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Related Concept Videos

Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
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.
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 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...
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

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...
Hormones Regulating Blood Glucose01:16

Hormones Regulating Blood Glucose

Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...

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Related Experiment Video

Updated: Jul 19, 2026

A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform
09:35

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Serum visfatin increases with progressive beta-cell deterioration.

Abel López-Bermejo1, Berta Chico-Julià, Mercè Fernàndez-Balsells

  • 1Diabetes, Endocrinology and Nutrition, Dr. Josep Trueta Hospital, Av. Francia s/n, 17007 Girona, Spain. uden.alopez@htrueta.scs.es

Diabetes
|September 28, 2006
PubMed
Summary

Circulating visfatin levels are linked to impaired insulin secretion in non-diabetic individuals. Visfatin increases with progressive beta-cell deterioration in both type 1 and type 2 diabetes.

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Area of Science:

  • Endocrinology
  • Metabolic Research
  • Diabetes Pathophysiology

Background:

  • Visfatin, an adipokine, is elevated in type 2 diabetes but its relationship with insulin sensitivity is unclear.
  • Previous research suggests visfatin may play a role in metabolic regulation.

Purpose of the Study:

  • To investigate the association between circulating visfatin levels and insulin secretion in humans.
  • To examine visfatin levels in relation to insulin sensitivity and metabolic parameters in non-diabetic, type 2 diabetic, and type 1 diabetic individuals.

Main Methods:

  • Cross-sectional study involving 118 non-diabetic men, 64 type 2 diabetic patients, and 58 type 1 diabetic patients.
  • Circulating visfatin measured by enzyme immunoassay.
  • Insulin secretion assessed via acute insulin response to glucose (AIRg) during intravenous glucose tolerance tests.
  • Insulin sensitivity (Si) and other metabolic/anthropometric parameters were evaluated.

Main Results:

  • In non-diabetic subjects, visfatin was independently associated with insulin secretion (AIRg) but not insulin sensitivity (Si).
  • Circulating visfatin was significantly increased in type 2 diabetes compared to non-diabetic subjects, an association attenuated by HbA1c.
  • Visfatin levels were markedly elevated in long-standing type 1 diabetes, even after adjusting for HbA1c, indicating progressive beta-cell deterioration.

Conclusions:

  • Circulating visfatin is associated with impaired insulin secretion in non-diabetic individuals.
  • Elevated visfatin levels correlate with progressive beta-cell dysfunction in both type 1 and type 2 diabetes.
  • Further research into the role and regulation of visfatin in diabetes is warranted.