Monocyte chemoattractant protein-1 in subcutaneous abdominal adipose tissue: characterization of interstitial concentration and regulation of gene expression by insulin

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Fältnamn	Indikatorer	Metadata
000		05088naa a2200553 4500
001		oai:gup.ub.gu.se/50448
003		SwePub
008		240528s2007 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://gup.ub.gu.se/publication/504482 URI
024	7	a https://doi.org/10.1210/jc.2006-28142 DOI
040		a (SwePub)gu
041		a eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Murdolo, Giuseppe,d 1966u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine4 aut0 (Swepub:gu)xmurgi
245	1 0	a Monocyte chemoattractant protein-1 in subcutaneous abdominal adipose tissue: characterization of interstitial concentration and regulation of gene expression by insulin
264	1	b The Endocrine Society,c 2007
520		a CONTEXT: The chemokine monocyte chemoattractant protein-1 (MCP-1) is implicated in obesity-associated chronic inflammation, insulin resistance, and atherosclerosis. OBJECTIVES: The objectives of this study were to: 1) characterize the interstitial levels and the gene expression of MCP-1 in the sc abdominal adipose tissue (SCAAT), 2) elucidate the response of MCP-1 to acute hyperinsulinemia, and 3) determine the relationship between MCP-1 and arterial stiffness. DESIGN: Nine lean (L) and nine uncomplicated obese (OB) males were studied in the fasting state and during a euglycemic-hyperinsulinemic clamp combined with the microdialysis technique. Interstitial and serum MCP-1 (iMCP-1 and sMCP-1, respectively) levels, pulse wave analysis, and SCAAT biopsies were characterized at baseline and after hyperinsulinemia. RESULTS: OB showed elevated sMCP-1 (P < 0.01) but similar iMCP-1 levels as compared with L. Basal iMCP-1 concentrations were considerably higher than sMCP-1 (P < 0.0001), and a gradient between iMCP-1 and sMCP-1 levels was maintained throughout the hyperinsulinemia. At baseline, SCAAT gene expression profile revealed a "co-upregulation" of MCP-1, MCP-2, macrophage inflammatory protein-1alpha, and CD68 in OB, and whole-body glucose disposal inversely correlated with the MCP-1 gene expression. After hyperinsulinemia, MCP-1 and MCP-2 mRNA levels significantly increased in L, but not in OB. Finally, sMCP-1 excess in the OB positively correlated with the stiffer vasculature. CONCLUSIONS: These observations demonstrate similar interstitial concentrations and a differential gene response to hyperinsulinemia of MCP-1 in the SCAAT from L and OB individuals. In human obesity, we suggest the SCAAT MCP-1 gene overexpression as a biomarker of an "inflamed" adipose organ and impaired glucose metabolism.
653		a Adipocytes/cytology/physiology
653		a Adult
653		a Biological Markers
653		a Cell Size
653		a Chemokine CCL2/*genetics
653		a Diabetes Mellitus
653		a Type 2/*genetics/immunology/physiopathology
653		a Gene Expression Profiling
653		a Gene Expression Regulation/immunology
653		a *Genetic Markers
653		a Humans
653		a Hyperinsulinism/genetics/immunology/physiopathology
653		a Insulin/*blood
653		a Insulin Resistance
653		a Male
653		a Middle Aged
653		a Obesity/genetics/immunology/physiopathology
653		a Subcutaneous Fat/*physiology
700	1	a Hammarstedt, Ann,d 1975u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine4 aut0 (Swepub:gu)xhaman
700	1	a Sandqvist, Madelene,d 1974u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine4 aut0 (Swepub:gu)xsamad
700	1	a Schmelz, M.4 aut
700	1	a Herder, C.4 aut
700	1	a Smith, Ulf,d 1943u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine4 aut0 (Swepub:gu)xsmiul
700	1	a Jansson, Per-Anders,d 1961u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine4 aut0 (Swepub:gu)xjansp
710	2	a Göteborgs universitetb Institutionen för medicin, avdelningen för molekylär och klinisk medicin4 org
773	0	t J Clin Endocrinol Metabd : The Endocrine Societyg 92:7, s. 2688-95q 92:7<2688-95x 0021-972X
773	0	t The Journal of Clinical Endocrinology & Metabolismd : The Endocrine Societyg 92:7, s. 2688-95q 92:7<2688-95x 1945-7197
856	4	u https://academic.oup.com/jcem/article-pdf/92/7/2688/11059447/jcem2688.pdf
856	4 8	u https://gup.ub.gu.se/publication/50448
856	4 8	u https://doi.org/10.1210/jc.2006-2814

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Av författaren/redakt...: Murdolo, Giusepp ...; Hammarstedt, Ann ...; Sandqvist, Madel ...; Schmelz, M.; Herder, C.; Smith, Ulf, 1943; visa fler...; Jansson, Per-And ...; visa färre...

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