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15.03.2018 – They can be used to treat diabetes mellitus type 2. J Proteome Res ;9: Data were normalized to the protein level of actin and are expressed relative to day 0.
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3. 7 J Biol Chem ; http://softik.org/ccleaner-gratis-y-en-espanol/ http://softik.org/ccleaner-gratis-para-windows-10/DPP4 is a multifunctional, type II integral membrane glycoprotein exhibiting ubiquitous expression, including adipose tissue 23being highly abundant in the kidney, on T lymphocytes and endothelial cells Don J, Stelzer G.
4. 3 DPP4 released from adipose tissue correlated positively with an increasing risk score for the metabolic syndrome. Origin, development and regulation of human Leydig cells.Dpp1 5 29917ru mp 25 10 2011Expression of stimulated by retinoic acid gene 8 Stra8 and maturation of murine gonocytes and spermatogonia induced by retinoic acid in vitro. Reduced-resolution RAW image files June 25,
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6. 4 Intermediate filaments and epithelial differentiation of male rat embryonic gonad. Glucose lowering and anti-atherogenic effects of incretin-based therapies:
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This study assessed 2011 functional implications of the adipokine DPP4 and its association to the metabolic syndrome. In lean and obese subjects, depot-specific expression of DPP4 and its release from adipose tissue explants were determined and correlated to parameters of the metabolic syndrome.
Direct addition of Dpp1 to fat and skeletal and smooth muscle cells impairs insulin signaling. A fivefold higher level of DPP4 protein expression was seen in visceral compared with subcutaneous fat of obese patients, with no regional difference in lean subjects.
DPP4 serum concentrations significantly correlated with adipocyte size. By using adipose tissue explants from lean and obese subjects, we observed a twofold increase in DPP4 release that strongly correlated with adipocyte volume and parameters of the metabolic syndrome and was decreased to the lean level after weight reduction.
DPP4 released from adipose tissue correlated positively with an increasing risk score for the metabolic syndrome. Furthermore, DPP4 release strongly correlates with adipocyte size, potentially representing an important source of DPP4 in obesity.
Therefore, we suggest that DPP4 may be involved in linking adipose tissue and the metabolic syndrome. Obesity is the hallmark of the metabolic syndrome and represents a major global health problem that frequently associates with the development of chronic diseases, including type 2 diabetes and cardiovascular disease 1.
A complex interorgan cross-talk scenario between adipose tissue and other central dpp1 peripheral organs underlies the progression of these diseases, with adipose tissue on top of the cross-talk hierarchy 2.
This is attributed to the huge diversity of signaling and mediator molecules released from adipose tissue, which is now considered one of the major endocrine organs 34.
Recent data show that adipokines, which are proteins and peptides released by various adipose tissue cells, create a complex interconnected network of feedback loops 5. Enlargement of adipose tissue leads to dysregulation of adipokine secretion, representing a potential critical pathogenic link among obesity, insulin resistance IRand type 2 diabetes 1.
Therefore, we conducted a comprehensive proteomic profiling of conditioned media derived from differentiated, primary human adipocytes. This resulted in the identification of novel adipokines, including the exoprotease dipeptidyl peptidase 4 DPP4.
DPP4 is a ubiquitously expressed transmembrane glycoprotein that cleaves N-terminal dipeptides from a variety of substrates, including growth factors and hormones, neuropeptides, and chemokines 6.
Because GLP-1 remains active under hyperglycemic conditions in type 2 diabetes, DPP4 has gained considerable interest as a therapeutic target, and a variety of DPP4-inhibitors that prolong the insulinotropic effect of GLP1 are now in clinical use as antidiabetic drugs 8.
Substantial DPP4 activity is also found in plasma and other body fluids because of a soluble form of DPP4 lacking the cytoplasmic tail and the transmembrane region of this protein 9.
Both the membrane abundance and the circulating activity of DPP4 have been found to be altered in a variety of neurologic and inflammatory diseases 6. However, although a fraction of soluble DPP4 most likely originates from cells of the immune system 10the major source of circulating DPP4 and its regulation remain unknown.
Furthermore, essentially no data are currently available regarding the potential effects of soluble DPP4 on insulin target tissues, including muscle and fat. In the present investigation, we combined in vitro experiments with two independent clinical studies, aiming to validate DPP4 as a novel adipokine and to characterize the association of DPP4 to different parameters of the metabolic syndrome.
