Resistin / Fizz3 Expression in Relation to Obesity and Peroxisome Proliferator–Activated Receptor-γ Action in Humans
Resistin / Fizz3 Expression in Relation to Obesity and Peroxisome Proliferator–Activated Receptor-γ Action in Humans David B. Savage 1 , Ciaran P. Sewter 1 , Ellen S. Klenk 2 , David G. Segal 2 , Antonio Vidal-Puig 1 , Robert V. Considine 2 and Stephen O’Rahilly 1 1 University Departments of Medicin...
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| Published in | Diabetes (New York, N.Y.) Vol. 50; no. 10; pp. 2199 - 2202 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Alexandria, VA
American Diabetes Association
01.10.2001
|
| Subjects | |
| Online Access | Get full text |
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| Abstract | Resistin / Fizz3 Expression in Relation to Obesity and Peroxisome Proliferator–Activated Receptor-γ Action in Humans
David B. Savage 1 ,
Ciaran P. Sewter 1 ,
Ellen S. Klenk 2 ,
David G. Segal 2 ,
Antonio Vidal-Puig 1 ,
Robert V. Considine 2 and
Stephen O’Rahilly 1
1 University Departments of Medicine and Clinical Biochemistry, Addenbrooke’s Hospital, Cambridge, United Kingdom
2 Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana
Abstract
Recent studies in murine models suggest that resistin (also called Fizz3 [ 1 ]), a novel cysteine-rich protein secreted by adipocytes, may represent the long-sought link between obesity and insulin resistance
( 2 ). Furthermore, peroxisome proliferator–activated receptor-γ (PPAR-γ) agonists appear to inhibit resistin expression in murine
adipocytes, providing a possible explanation for the mode of action of this class of insulin sensitizers ( 2 ). Using a fluorescent real-time reverse transcriptase–polymerase chain reaction–based assay, we found that resistin mRNA
levels in whole adipose tissue samples were increased in morbidly obese humans compared with lean control subjects. However,
in freshly isolated human adipocytes, resistin mRNA levels were very low and showed no correlation with BMI. Resistin mRNA
was undetectable in preadipocytes, endothelial cells, and vascular smooth muscle cells, but it was readily detectable in circulating
mononuclear cells. Although exposure of human mononuclear cells to PPAR-γ agonists markedly upregulated fatty acid–binding
protein-4 expression, these agents had no effect on mononuclear cell resistin expression. Finally, resistin mRNA was undetectable
in adipocytes from a severely insulin-resistant subject with a dominant-negative mutation in PPAR-γ ( 3 ). We conclude that the recently described relationships of murine resistin/Fizz3 expression with obesity, insulin resistance,
and PPAR-γ action may not readily translate to humans. Further studies of this novel class of proteins are needed to clarify
their roles in human metabolism.
Footnotes
Address correspondence and reprint requests to S. O’Rahilly, Department of Medicine, Box 157, Addenbrooke’s Hospital, Cambridge,
CB2 2QR, U.K. E-mail: sorahill{at}hgmp.mrc.ac.uk .
Received for publication 24 April 2001 and accepted in revised form 7 August 2001. Posted on the World Wide Web at http://www.diabetes.org/diabetes_rapids on 6 September 2001.
