Transcriptomics applied to obesity and caloric restriction

N. Viguerie, C. Poitou, R. Cancello, V. Stich, K. Clément, D. Langin

Research output: Contribution to journalArticle

Abstract

Caloric restriction still remains the most efficient way to promote weight loss. Deciphering the molecular basis of adaptation to energy restriction is critical for the tailoring of new therapeutic strategies. This review focuses on the recent input of gene profiling on adipose tissue in obesity pathogenesis and on the new insights on adaptations occurring during very low caloric diet (VLCD) in humans. Hypocaloric diets improve a wide range of metabolic parameters including lipolytic efficiency, insulin sensitivity, and inflammatory profile. In the subcutaneous white adipose tissue (scWAT) the VLCD induced a decrease in the mRNA levels for the antilipolytic α2-adrenergic receptor associated with changes in catecholamine-induced adipocyte lipolytic capacity. The improvement in insulin sensitivity was not associated with a change in subcutaneous adipose tissue adiponectin gene expression or in its plasma level, suggesting that adiponectin is not involved in the regulation of VLCD-induced improvement of insulin sensitivity and that there is a small contribution of subcutaneous adipose tissue to plasma adiponectin levels. Pangenomic microarray studies in human scWAT revealed that a panel of inflammatory markers and acute phase reactants were over expressed in obese compared to lean subjects. Caloric restriction improved the inflammatory profile of obese subjects through a decrease of pro-inflammatory factors and an increase of anti-inflammatory molecules. These genes were mostly expressed in the stroma vascular fraction of the adipose tissue. Specific cell-type isolation and immunohistochemistry demonstrated that monocyte/macrophage lineage cells were responsible for the expression of both mRNA and protein inflammatory markers. The acute phase proteins serum amyloid A was highly expressed in mature adipocytes from obese subjects. Caloric restriction decreased both serum amyloid mRNA and circulating levels. Obesity now clearly appears as chronic low-grade inflammation state. Modulation of the inflammatory pathways may represent new therapeutic targets for the treatment of obesity-related complications.

Original languageEnglish
Pages (from-to)117-123
Number of pages7
JournalBiochimie
Volume87
Issue number1 SPEC. ISS.
DOIs
Publication statusPublished - Jan 2005

Fingerprint

Caloric Restriction
Subcutaneous Fat
Adiponectin
Obesity
Tissue
Nutrition
Diet
Insulin Resistance
White Adipose Tissue
Acute-Phase Proteins
Adipocytes
Messenger RNA
Adipose Tissue
Insulin
Serum Amyloid A Protein
Cell Separation
Genes
Amyloid
Adrenergic Receptors
Catecholamines

Keywords

  • Caloric restriction
  • Inflammation
  • Macrophages
  • Microarrays
  • Obesity

ASJC Scopus subject areas

  • Biochemistry

Cite this

Viguerie, N., Poitou, C., Cancello, R., Stich, V., Clément, K., & Langin, D. (2005). Transcriptomics applied to obesity and caloric restriction. Biochimie, 87(1 SPEC. ISS.), 117-123. https://doi.org/10.1016/j.biochi.2004.12.011

Transcriptomics applied to obesity and caloric restriction. / Viguerie, N.; Poitou, C.; Cancello, R.; Stich, V.; Clément, K.; Langin, D.

In: Biochimie, Vol. 87, No. 1 SPEC. ISS., 01.2005, p. 117-123.

Research output: Contribution to journalArticle

Viguerie, N, Poitou, C, Cancello, R, Stich, V, Clément, K & Langin, D 2005, 'Transcriptomics applied to obesity and caloric restriction', Biochimie, vol. 87, no. 1 SPEC. ISS., pp. 117-123. https://doi.org/10.1016/j.biochi.2004.12.011
Viguerie N, Poitou C, Cancello R, Stich V, Clément K, Langin D. Transcriptomics applied to obesity and caloric restriction. Biochimie. 2005 Jan;87(1 SPEC. ISS.):117-123. https://doi.org/10.1016/j.biochi.2004.12.011
Viguerie, N. ; Poitou, C. ; Cancello, R. ; Stich, V. ; Clément, K. ; Langin, D. / Transcriptomics applied to obesity and caloric restriction. In: Biochimie. 2005 ; Vol. 87, No. 1 SPEC. ISS. pp. 117-123.
@article{d393d3f732a247938cb4e9dd8f519359,
title = "Transcriptomics applied to obesity and caloric restriction",
abstract = "Caloric restriction still remains the most efficient way to promote weight loss. Deciphering the molecular basis of adaptation to energy restriction is critical for the tailoring of new therapeutic strategies. This review focuses on the recent input of gene profiling on adipose tissue in obesity pathogenesis and on the new insights on adaptations occurring during very low caloric diet (VLCD) in humans. Hypocaloric diets improve a wide range of metabolic parameters including lipolytic efficiency, insulin sensitivity, and inflammatory profile. In the subcutaneous white adipose tissue (scWAT) the VLCD induced a decrease in the mRNA levels for the antilipolytic α2-adrenergic receptor associated with changes in catecholamine-induced adipocyte lipolytic capacity. The improvement in insulin sensitivity was not associated with a change in subcutaneous adipose tissue adiponectin gene expression or in its plasma level, suggesting that adiponectin is not involved in the regulation of VLCD-induced improvement of insulin sensitivity and that there is a small contribution of subcutaneous adipose tissue to plasma adiponectin levels. Pangenomic microarray studies in human scWAT revealed that a panel of inflammatory markers and acute phase reactants were over expressed in obese compared to lean subjects. Caloric restriction improved the inflammatory profile of obese subjects through a decrease of pro-inflammatory factors and an increase of anti-inflammatory molecules. These genes were mostly expressed in the stroma vascular fraction of the adipose tissue. Specific cell-type isolation and immunohistochemistry demonstrated that monocyte/macrophage lineage cells were responsible for the expression of both mRNA and protein inflammatory markers. The acute phase proteins serum amyloid A was highly expressed in mature adipocytes from obese subjects. Caloric restriction decreased both serum amyloid mRNA and circulating levels. Obesity now clearly appears as chronic low-grade inflammation state. Modulation of the inflammatory pathways may represent new therapeutic targets for the treatment of obesity-related complications.",
keywords = "Caloric restriction, Inflammation, Macrophages, Microarrays, Obesity",
author = "N. Viguerie and C. Poitou and R. Cancello and V. Stich and K. Cl{\'e}ment and D. Langin",
year = "2005",
month = "1",
doi = "10.1016/j.biochi.2004.12.011",
language = "English",
volume = "87",
pages = "117--123",
journal = "Biochimie",
issn = "0300-9084",
publisher = "Elsevier",
number = "1 SPEC. ISS.",