We show that 1 DPP4 is a novel adipokine released from differentiated human adipocytes and that it may exert autocrine and paracrine effects leading to IR; 2 DPP4 expression is substantially elevated in visceral fat of obese subjects and that serum DPP4 correlates with adipocyte size and all parameters of the metabolic syndrome; and 3 adipose tissue explants from obese subjects release substantially more DPP4 with a prominent decrease after weight reduction.
In light of the well accepted interference of DPP4 with the incretin system, we now suggest that DPP4 may play a role in linking obesity to IR and the metabolic syndrome.
Polyclonal antibodies for adiponectin and actin were supplied by Abcam Cambridge, U. Adiponectin was purchased from Biovendor Heidelberg, Germany. Complete protease inhibitor cocktail and PhosStop phosphatase inhibitor cocktail were provided by Roche Mannheim, Germany.
All other chemicals were of the highest analytic grade commercially available and purchased from Sigma-Aldrich. For all studies, protocols were approved by local ethics committees, and all participants gave written, informed consent.
Study 1 included 20 male obese patients and 20 lean controls who were recruited at Gent University Hospital Belgian registration number B For all patients, anthropometric and routine blood parameters were assessed.
Fasting blood samples were collected, and adipose tissue biopsies were fixed for microscopic evaluation of adipocyte 2011 area analysis. Sixteen obese women were reinvestigated 18—24 months after gastric bypass in a weight-stable period for at least 3 months, according to self-report reduction of BMI from A venous blood sample was obtained for the analysis of glucose and insulin to be used as an estimation of insulin sensitivity in vivo with the homeostasis model assessment HOMA index as described Thereafter, abdominal subcutaneous adipose tissue biopsies were obtained by needle aspiration as described previously One part of the tissue was used for measurements of DPP4 release as described previously Methodological experiments revealed that DPP4 release was linear with time for at least 3 h, suggesting no important cell damage data not shown.
Another part of the tissue was subjected to collagenase treatment, and mean adipocyte volume and weight were determined as described previously For calculation of the risk score for the metabolic syndrome, we used Adult Treatment Panel-III definitions as follows: The risk score 29917ru equal to the number of criteria fulfilled.
Subcutaneous adipose tissue was obtained from lean or moderately overweight women undergoing plastic surgery for mammary reduction or breast reconstruction with subcutaneous abdominal adipose tissue.
All subjects were healthy and free of medication and had no evidence of diabetes according to routine laboratory test results. Preadipocytes were isolated by collagenase digestion of adipose tissue as previously described by Dietze-Schroeder et al.
The degree of 29917ru was determined by Oil Red staining and induction of adiponectin expression. Differentiated adipocytes were used for the generation of adipocyte-conditioned media, as recently described by Dietze-Schroeder et al.
Macrophages were isolated from human adipose tissue and cultured using a method described by Curat et al. For an individual experiment, myoblasts were seeded in six-well culture dishes 9.
Primary human coronary artery smooth muscle cells were obtained from PromoCell Heidelberg, Germany. For all experiments, subconfluent cells of passage three were used. Filters were blocked with Tris-buffered saline containing 0.
The Shapiro—Wilcoxon test was used to test the Gaussian distribution of biological parameters. Student t test and ANOVA followed by P for linear trend post-test when appropriate were used for comparison between groups.
Correlations were performed by Pearson. For adjustment BMI, agewe applied a multiple linear regression modeling using least-squares means tests. Corresponding significance levels are indicated in Figs.
Comprehensive proteomic profiling of the adipocyte secretome led to the identification of proteins, with proteins being predicted or annotated as secretory proteins data to be presented in another publication.
To validate this novel adipokine, we used in vitro differentiated human adipocytes and macrophages isolated from adipose tissue. DPP4 expression in human adipocytes is significantly increased during differentiation with a maximum reached at day 7 fourfold over undifferentiated control Fig.
DPP4 expression is paralleled by a marked release of this adipokine Fig. As shown in Fig. In addition to adipocytes, adipose tissue-derived macrophages release measurable amounts of DPP4 Fig.
However, this is only one third compared with adipocytes, pointing to a major contribution of adipocytes to DPP4 output from adipose tissue. DPP4 protein level and release during adipocyte differentiation and after stimulation with different regulatory factors.
