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Related Concept Videos

Type I Diabetes II: Pathophysiology01:26

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...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

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.
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...
Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1 diabetes is an...
Diabetes Mellitus: Introduction01:26

Diabetes Mellitus: Introduction

Diabetes mellitus consists of chronic metabolic disorders characterized by persistent hyperglycemia. This elevated blood glucose results from defects in insulin secretion, impaired insulin action, or both. Insulin, produced by pancreatic β-cells, is essential for maintaining glucose homeostasis by facilitating cellular glucose uptake for energy or storage. Disruptions in insulin production or function lead to glucose accumulation in the bloodstream, causing the clinical features and long-term...

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Differentiated Mouse Adipocytes in Primary Culture: A Model of Insulin Resistance
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[Beyond immunopathogenesis. Insulin resistance and "epidermal dysfunction"].

W-H Boehncke1, S Boehncke, C Buerger

  • 1Klinik für Dermatologie, Venerologie und Allergologie, Klinikum der Johann Wolfgang Goethe-Universität, Theodor-Stern-Kai 7, 60590, Frankfurt am Main, Deutschland. Boehncke@em.uni-frankfurt.de

Der Hautarzt; Zeitschrift Fur Dermatologie, Venerologie, Und Verwandte Gebiete
|February 22, 2012
PubMed
Summary
This summary is machine-generated.

Insulin resistance impacts more than diabetes, affecting skin health and psoriasis. Targeting kinases could normalize epidermal function, complementing current psoriasis treatments.

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Area of Science:

  • Endocrinology
  • Dermatology
  • Cell Biology

Background:

  • Insulin resistance is central to type 2 diabetes and atherosclerosis.
  • Insulin also plays a critical role in maintaining epidermal homeostasis.
  • Cytokine-induced insulin resistance is implicated in skin conditions like psoriasis.

Purpose of the Study:

  • To summarize the effects of insulin on human keratinocyte proliferation and differentiation.
  • To explore the relevance of cytokine-induced insulin resistance in psoriasis pathogenesis.
  • To identify potential therapeutic targets for epidermal dysfunction.

Main Methods:

  • Review of existing literature on insulin signaling in keratinocytes.
  • Analysis of the role of insulin resistance in psoriasis.
  • Identification of kinase signaling pathways common to insulin and cytokine receptors.

Main Results:

  • Insulin influences human keratinocyte proliferation and differentiation.
  • Insulin resistance contributes to epidermal homeostasis alterations seen in psoriasis.
  • Kinases in insulin and cytokine signaling pathways are potential therapeutic targets.

Conclusions:

  • Insulin resistance has broad implications beyond metabolic diseases, including skin homeostasis.
  • Targeting specific kinases may offer a novel approach to treat epidermal dysfunction in psoriasis.
  • Pharmacological normalization of epidermal dysfunction could complement existing immunomodulatory therapies for psoriasis.