotherapy.

Veterinary journal (London, England : 1997)·2024
Same journal

Pharmaceutical and Nutraceutical Therapies for Liver Disease.

The Veterinary clinics of North America. Equine practice·2026
Same journal

Clinical Signs of Liver Disease in Horses.

The Veterinary clinics of North America. Equine practice·2026
Same journal

Syndrome of High Gamma-Glutamyl Transferase in Racehorses.

The Veterinary clinics of North America. Equine practice·2026
Same journal

Equine Hepatology in Practice: Insights, Challenges, and Progress.

The Veterinary clinics of North America. Equine practice·2026
Same journal

Pathophysiology and Treatment of Hepatic Encephalopathy.

The Veterinary clinics of North America. Equine practice·2026
Same journal

Viral Hepatitis.

The Veterinary clinics of North America. Equine practice·2026
See all related articles

Related Experiment Video

Updated: Jun 10, 2026

Hyperinsulinemic-Euglycemic Clamp in the Conscious Rat
11:12

Hyperinsulinemic-Euglycemic Clamp in the Conscious Rat

Published on: February 7, 2011

Hyperinsulinemic laminitis.

Melody A de Laat1, Catherine M McGowan, Martin N Sillence

  • 1Australian Equine Laminitis Research Unit, School of Veterinary Science, The University of Queensland, Gatton, Queensland 4343, Australia. m.delaat@uq.edu.au

The Veterinary Clinics of North America. Equine Practice
|August 12, 2010
PubMed
Summary
This summary is machine-generated.

Hyperinsulinemia, not insulin resistance, directly causes equine laminitis. Research is exploring how high insulin levels harm lamellar tissue, improving understanding of this equine disease.

More Related Videos

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
11:10

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

Published on: November 16, 2011

Preclinical Model of Hind Limb Ischemia in Diabetic Rabbits
07:34

Preclinical Model of Hind Limb Ischemia in Diabetic Rabbits

Published on: June 2, 2019

Related Experiment Videos

Last Updated: Jun 10, 2026

Hyperinsulinemic-Euglycemic Clamp in the Conscious Rat
11:12

Hyperinsulinemic-Euglycemic Clamp in the Conscious Rat

Published on: February 7, 2011

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice
11:10

Hyperinsulinemic-euglycemic Clamps in Conscious, Unrestrained Mice

Published on: November 16, 2011

Preclinical Model of Hind Limb Ischemia in Diabetic Rabbits
07:34

Preclinical Model of Hind Limb Ischemia in Diabetic Rabbits

Published on: June 2, 2019

Area of Science:

  • Equine Medicine
  • Veterinary Science
  • Endocrinology

Background:

  • Laminitis is a common and serious equine condition.
  • Hyperinsulinemia (high insulin levels) is frequently observed in horses with laminitis.
  • Recent findings indicate hyperinsulinemia is the direct cause, not just insulin resistance.

Purpose of the Study:

  • To investigate the direct causal link between hyperinsulinemia and equine laminitis.
  • To elucidate the pathophysiological mechanisms by which elevated insulin affects lamellar tissue.
  • To utilize a novel insulin infusion model to advance research in insulin-associated laminitis.

Main Methods:

  • Employing a new insulin infusion model in equine research.
  • Focusing on the metabolic and vascular effects of insulin within the lamellar microenvironment.
  • Investigating the direct impact of elevated serum insulin concentrations on lamellar function.

Main Results:

  • New evidence implicates hyperinsulinemia as the direct cause of laminitis.
  • The precise mechanism of insulin-induced lamellar dysfunction is under active investigation.
  • The insulin infusion model is expected to accelerate progress in understanding insulin-associated laminitis.

Conclusions:

  • Hyperinsulinemia is the primary driver of this specific form of equine laminitis.
  • Further research into insulin's actions in the lamellar microenvironment is crucial.
  • Understanding these pathophysiological processes will lead to better disease management and prevention.