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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.
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Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

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Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

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Type II Diabetes II: Pathophysiology01:24

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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.
Diabetes Mellitus: Overview and Type I Subtype01:22

Diabetes Mellitus: Overview and Type I Subtype

Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
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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...

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Combined Intravital Microscopy and Contrast-enhanced Ultrasonography of the Mouse Hindlimb to Study Insulin-induced Vasodilation and Muscle Perfusion
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Insulin and aging.

Andrzej Bartke1

  • 1Department of Internal Medicine and Department of Physiology, Southern Illinois University School of Medicine, Springfield, Illinois 62794-9628, USA. abartke@siumed.edu

Cell Cycle (Georgetown, Tex.)
|October 25, 2008
PubMed
Summary
This summary is machine-generated.

Insulin signaling pathways significantly impact aging and longevity across species. Genetic modifications affecting insulin signaling in mice and studies in long-lived humans suggest its crucial role in aging processes.

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Area of Science:

  • Aging research
  • Molecular biology
  • Genetics

Background:

  • Insulin and IGF-1 signaling pathways regulate longevity in invertebrates.
  • These pathways are implicated in mammalian aging, but distinguishing roles of insulin, IGF-1, and GH is challenging.

Purpose of the Study:

  • To investigate the role of insulin signaling in mammalian aging and longevity.
  • To explore the relationship between insulin signaling, GH, and lifespan extension.

Main Methods:

  • Analysis of genetically modified mice with disrupted insulin signaling (e.g., adipose tissue insulin receptor knockout).
  • Examination of mice with deletions in insulin receptor substrates (IRS1, IRS2).
  • Study of growth hormone (GH) deficient or resistant mice.

Main Results:

  • Selective disruption of the insulin receptor in adipose tissue extended mouse longevity.
  • Deletion of IRS1 or IRS2 in mice also increased lifespan.
  • GH deficiency/resistance in mice resulted in hypoinsulinemia, enhanced insulin sensitivity, and extended longevity, mimicking calorie restriction.

Conclusions:

  • Insulin signaling pathways are critical regulators of aging and longevity in mammals.
  • Manipulating insulin signaling components offers potential strategies for lifespan extension.
  • Human studies on long-lived individuals support the role of insulin signaling in human aging.