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Insulin: The Receptor and Signaling Pathways01:28

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Live Images of GLUT4 Protein Trafficking in Mouse Primary Hypothalamic Neurons Using Deconvolution Microscopy
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T Cell-based RAS Activity and Insulin Levels in Obese Subjects with Low Grade Inflammation.

M Coppo1, M Bandinelli1, M Chiostri1

  • 1Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy.

The American Journal of the Medical Sciences
|September 27, 2021
PubMed
Summary
This summary is machine-generated.

Obesity amplifies the renin-angiotensin system (RAS) response in T cells, especially with inflammation. Insulin may protect against inflammation, suggesting a link between obesity, inflammation, and insulin resistance.

Keywords:
Angiotensin IIInsulin resistanceObesityRenin-angiotensin systemT-cell

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Area of Science:

  • Endocrinology
  • Immunology
  • Metabolic Syndrome

Background:

  • Obesity contributes to inflammation and oxidative stress, key drivers of insulin resistance (IR) and diabetes.
  • The renin-angiotensin system (RAS) is implicated as a link between IR and obesity.
  • This study investigates RAS activity in circulating T cells of obese individuals with varying IR and inflammation levels.

Purpose of the Study:

  • To investigate renin-angiotensin system (RAS) activity in circulating T cells.
  • To assess the impact of obesity, insulin resistance (IR), and low-grade inflammation on T cell RAS.
  • To explore the relationship between T cell RAS, inflammation, and insulin levels.

Main Methods:

  • Quantified angiotensin converting enzyme (ACE) and angiotensin 1-receptor (AT1-R) mRNA in T cells via RT-PCR.
  • Measured serum levels of high-sensitivity C-reactive protein (hs-CRP), insulin, and inflammatory cytokines.
  • Assessed plasma renin activity (PRA), ACE activity, and angiotensin II (Ang II) levels in T cells.

Main Results:

  • Obese subjects showed higher baseline T cell RAS gene expression, ACE activity, and Ang II levels compared to controls.
  • Ang II-induced RAS response was significantly amplified in T cells from obese subjects with hs-CRP ≥3 mg/dl.
  • T cell RAS gene expression and cytokine levels were inversely correlated with insulin concentration in obese subjects with IR and inflammation.

Conclusions:

  • Low-grade inflammation exacerbates the T cell RAS response to Ang II stimulation.
  • T cell RAS gene expression and inflammatory cytokine levels show an inverse relationship with insulin concentration.
  • Insulin may exert a protective role against the development of inflammatory processes.