FABP4, fatty acid–binding protein-4; FBS, fetal bovine serum; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PBMC, peripheral
blood mononuclear cell; PBS, phosphate-buffered saline; PCR, polymerase chain reaction; PPAR-γ, peroxisome proliferator–activated
receptor-γ; RT, reverse transcriptase; TNF-α, tumor necrosis factor-α; WAT, white adipose tissue. |
|---|---|
| AbstractList | Resistin / Fizz3 Expression in Relation to Obesity and Peroxisome Proliferator–Activated Receptor-γ Action in Humans
David B. Savage 1 ,
Ciaran P. Sewter 1 ,
Ellen S. Klenk 2 ,
David G. Segal 2 ,
Antonio Vidal-Puig 1 ,
Robert V. Considine 2 and
Stephen O’Rahilly 1
1 University Departments of Medicine and Clinical Biochemistry, Addenbrooke’s Hospital, Cambridge, United Kingdom
2 Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana
Abstract
Recent studies in murine models suggest that resistin (also called Fizz3 [ 1 ]), a novel cysteine-rich protein secreted by adipocytes, may represent the long-sought link between obesity and insulin resistance
( 2 ). Furthermore, peroxisome proliferator–activated receptor-γ (PPAR-γ) agonists appear to inhibit resistin expression in murine
adipocytes, providing a possible explanation for the mode of action of this class of insulin sensitizers ( 2 ). Using a fluorescent real-time reverse transcriptase–polymerase chain reaction–based assay, we found that resistin mRNA
levels in whole adipose tissue samples were increased in morbidly obese humans compared with lean control subjects. However,
in freshly isolated human adipocytes, resistin mRNA levels were very low and showed no correlation with BMI. Resistin mRNA
was undetectable in preadipocytes, endothelial cells, and vascular smooth muscle cells, but it was readily detectable in circulating
mononuclear cells. Although exposure of human mononuclear cells to PPAR-γ agonists markedly upregulated fatty acid–binding
protein-4 expression, these agents had no effect on mononuclear cell resistin expression. Finally, resistin mRNA was undetectable
in adipocytes from a severely insulin-resistant subject with a dominant-negative mutation in PPAR-γ ( 3 ). We conclude that the recently described relationships of murine resistin/Fizz3 expression with obesity, insulin resistance,
and PPAR-γ action may not readily translate to humans. Further studies of this novel class of proteins are needed to clarify
their roles in human metabolism.
Footnotes
Address correspondence and reprint requests to S. O’Rahilly, Department of Medicine, Box 157, Addenbrooke’s Hospital, Cambridge,
CB2 2QR, U.K. E-mail: sorahill{at}hgmp.mrc.ac.uk .
Received for publication 24 April 2001 and accepted in revised form 7 August 2001. Posted on the World Wide Web at http://www.diabetes.org/diabetes_rapids on 6 September 2001.
FABP4, fatty acid–binding protein-4; FBS, fetal bovine serum; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; PBMC, peripheral
blood mononuclear cell; PBS, phosphate-buffered saline; PCR, polymerase chain reaction; PPAR-γ, peroxisome proliferator–activated
receptor-γ; RT, reverse transcriptase; TNF-α, tumor necrosis factor-α; WAT, white adipose tissue. Recent studies in murine models suggest that resistin (also called Fizz3 [1]), a novel cysteine-rich protein secreted by adipocytes, may represent the long-sought link between obesity and insulin resistance (2). Furthermore, peroxisome proliferator–activated receptor-γ (PPAR-γ) agonists appear to inhibit resistin expression in murine adipocytes, providing a possible explanation for the mode of action of this class of insulin sensitizers (2). Using a fluorescent real-time reverse transcriptase–polymerase chain reaction–based assay, we found that resistin mRNA levels in whole adipose tissue samples were increased in morbidly obese humans compared with lean control subjects. However, in freshly isolated human adipocytes, resistin mRNA levels were very low and showed no correlation with BMI. Resistin mRNA was undetectable in preadipocytes, endothelial cells, and vascular smooth muscle cells, but it was readily detectable in circulating mononuclear cells. Although exposure of human mononuclear cells to PPAR-γ agonists markedly upregulated fatty acid–binding protein-4 expression, these agents had no effect on mononuclear cell resistin expression. Finally, resistin mRNA was undetectable in adipocytes from a severely insulin-resistant subject with a dominant-negative mutation in PPAR-γ (3). We conclude that the recently described relationships of murine resistin/Fizz3 expression with obesity, insulin resistance, and PPAR-γ action may not readily translate to humans. Further studies of this novel class of proteins are needed to clarify their roles in human metabolism. Recent studies in murine models suggest that resistin (also called Fizz3 [1]), a novel cysteine-rich protein secreted by adipocytes, may