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Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Inflammation: Introduction01:28

Inflammation: Introduction

Inflammation is a fundamental, protective biological response of vascularized tissues to cellular injury, infection, or harmful stimuli. Its primary function is to eliminate the initial cause of injury, clear necrotic cells and damaged tissue, and initiate the necessary repair processes.Cardinal SignsAcute inflammation presents with classic signs. Redness results from vasodilation and increased blood flow. Heat is due to increased metabolism and circulation. Swelling results from the...
Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
Acute Inflammation II: Local and Systemic Effects01:25

Acute Inflammation II: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...

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Related Experiment Video

Updated: May 10, 2026

Identification and Dissection of Diverse Mouse Adipose Depots
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Identification and Dissection of Diverse Mouse Adipose Depots

Published on: July 11, 2019

Adiponectin and inflammation: consensus and controversy.

Giamila Fantuzzi1

  • 1Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL 60612, USA. giamila@uic.edu

The Journal of Allergy and Clinical Immunology
|December 7, 2007
PubMed
Summary
This summary is machine-generated.

Adiponectin levels decrease with obesity and type 2 diabetes, but increase in autoimmune diseases. This study explores the paradox of adiponectin

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An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function
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An Adipocyte Cell Culture Model to Study the Impact of Protein and Micro-RNA Modulation on Adipocyte Function

Published on: May 4, 2021

Area of Science:

  • Endocrinology
  • Immunology
  • Metabolic Syndrome

Background:

  • Circulating adiponectin levels are inversely correlated with visceral obesity, type 2 diabetes, metabolic syndrome, and cardiovascular disease.
  • Adiponectin exhibits anti-inflammatory properties, yet chronic inflammation associated with obesity may inhibit its production, creating a perpetuating cycle.
  • Conversely, adiponectin levels are elevated in chronic inflammatory/autoimmune diseases unrelated to obesity, such as rheumatoid arthritis and SLE.

Purpose of the Study:

  • To investigate the paradoxical regulation of adiponectin in obesity-associated inflammation versus classic chronic inflammatory/autoimmune diseases.
  • To explore potential explanations for the differential functions and regulation of adiponectin in distinct inflammatory conditions.

Main Methods:

  • Review and synthesis of existing scientific literature on adiponectin levels, inflammation markers, and disease states.
  • Comparative analysis of adiponectin's role in obesity-related metabolic disorders versus autoimmune conditions.

Main Results:

  • Adiponectin levels decrease with increasing visceral obesity and are negatively correlated with inflammation markers in metabolic diseases.
  • Adiponectin levels increase in chronic inflammatory/autoimmune diseases and positively correlate with inflammation markers.
  • Proinflammatory effects of adiponectin have been reported in specific tissues within these autoimmune conditions.

Conclusions:

  • Adiponectin exhibits opposing regulatory patterns and potentially differential functions in obesity-associated inflammation compared to classic inflammatory diseases.
  • The study highlights a complex interplay between adiponectin, inflammation, and metabolic versus autoimmune conditions, necessitating further investigation into underlying mechanisms.