The Expression of Adipose Tissue-Derived Cardiotrophin-1 in Humans with Obesity

Jacqueline Stephens1, Eric Ravussin2, Ursula White3

  • 1Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA. jsteph1@lsu.edu.

Biology
|April 25, 2019
PubMed

Insights

Cardiotrophin-1 (CT-1) expression in human fat tissue varies by location and is linked to metabolic health. Higher CT-1 in subcutaneous fat may protect against obesity and metabolic syndrome complications.

Area of Science:

  • Endocrinology
  • Metabolic Research
  • Molecular Biology

Background:

  • Cardiotrophin-1 (CT-1) is a cytokine linked to heart failure, obesity, and metabolic syndrome (MetS).
  • Adipose tissue (AT) is an endocrine organ and a source of CT-1, but its human adipose-derived expression is unstudied.
  • Rodent studies suggest CT-1 may be a therapeutic target for obesity and MetS.

Purpose of the Study:

  • To analyze CT-1 mRNA expression in human subcutaneous adipose tissue depots.
  • To investigate the association of adipose-derived CT-1 with clinical variables in obesity and during overfeeding.

Main Methods:

  • Analysis of CT-1 mRNA expression in subcutaneous abdominal (scABD) and femoral (scFEM) adipose tissue depots.
  • Correlation of CT-1 expression with visceral adiposity, intrahepatic lipid, and insulin sensitivity in obese women and men undergoing 8-week overfeeding.

Main Results:

  • CT-1 expression was higher in scABD than scFEM adipose depots.
  • In obese women, scFEM CT-1 expression negatively correlated with visceral adiposity and intrahepatic lipid, and positively with insulin sensitivity.
  • In men, higher baseline CT-1 levels correlated with preserved insulin sensitivity after overfeeding.

Conclusions:

  • Adipose-derived CT-1 expression differs between human subcutaneous fat depots.
  • CT-1 may play a protective role in metabolic health, influencing visceral adiposity and insulin sensitivity in obesity.
  • CT-1 warrants further investigation as a potential therapeutic target for obesity and related metabolic disorders.

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