Adiponectin expression served as a control of differentiation. Data were normalized to the protein level of actin and are expressed relative to day 0. DPP4 release by preadipocytes, differentiated adipocytes, and adipose tissue—derived and cultured human macrophages was analyzed by ELISA.
The soluble form of DPP4 may bind to the extracellular matrix 22 and affect a variety of cells, yet this has not been investigated so far. To assess potential direct effects of soluble DPP4 on peripheral cells, we studied insulin signaling in adipocytes and skeletal muscle cells.
This demonstrates an autocrine effect of DPP4 on adipocytes. Validation experiments using this compound proved inhibition of DPP4 in vitro, which remained unaltered for a period of at least 8 h data not shown.
Similar to adipocytes, DPP4 also induces IR in skeletal muscle cells at the level of Akt phosphorylation in a dose-dependent way but less prominent compared with adipocytes Fig.
To prove whether DPP4 has a functional impact not only on insulin signaling, we determined DPP4-stimulated proliferation and insulin signaling in primary human smooth muscle cells. Effect of DPP4 on insulin-stimulated Akt phosphorylation in adipocytes and skeletal muscle cells.
Differentiated human adipocytes A and B and skeletal muscle cells C and D were treated with the indicated amounts of DPP4 without and with concomitant administration of a specific DPP4 inhibitor for 24 h.
After incubation with the appropriate HRP-coupled secondary antibody, the signal was detected by enhanced chemiluminescence. Representative Western blots are presented. For Alanes were excised from a single 2011 blot and displayed in the presented order.
Basal white bars ; insulin-stimulated black bars. Effect of DPP4 on insulin-stimulated Akt phosphorylation and proliferation in smooth muscle cells. Smooth muscle cells were treated with the indicated amounts of DPP4 without and with concomitant administration of a specific DPP4 inhibitor for 24 h.
Measuring DPP4 in serum from age-matched lean and morbidly obese subjects patient characteristics in Supplementary Table 1 revealed that obese subjects are characterized by significantly increased DPP4 concentrations Fig.
DPP4 expression in adipose tissue biopsies from the same patients revealed that DPP4 protein expression is regulated by both the fatness of the individual and the adipose tissue depot Fig.
Although there is only a trend for higher DPP4 expression in visceral fat of lean subjects, obese patients are characterized by significantly higher DPP4 in visceral adipose tissue compared with subcutaneous adipose tissue.
Furthermore, expression of DPP4 in both depots is significantly higher in obese subjects compared with lean subjects. DPP4 levels positively correlate with BMI, the size of subcutaneous and visceral adipocytes, insulin, and leptin, whereas a negative correlation with age and adiponectin could be found Fig.
Adjusting DPP4 for age has no impact on these correlations. DPP4 serum concentration and expression in adipose tissue from lean compared with obese patients clinical study 1.
Data were normalized to the protein level of actin and are expressed relative to subcutaneous adipose tissue from lean subjects. DPP4 serum concentrations correlate with various clinical and biochemical parameters clinical study 1.
Linear regression analysis of DPP4 serum concentration and patient characteristics such as age ABMI Bsize of subcutaneous C and visceral D adipocytes, insulin concentration Eadiponectin concentration Fand leptin concentration G.
Statistical evaluation is indicated in each graph. We investigated lean and obese subjects after weight reduction and analyzed the release of DPP4 from whole adipose tissue.
Adipocytes from lean subjects were significantly smaller than those from obese patients Fig. Surgery-induced weight loss reduced the average size of adipocytes 29917ru the size from lean subjects.
DPP4 release is significantly increased from adipose tissue of obese subjects compared with lean subjects Fig. This was paralleled by a significant reduction in the circulating DPP4 level, supporting dpp1 notion that adipose tissue is an important source of serum DPP4 Fig.
In the group of lean and obese subjects, DPP4 release from adipose tissue significantly correlates with BMI, waist circumference, percent body fat, triglycerides, HOMA, adipocyte volume, and leptin, whereas the correlation is negative with HDL-cholesterol Fig.
All of these factors are denominators of the metabolic syndrome.
