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Related Concept Videos

Insulin: The Receptor and Signaling Pathways01:28

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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...
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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.
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Insulin: Dosing Regimen and Adverse Effects01:16

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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.
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Glucagon-like Receptor Agonists01:24

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Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
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Insulin Secretory Vesicles01:05

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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...
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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.
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Updated: May 2, 2026

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Insulin and bone: Recent developments.

Gordon L Klein1

  • 1Gordon L Klein, Department of Orthopaedic Surgery and Rehabilitation, University of Texas and Shriners Burns Hospital, Galveston, TX 77555, United States.

World Journal of Diabetes
|February 26, 2014
PubMed
Summary
This summary is machine-generated.

Insulin, like insulin-like growth factor I, shows anabolic properties for bone by stimulating osteoblast differentiation. Insulin resistance, seen in type 2 diabetes, correlates with lower osteocalcin and reduced bone strength.

Keywords:
BoneInsulinInsulin resistanceOsteoblastsType 2 diabetes

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Area of Science:

  • Endocrinology
  • Bone Biology
  • Metabolic Diseases

Background:

  • Insulin-like growth factor I is a known bone anabolic agent.
  • Emerging evidence suggests insulin also possesses anabolic properties for bone.
  • Insulin's role in bone metabolism is increasingly recognized.

Purpose of the Study:

  • To explore the anabolic effects of insulin on bone.
  • To investigate insulin's potential to stimulate osteoblast differentiation and osteocalcin production.
  • To examine the relationship between insulin resistance, osteocalcin levels, and bone strength.

Main Methods:

  • Review of current scientific literature on insulin and bone metabolism.
  • Analysis of studies investigating insulin's effects on osteoblast differentiation.
  • Examination of data linking insulin resistance to bone health markers.

Main Results:

  • Insulin may stimulate osteoblast differentiation, enhancing osteocalcin production.
  • Osteocalcin is a key peptide linking bone health to pancreatic beta-cell function and insulin sensitivity.
  • Insulin's direct or indirect effects on bone, via muscle work and skeletal loading, require further elucidation.

Conclusions:

  • Insulin demonstrates anabolic potential for bone, potentially through osteoblast stimulation.
  • Insulin resistance, common in type 2 diabetes, is associated with decreased osteocalcin and impaired bone strength.
  • Further research is needed to clarify the precise mechanisms of insulin's action on bone and the implications of insulin resistance.