represent the long-sought link between obesity and insulin resistance (2). Furthermore, peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists appear to inhibit resistin expression in murine adipocytes, providing a possible explanation for the mode of action of this class of insulin sensitizers (2). Using a fluorescent real-time reverse transcriptase-polymerase chain reaction-based assay, we found that resistin mRNA levels in whole adipose tissue samples were increased in morbidly obese humans compared with lean control subjects. However, in freshly isolated human adipocytes, resistin mRNA levels were very low and showed no correlation with BMI. Resistin mRNA was undetectable in preadipocytes, endothelial cells, and vascular smooth muscle cells, but it was readily detectable in circulating mononuclear cells. Although exposure of human mononuclear cells to PPAR-gamma agonists markedly upregulated fatty acid-binding protein-4 expression, these agents had no effect on mononuclear cell resistin expression. Finally, resistin mRNA was undetectable in adipocytes from a severely insulin-resistant subject with a dominant-negative mutation in PPAR-gamma (3). We conclude that the recently described relationships of murine resistin/Fizz3 expression with obesity, insulin resistance, and PPAR-gamma action may not readily translate to humans. Further studies of this novel class of proteins are needed to clarify their roles in human metabolism.Recent studies in murine models suggest that resistin (also called Fizz3 [1]), a novel cysteine-rich protein secreted by adipocytes, may represent the long-sought link between obesity and insulin resistance (2). Furthermore, peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists appear to inhibit resistin expression in murine adipocytes, providing a possible explanation for the mode of action of this class of insulin sensitizers (2). Using a fluorescent real-time reverse transcriptase-polymerase chain reaction-based assay, we found that resistin mRNA levels in whole adipose tissue samples were increased in morbidly obese humans compared with lean control subjects. However, in freshly isolated human adipocytes, resistin mRNA levels were very low and showed no correlation with BMI. Resistin mRNA was undetectable in preadipocytes, endothelial cells, and vascular smooth muscle cells, but it was readily detectable in circulating mononuclear cells. Although exposure of human mononuclear cells to PPAR-gamma agonists markedly upregulated fatty acid-binding protein-4 expression, these agents had no effect on mononuclear cell resistin expression. Finally, resistin mRNA was undetectable in adipocytes from a severely insulin-resistant subject with a dominant-negative mutation in PPAR-gamma (3). We conclude that the recently described relationships of murine resistin/Fizz3 expression with obesity, insulin resistance, and PPAR-gamma action may not readily translate to humans. Further studies of this novel class of proteins are needed to clarify their roles in human metabolism. Recent studies in murine models suggest that resistin (also called Fizz3 [1]), a novel cysteine-rich protein secreted by adipocytes, may represent the long-sought link between obesity and insulin resistance (2). Furthermore, peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists appear to inhibit resistin expression in murine adipocytes, providing a possible explanation for the mode of action of this class of insulin sensitizers (2). Using a fluorescent real-time reverse transcriptase-polymerase chain reaction-based assay, we found that resistin mRNA levels in whole adipose tissue samples were increased in morbidly obese humans compared with lean control subjects. However, in freshly isolated human adipocytes, resistin mRNA levels were very low and showed no correlation with BMI. Resistin mRNA was undetectable in preadipocytes, endothelial cells, and vascular smooth muscle cells, but it was readily detectable in circulating mononuclear cells. Although exposure of human mononuclear cells to PPAR-gamma agonists markedly upregulated fatty acid-binding protein-4 expression, these agents had no effect on mononuclear cell resistin expression. Finally, resistin mRNA was undetectable in adipocytes from a severely insulin-resistant subject with a dominant-negative mutation in PPAR-gamma (3). We conclude that the recently described relationships of murine resistin/Fizz3 expression with obesity, insulin resistance, and PPAR-gamma action may not readily translate to humans. Further studies of this novel class of proteins are needed to clarify their roles in human metabolism. |
| Audience | Professional |
| Author | Robert V. Considine David B. Savage Ciaran P. Sewter David G. Segal Ellen S. Klenk Stephen O’Rahilly Antonio Vidal-Puig |
