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Related Concept Videos

Diabetes Mellitus: Type 2 and Gestational01:22

Diabetes Mellitus: Type 2 and Gestational

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Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
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Diabetes Mellitus: Overview and Type I Subtype01:22

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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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Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

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Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility,...
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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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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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Insulin Formulations: Types and Delivery01:27

Insulin Formulations: Types and Delivery

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Insulin preparations are categorized by their duration of action into short-acting and long-acting types. Two strategies are used to modify insulin's absorption and pharmacokinetic profile: slowing the absorption post-subcutaneous injection, or altering human insulin's amino acid sequence or protein structure. These changes retain the insulin's ability to bind to the insulin receptor, but alter its behavior in solution or after injection.
Short-acting insulins are divided into...
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Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. 1992.

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A Zebrafish Model of Diabetes Mellitus and Metabolic Memory
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Non-insulin-dependent diabetes mellitus

C N Hales1

  • 1Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.

British Medical Bulletin
|January 1, 1997
PubMed
Summary

Poor fetal growth may increase the risk of developing non-insulin-dependent diabetes mellitus (NIDDM) later in life. This suggests environmental factors during development impact adult glucose tolerance.

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Epidemiology

Background:

  • Non-insulin-dependent diabetes mellitus (NIDDM) typically emerges after age 50.
  • Distinguishing NIDDM from late-onset insulin-dependent diabetes can be challenging.
  • Genetic factors are traditionally considered primary causes of NIDDM.

Purpose of the Study:

  • To investigate the association between early life growth and adult glucose tolerance.
  • To explore potential mechanisms linking fetal development to NIDDM susceptibility.
  • To examine the role of environmental constraints on fetal growth.

Main Methods:

  • Epidemiological analysis of associations between growth indices and glucose tolerance.
  • Postulation of adaptive organogenesis changes due to fetal growth constraints.

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  • Utilizing an animal model (pregnant rats on reduced protein diet) to test hypotheses.

    • Main Results:

    • Statistical associations found between poor fetal/infant growth and reduced glucose tolerance in adulthood.
    • Proposed adaptive responses prioritize brain growth over visceral growth.
    • Altered liver function observed to aid survival under poor postnatal nutrition.

    Conclusions:

    • Environmental factors during fetal development may permanently alter organogenesis, influencing NIDDM risk.
    • Adaptive responses to fetal growth restriction can lead to impaired insulin secretion and insulin resistance.
    • Animal model results support the concept that early life nutrition impacts adult metabolic health.