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Related Concept Videos

Insulin: Dosing Regimen and Adverse Effects01:16

Insulin: Dosing Regimen and Adverse Effects

Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
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...
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...
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...
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...
Psychoneuroimmunology: Diabetes and Cancer01:19

Psychoneuroimmunology: Diabetes and Cancer

Chronic stress has been linked to both the onset and progression of serious health conditions, including Type 2 diabetes and cancer. Type 2 diabetes, a widespread chronic illness, is closely associated with obesity and insulin resistance, both of which often worsen under stress. Studies indicate that men experiencing high levels of chronic stress face a 45% higher risk of developing diabetes compared to those with minimal stress. Stress triggers physiological responses that elevate blood...

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Updated: Jul 10, 2026

A Method for Mouse Pancreatic Islet Isolation and Intracellular cAMP Determination
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Study Protocol: insulin and its role in cancer.

K Harish1, M Dharmalingam, M Himanshu

  • 1Department of Surgical Oncology, M, S, Ramaiah Medical College & Hospital, Bangalore 560054, India. drkhari@yahoo.com

BMC Endocrine Disorders
|October 24, 2007
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Hyperinsulinism, a condition linked to insulin resistance, may promote cancer by increasing free insulin growth factor 1 (IGF-1) levels. Further research is needed to confirm this link and explore therapeutic strategies targeting insulin pathways for cancer prevention and treatment.

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Last Updated: Jul 10, 2026

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Published on: June 25, 2014

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Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)
08:13

Study of In Vivo Glucose Metabolism in High-fat Diet-fed Mice Using Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT)

Published on: January 7, 2018

Area of Science:

  • Oncology
  • Endocrinology
  • Metabolic Syndrome

Background:

  • Metabolic syndrome and diabetes-related biochemical changes may contribute to cancer development.
  • Hyperinsulinism, common in early insulin resistance, can elevate free insulin growth factor 1 (IGF-1) levels.
  • Elevated free IGF-1 is known to accelerate tumor growth and progression.

Purpose of the Study:

  • To investigate the role of insulin resistance and sensitivity in carcinogenesis.
  • To examine the relationship between insulin resistance/sensitivity and free IGF-1 levels in cancer patients.
  • To test the hypothesis that hyperinsulinemia in insulin resistance increases free IGF-1, potentially driving carcinogenesis.

Main Methods:

  • A two-group case-control study design.
  • Recruitment of 800 untreated cancer patients (solid epithelial tumors, <50 years) and 200 healthy controls.
  • Measurement of insulin resistance/sensitivity and free IGF-1 levels in all participants, with statistical analysis of associations.

Main Results:

  • Pilot study results and power analysis informed the study design.
  • Association between insulin resistance/sensitivity and free IGF-1 levels will be statistically tested.

Conclusions:

  • Human studies are crucial to elucidate the complex interplay between insulin, insulin resistance, IGF-1, and carcinogenesis.
  • This research may offer insights into the mechanisms of cancer development related to insulin and IGF-1.
  • Future cancer prevention and treatment strategies might focus on modulating insulin and insulin resistance.