| Author_xml | – sequence: 1 givenname: David B. surname: Savage fullname: Savage, David B. organization: University Departments of Medicine and Clinical Biochemistry, Addenbrooke’s Hospital, Cambridge, United Kingdom – sequence: 2 givenname: Ciaran P. surname: Sewter fullname: Sewter, Ciaran P. organization: University Departments of Medicine and Clinical Biochemistry, Addenbrooke’s Hospital, Cambridge, United Kingdom – sequence: 3 givenname: Ellen S. surname: Klenk fullname: Klenk, Ellen S. organization: Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana – sequence: 4 givenname: David G. surname: Segal fullname: Segal, David G. organization: Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana – sequence: 5 givenname: Antonio surname: Vidal-Puig fullname: Vidal-Puig, Antonio organization: University Departments of Medicine and Clinical Biochemistry, Addenbrooke’s Hospital, Cambridge, United Kingdom – sequence: 6 givenname: Robert V. surname: Considine fullname: Considine, Robert V. organization: Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana – sequence: 7 givenname: Stephen surname: O’Rahilly fullname: O’Rahilly, Stephen organization: University Departments of Medicine and Clinical Biochemistry, Addenbrooke’s Hospital, Cambridge, United Kingdom |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14146845$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/11574398$$D View this record in MEDLINE/PubMed |
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| PublicationDate_xml | – month: 10 year: 2001 text: 2001-10-01 day: 01 |
| PublicationDecade | 2000 |
| PublicationPlace | Alexandria, VA |
| PublicationPlace_xml | – name: Alexandria, VA – name: United States – name: New York |
| PublicationTitle | Diabetes (New York, N.Y.) |
| PublicationTitleAlternate | Diabetes |
| PublicationYear | 2001 |
| Publisher | American Diabetes Association |
| Publisher_xml | – name: American Diabetes Association |
| References | 2022031212265572600_R12 2022031212265572600_R13 2022031212265572600_R14 2022031212265572600_R15 2022031212265572600_R16 2022031212265572600_R9 2022031212265572600_R8 2022031212265572600_R7 2022031212265572600_R10 2022031212265572600_R11 2022031212265572600_R2 2022031212265572600_R1 2022031212265572600_R6 2022031212265572600_R5 2022031212265572600_R4 2022031212265572600_R3 |
| References_xml | – ident: 2022031212265572600_R1 doi: 10.1093/emboj/19.15.4046 – ident: 2022031212265572600_R7 doi: 10.1021/jm990554g – ident: 2022031212265572600_R10 doi: 10.1172/JCI117936 – ident: 2022031212265572600_R15 doi: 10.2337/diabetes.47.9.1384 – ident: 2022031212265572600_R3 doi: 10.1038/47254 – ident: 2022031212265572600_R6 doi: 10.1172/JCI119870 – ident: 2022031212265572600_R2 doi: 10.1038/35053000 – ident: 2022031212265572600_R9 doi: 10.2337/diabetes.46.3.342 – ident: 2022031212265572600_R11 doi: 10.1111/j.1365-2362.1995.tb01690.x – ident: 2022031212265572600_R8 doi: 10.1074/jbc.C100028200 – ident: 2022031212265572600_R16 doi: 10.2337/diab.45.7.881 – ident: 2022031212265572600_R13 doi: 10.1172/JCI10843 – ident: 2022031212265572600_R14 doi: 10.1126/science.7678183 – ident: 2022031212265572600_R5 doi: 10.1210/jc.85.10.3551 – ident: 2022031212265572600_R12 doi: 10.1210/jc.83.11.3925 – ident: 2022031212265572600_R4 doi: 10.1074/jbc.C100189200 |
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| Snippet | Resistin / Fizz3 Expression in Relation to Obesity and Peroxisome Proliferator–Activated Receptor-γ Action in Humans
David B. Savage 1 ,
Ciaran P. Sewter 1 ,... Recent studies in murine models suggest that resistin (also called Fizz3 [1]), a novel cysteine-rich protein secreted by adipocytes, may represent the... |
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| SubjectTerms | Adipocytes Adipocytes - metabolism Adult Biological and medical sciences Body fat Body Mass Index Cells, Cultured Comorbidity Complications and side effects Computer Systems Diabetes Diabetes research Fatty acids Female Hormones, Ectopic - genetics Hormones, Ectopic - metabolism Humans Insulin resistance Intercellular Signaling Peptides and Proteins Male Medical sciences Men Metabolic diseases Monocytes - metabolism Obesity Obesity - metabolism Obesity - pathology Polymerase chain reaction Proteins Receptors, Cytoplasmic and Nuclear - agonists Receptors, Cytoplasmic and Nuclear - physiology Resistin Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - blood RNA, Messenger - metabolism Smooth muscle Transcription Factors - agonists Transcription Factors - physiology White people |
| Title | Resistin / Fizz3 Expression in Relation to Obesity and Peroxisome Proliferator–Activated Receptor-γ Action in Humans |
| URI | http://diabetes.diabetesjournals.org/content/50/10/2199.abstract https://www.ncbi.nlm.nih.gov/pubmed/11574398 https://www.proquest.com/docview/216488564 https://www.proquest.com/docview/71201276 |
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