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An adipose-specific knockout of DPP4 would be required to prove a causal role of this protein, and this mouse model is currently under development in our laboratory. It is noteworthy that we measured DPP4 serum concentration and not its activity. Not all germ cells are created equal: For typical on-screen use for websites, email or Microsoft PowerPoint presentations, these sRAW files provide more than enough resolution for image display. Substantial DPP4 activity is also found in plasma and other body fluids because of a soluble form of DPP4 lacking the cytoplasmic tail and the transmembrane region of this protein 9.
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In assignments like those, it may be preferable to shoot at smaller resolutions — still perfectly acceptable for online viewing, but much more manageable file sizes that are easier to store long-term.
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Reduced-resolution RAW image files June 25, The new small RAW options have the potential to save a lot of hard drive storage space over time. This article was originally published on March 28, and has been updated to include current product information.
What are the benefits of shooting RAW images? Therefore, enhanced abundance of both resident and soluble DPP4 within adipose tissue of obese subjects may substantially augment the lipolytic activity of enlarged adipocytes.
Finally, DPP4 inactivates or alters the specificity of many chemokines, including RANTES, eotaxin, macrophage-derived chemokine, stromal-derived factor-1, and many others 22 , making it likely that DPP4 plays a yet undefined functional role in the intraorgan cross-talk among macrophages, adipocytes, and other components of the stroma-vascular fraction.
So far, the direct effects of soluble DPP4 on isolated cells have not been investigated, although it binds to the extracellular matrix and may exert signaling functions We demonstrate for the first time that DPP4 consistently impairs insulin signaling at the level of Akt in three different primary cell types, namely, adipocytes, skeletal muscle, and smooth muscle cells.
This issue is currently under investigation in our laboratory. DPP4 induces proliferation of human vascular cells in parallel to an impairment of insulin signaling, suggesting a potential role in obesity-associated vascular complications.
In this study, we used DPP4 concentrations that match circulating levels that were measured in both lean and obese subjects. Because obese patients are characterized by significantly increased circulating DPP4, it may be speculated that DPP4 may interfere with insulin sensitivity not only in adipose tissue but also in other insulin-sensitive peripheral organs.
This would substantially extend the current view of DPP4 as a target for treatment of type 2 diabetes. Future work will be needed to address the mechanism and the functional role of these effects in the pathogenesis of IR and obesity-associated complications.
Serum DPP4 is altered in many pathophysiologic conditions, such as different types of cancer, allergic asthma, or hepatitis C To the best of our knowledge, this is the first study to analyze circulating DPP4 in the context of obesity and adipose tissue.
Morbidly obese men are characterized by elevated DPP4 levels compared with lean controls. DPP4 serum concentrations are significantly correlated with the BMI, the size of adipocytes in subcutaneous and visceral fat, and the adipocyte hormones adiponectin negatively and leptin, showing that DPP4 is related to not only increased body weight but also other important parameters of adipose tissue in particular.
DPP4 is negatively associated with age, but all of the above mentioned parameters are still significantly correlated with DPP4, even after adjustment for age. In a different manner, BMI adjustment causes the disappearance of most of these correlations, with the exception of the size of subcutaneous adipocytes.
In addition to circulating DPP4, the protein expression of this adipokine is significantly different not only between lean and obese subjects but also between their fat depots.
Former studies report contradicting data, describing both decreased and increased mRNA expression of DPP4 in adipose tissue of obese men 23 , We now clearly demonstrate at the protein level that obesity leads to a prominent induction of DPP4 abundance in both subcutaneous and visceral adipose tissue and that the visceral fat exhibits the highest DPP4 level in obese subjects.
Therefore, we conclude that enlargement of visceral adipocytes in obesity may substantially contribute to the augmented level of circulating DPP4 in obese patients. It is noteworthy that we measured DPP4 serum concentration and not its activity.
However, in additional experiments, other samples from the same patients were used to determine DPP4 activity that is significantly correlated with circulating DPP4 levels data not shown. Thus, DPP4 activity is also significantly increased in obese compared with lean subjects.
DPP4 expression in adipose tissue is increased in obese compared with lean individuals, a fact that is reflected by an increased release of DPP4 from adipose tissue explants of obese patients compared with lean controls.
Similar to circulating DPP4, its release from adipose tissue correlates with various classic markers for the metabolic syndrome, namely, BMI, waist circumference and plasma triglycerides, and HOMA as an index of IR, as well as with fat cell volume and the adipokine leptin.
