Plasma Osteopontin Levels and Expression in Adipose Tissue Are Increased in Obesity

Gómez-Ambrosi, Javier; Catalán, Victoria; Ramírez, Beatriz; Rodríguez, Amaia; Colina, Inmaculada; Silva, Camilo; Rotellar, Fernando; Mugueta, Carmen; Gil, Marı́a J.; Cienfuegos, Javier A.; Salvador, Javier; Frühbeck, Gema

doi:10.1210/jc.2007-0349

Cited by 187 publications

(158 citation statements)

References 58 publications

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“…In other words, the production of OPN was increased under various inflammatory conditions, such as that involved with calcified aortas, 17 coronary artery plaques 26 and obesity. 27 In addition, it was reported that in OPN-defective mice, fibrosis and arteriosclerotic changes were attenuated. 28,29 In this study, OPN gene transcription activity was enhanced dose-dependently and timedependently in Aldo-stimulated rVSMCs, which is consistent with reports in other various cell species, such as renal mesangium cells, 19 renal fibroblasts 21 and vascular endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Aldosterone-induced osteopontin gene transcription in vascular smooth muscle cells involves glucocorticoid response element

et al. 2011

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Osteopontin (OPN) is known to be one of the cytokines that is involved in the vascular inflammation caused by aldosterone (Aldo). Previous reports have shown that Aldo increases OPN transcripts, and the mechanisms for this remain to be clarified. In this study, we investigated how Aldo increases OPN transcripts in the vascular smooth muscle cells of rats. Aldosterone increased OPN transcripts time-dependently as well as dose-dependently. This increase was diminished by eplerenone, a mineralocorticoid receptor (MR) antagonist. Luciferase promoter assays showed that the OPN promoter deleted to the À1599 site retained the same promoting ability as the full-length OPN promoter when stimulated by 10 À7 M Aldo, but the promoter deleted to the À1300 site lost the promoting ability. A glucocorticoid response element (GRE) is located in that deleted region. Luciferase assays of a mutated promoter without the GRE lost the luciferase upregulation, although mutated promoters with the deletion of other consensus sites maintained the promoter activity. The binding of the Aldo-MR complex to the GRE fragment was confirmed by an electrophoretic-mobility shift assay. This is the first report showing that Aldo regulates the transcriptional levels of OPN and inflammatory responses in the vasculature through a specific GRE site in the OPN promoter region.

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Section: Discussionmentioning

confidence: 99%

Aldosterone-induced osteopontin gene transcription in vascular smooth muscle cells involves glucocorticoid response element

et al. 2011

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“…Plasma glucose and insulin was analyzed as previously described. 49,50 An indirect measure of insulin resistance was calculated by using the homeostatic model assessment. 51 Total cholesterol and triglyceride concentrations were determined by enzymatic spectrophotometric methods (Roche, Basel, Switzerland).…”

Section: Body Compositionmentioning

confidence: 99%

Body mass index classification misses subjects with increased cardiometabolic risk factors related to elevated adiposity

et al. 2011

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Context: Body mass index (BMI) is widely used as a measure of overweight and obesity, but underestimates the prevalence of both conditions, defined as an excess of body fat. Objective: We assessed the degree of misclassification on the diagnosis of obesity using BMI as compared with direct body fat percentage (BF%) determination and compared the cardiovascular and metabolic risk of non-obese and obese BMI-classified subjects with similar BF%. Design: We performed a cross-sectional study. Subjects: A total of 6123 (924 lean, 1637 overweight and 3562 obese classified according to BMI) Caucasian subjects (69% females), aged 18-80 years. Methods: BMI, BF% determined by air displacement plethysmography and well-established blood markers of insulin sensitivity, lipid profile and cardiovascular risk were measured. Results: We found that 29% of subjects classified as lean and 80% of individuals classified as overweight according to BMI had a BF% within the obesity range. Importantly, the levels of cardiometabolic risk factors, such as C-reactive protein, were higher in lean and overweight BMI-classified subjects with BF% within the obesity range (men 4.3 ± 9.2, women 4.9 ± 19.5 mg l À1 ) as well as in obese BMI-classified individuals (men 4.2 ± 5.5, women 5.1 ± 13.2 mg l À1 ) compared with lean volunteers with normal body fat amounts (men 0.9 ± 0.5, women 2.1 ± 2.6 mg l À1 ; Po0.001 for both genders). Conclusion: Given the elevated concentrations of cardiometabolic risk factors reported herein in non-obese individuals according to BMI but obese based on body fat, the inclusion of body composition measurements together with morbidity evaluation in the routine medical practice both for the diagnosis and the decision-making for instauration of the most appropriate treatment of obesity is desirable.

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“…At 20 min, regular insulin (Actrapid, Novo, Denmark; 0.03 U kg À1 ) was injected as a bolus. Additional samples were obtained from a contralateral antecubital vein at times 1,2,3,4,5,6,7,8,10,12,14,16,19,20,22,23,24,25,27,30,40,50,60,70,80,90, 100, 120, 140, 160 and 180 min. Samples were rapidly collected through a three-way stopcock connected to the butterfly needle.…”

Section: Study Of Insulin Sensitivitymentioning

confidence: 99%

“…19 Insulin was measured using an enzyme-amplified chemiluminescence assay (Immulite, Diagnostic Products Corp., Los Angeles, CA, USA). To estimate insulin resistance, the homeostasis model assessment (HOMA) index was calculated as fasting insulin concentration (mU ml À1 ) Â fasting glucose concentration (mmol l À1 )/22.5.…”

Section: Weight Loss Studymentioning

confidence: 99%

Circulating lipopolysaccharide-binding protein (LBP) as a marker of obesity-related insulin resistance

et al. 2011

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OBJECTIVE: Lipopolysaccharide-binding protein (LBP) is a 65-kDa acute-phase protein present in blood at high concentrations, known to be derived from the liver. We aimed to gain insights into the association of circulating LBP with insulin resistance in humans and mice. METHODS, DESIGN AND MEASUREMENTS: We studied the cross-sectional (n ¼ 222) and weight loss-induced (n ¼ 34) associations of LBP (enzyme-linked immunosorbent assay) with inflammatory and metabolic parameters (including minimal model-measured insulin sensitivity), and the effects of high-fat diet (HFD), metformin and genetic insulin sensitization (glucagon-like peptide 1 receptor knockout model) in mice. RESULTS: Circulating LBP concentration was significantly increased in subjects with type 2 diabetes and dramatically increased in subjects with morbid obesity. LBP was significantly associated with insulin sensitivity and different inflammatory markers and decreased after weight loss (22.2 ± 5.8 vs 16.2 ± 9.3 mg ml À1 , Po0.0001) in association with changes in body mass index and insulin sensitivity. Circulating LBP concentration was increased in HFD mice, whereas decreased in glucagon-like peptide 1 receptor knockout mice (significantly more insulin sensitive than wild-type mice) and after metformin administration. CONCLUSION: LBP is an inflammatory marker associated with obesity-related insulin resistance.

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Plasma Osteopontin Levels and Expression in Adipose Tissue Are Increased in Obesity

Cited by 187 publications

References 58 publications

Aldosterone-induced osteopontin gene transcription in vascular smooth muscle cells involves glucocorticoid response element

Aldosterone-induced osteopontin gene transcription in vascular smooth muscle cells involves glucocorticoid response element

Body mass index classification misses subjects with increased cardiometabolic risk factors related to elevated adiposity

Circulating lipopolysaccharide-binding protein (LBP) as a marker of obesity-related insulin resistance

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