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Related Concept Videos

Insulin: Dosing Regimen and Adverse Effects01:16

Insulin: Dosing Regimen and Adverse Effects

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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.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
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Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

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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.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment...
388
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

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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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Oral Hypoglycemic Agents: Sulfonylureas01:17

Oral Hypoglycemic Agents: Sulfonylureas

212
Sulfonylureas are oral hypoglycemic agents utilized in treating type 2 diabetes. They are characterized by their unique sulfonylurea chemical structure. The family of sulfonylureas is divided into generations. First-generation sulfonylureas, including tolbutamide (Orinase), chlorpropamide (Diabinese), and tolazamide (Tolinase), trigger insulin release from pancreatic β cells and enhance peripheral tissues' insulin sensitivity. The second-generation members, such as glipizide...
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Insulin Secretory Vesicles01:05

Insulin Secretory Vesicles

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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

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

1.3K
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...
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Related Experiment Video

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Hyperinsulinemic-Euglycemic Clamp in the Conscious Rat
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ALSUntangled #72: Insulin.

Andrew Brown1, Carmel Armon2, Paul Barkhaus3

  • 1Department of Neurology, University of Miami, Miami, FL, USA.

Amyotrophic Lateral Sclerosis & Frontotemporal Degeneration
|November 29, 2023
PubMed
Summary
This summary is machine-generated.

Insulin may have a role in slowing amyotrophic lateral sclerosis (ALS) progression due to its biological mechanisms. However, current evidence is limited, and potential serious side effects prevent endorsement for ALS treatment.

Keywords:
Amyotrophic lateral sclerosis (ALS)insulinmetabolismoff-label treatment

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Area of Science:

  • Neurodegenerative diseases
  • Endocrinology
  • Pharmacology

Background:

  • Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease with limited treatment options.
  • Investigating alternative and off-label treatments is crucial for improving patient outcomes.
  • Insulin presents a potential therapeutic avenue due to plausible biological mechanisms for neuroprotection.

Approach:

  • This review examines the current evidence for insulin as a treatment to slow ALS progression.
  • The review focuses on pre-clinical data and the potential mechanisms of action.
  • Safety considerations and the lack of clinical trials in people with ALS are critically assessed.

Key Points:

  • Insulin has a plausible biological mechanism that might slow ALS progression.
  • Pre-clinical studies on insulin for ALS are limited.
  • There are no completed clinical trials of insulin in people with ALS.
  • Insulin use in individuals without a metabolic need carries significant risks of severe side effects.

Conclusions:

  • While insulin's potential benefits warrant further investigation, current evidence is insufficient to support its use.
  • The serious risks associated with insulin administration in non-diabetic individuals cannot be overlooked.
  • Further rigorous clinical trials are required to determine the safety and efficacy of insulin in slowing ALS progression.