}

TY - JOUR

T1 - Transcriptomics applied to obesity and caloric restriction

AU - Viguerie, N.

AU - Poitou, C.

AU - Cancello, R.

AU - Stich, V.

AU - Clément, K.

AU - Langin, D.

PY - 2005/1

Y1 - 2005/1

N2 - Caloric restriction still remains the most efficient way to promote weight loss. Deciphering the molecular basis of adaptation to energy restriction is critical for the tailoring of new therapeutic strategies. This review focuses on the recent input of gene profiling on adipose tissue in obesity pathogenesis and on the new insights on adaptations occurring during very low caloric diet (VLCD) in humans. Hypocaloric diets improve a wide range of metabolic parameters including lipolytic efficiency, insulin sensitivity, and inflammatory profile. In the subcutaneous white adipose tissue (scWAT) the VLCD induced a decrease in the mRNA levels for the antilipolytic α2-adrenergic receptor associated with changes in catecholamine-induced adipocyte lipolytic capacity. The improvement in insulin sensitivity was not associated with a change in subcutaneous adipose tissue adiponectin gene expression or in its plasma level, suggesting that adiponectin is not involved in the regulation of VLCD-induced improvement of insulin sensitivity and that there is a small contribution of subcutaneous adipose tissue to plasma adiponectin levels. Pangenomic microarray studies in human scWAT revealed that a panel of inflammatory markers and acute phase reactants were over expressed in obese compared to lean subjects. Caloric restriction improved the inflammatory profile of obese subjects through a decrease of pro-inflammatory factors and an increase of anti-inflammatory molecules. These genes were mostly expressed in the stroma vascular fraction of the adipose tissue. Specific cell-type isolation and immunohistochemistry demonstrated that monocyte/macrophage lineage cells were responsible for the expression of both mRNA and protein inflammatory markers. The acute phase proteins serum amyloid A was highly expressed in mature adipocytes from obese subjects. Caloric restriction decreased both serum amyloid mRNA and circulating levels. Obesity now clearly appears as chronic low-grade inflammation state. Modulation of the inflammatory pathways may represent new therapeutic targets for the treatment of obesity-related complications.

AB - Caloric restriction still remains the most efficient way to promote weight loss. Deciphering the molecular basis of adaptation to energy restriction is critical for the tailoring of new therapeutic strategies. This review focuses on the recent input of gene profiling on adipose tissue in obesity pathogenesis and on the new insights on adaptations occurring during very low caloric diet (VLCD) in humans. Hypocaloric diets improve a wide range of metabolic parameters including lipolytic efficiency, insulin sensitivity, and inflammatory profile. In the subcutaneous white adipose tissue (scWAT) the VLCD induced a decrease in the mRNA levels for the antilipolytic α2-adrenergic receptor associated with changes in catecholamine-induced adipocyte lipolytic capacity. The improvement in insulin sensitivity was not associated with a change in subcutaneous adipose tissue adiponectin gene expression or in its plasma level, suggesting that adiponectin is not involved in the regulation of VLCD-induced improvement of insulin sensitivity and that there is a small contribution of subcutaneous adipose tissue to plasma adiponectin levels. Pangenomic microarray studies in human scWAT revealed that a panel of inflammatory markers and acute phase reactants were over expressed in obese compared to lean subjects. Caloric restriction improved the inflammatory profile of obese subjects through a decrease of pro-inflammatory factors and an increase of anti-inflammatory molecules. These genes were mostly expressed in the stroma vascular fraction of the adipose tissue. Specific cell-type isolation and immunohistochemistry demonstrated that monocyte/macrophage lineage cells were responsible for the expression of both mRNA and protein inflammatory markers. The acute phase proteins serum amyloid A was highly expressed in mature adipocytes from obese subjects. Caloric restriction decreased both serum amyloid mRNA and circulating levels. Obesity now clearly appears as chronic low-grade inflammation state. Modulation of the inflammatory pathways may represent new therapeutic targets for the treatment of obesity-related complications.

KW - Caloric restriction

KW - Inflammation

KW - Macrophages

KW - Microarrays

KW - Obesity

UR - http://www.scopus.com/inward/record.url?scp=14544301451&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=14544301451&partnerID=8YFLogxK

U2 - 10.1016/j.biochi.2004.12.011

DO - 10.1016/j.biochi.2004.12.011

M3 - Article

C2 - 15733746

AN - SCOPUS:14544301451

VL - 87

SP - 117

EP - 123

JO - Biochimie

JF - Biochimie

SN - 0300-9084

IS - 1 SPEC. ISS.

ER -