In addition, DPP4 release can be reversed to normal levels by surgery-induced weight loss, which is also reflected by DPP4 being significantly reduced in serum of these patients.
With the exception of one study reporting on DPP4 levels in obese children before and after weight loss 28 , this is the first description of significantly decreased DPP4 levels after weight loss induced by obesity surgery in adults.
Thus, in obesity, both circulating levels of DPP4 and DPP4 release by adipose tissue are increased but can be reduced to control levels by substantial weight loss. Thus, DPP4 may be of relevance as a novel biomarker of the metabolic syndrome and for detection of obese subjects at high risk for obesity-associated complications.
Future studies are needed to address this important issue and to define the molecular pathways that link adipose DPP4 to the metabolic syndrome and type 2 diabetes.
An adipose-specific knockout of DPP4 would be required to prove a causal role of this protein, and this mouse model is currently under development in our laboratory. However, several lines of evidence support our notion that the novel adipokine links obesity to the metabolic syndrome.
First, DPP4 impairs the function of the incretin system, which is of key importance for glucose homeostasis Second, DPP4 inhibitors are well known to improve glucose tolerance in animal models of obesity Finally, preclinical data suggest that GLP-1 is cardioprotective 32 , and DPP4 inhibition was shown to improve cardiovascular outcomes in rodents Our data strongly support the current view 20 that adipocytes and specifically adipose tissue play a major, most likely causative role in the pathogenesis of metabolic diseases.
In summary, we showed that DPP4 is a novel adipokine that is substantially overexpressed in visceral fat from obese subjects and exhibits an augmented release in obesity.
Soluble DPP4 exerts autocrine and paracrine effects and impairs insulin signaling. We further observe a tight correlation of DPP4 release to adipocyte cell size, and plasma levels of DPP4 strongly correlate with the risk of having the metabolic syndrome.
Therefore, we suggest that DPP4 is a novel biomarker and a potential link between obesity and the metabolic syndrome. No other potential conflicts of interest relevant to this article were reported.
The authors thank Prof. This article contains Supplementary Data online at http: Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
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Skip to main content. Diabetes Jul; 60 7: Clinical studies of DPP-4 concentration in serum and DPP4 release from adipose tissue For all studies, protocols were approved by local ethics committees, and all participants gave written, informed consent.
Adipocyte isolation and culture Subcutaneous adipose tissue was obtained from lean or moderately overweight women undergoing plastic surgery for mammary reduction or breast reconstruction with subcutaneous abdominal adipose tissue.
Smooth muscle cell culture and proliferation Primary human coronary artery smooth muscle cells were obtained from PromoCell Heidelberg, Germany. RESULTS DPP4 is a novel adipokine exhibiting regulated release from human adipocytes Comprehensive proteomic profiling of the adipocyte secretome led to the identification of proteins, with proteins being predicted or annotated as secretory proteins data to be presented in another publication.
Soluble DPP4 exerts direct effects on fat and muscle cells The soluble form of DPP4 may bind to the extracellular matrix 22 and affect a variety of cells, yet this has not been investigated so far.
DPP4 is elevated in serum of obese patients and correlates with various anthropometric and clinical parameters clinical study 1 Measuring DPP4 in serum from age-matched lean and morbidly obese subjects patient characteristics in Supplementary Table 1 revealed that obese subjects are characterized by significantly increased DPP4 concentrations Fig.
DPP4 is released from subcutaneous adipose tissue in vitro clinical study 2 We investigated lean and obese subjects after weight reduction and analyzed the release of DPP4 from whole adipose tissue.
Footnotes This article contains Supplementary Data online at http: Inflammation, stress, and diabetes. J Clin Invest ; The adipocyte-myocyte axis in insulin resistance. Trends Endocrinol Metab ; The adipocyte in insulin resistance: Diabetes ; Robust signaling networks of the adipose secretome.
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Biochem Biophys Res Commun ; Dipeptidyl peptidase IV and related enzymes in cell biology and liver disorders. Clin Sci Lond ; Diabetes Obes Metab ; Dipeptidyl peptidase IV from human serum: J Biochem ; Characterization of the adenosine deaminase-adenosine deaminase complexing protein binding reaction.
J Biol Chem ; Dipeptidyl-peptidase IV CD26 —role in the inactivation of regulatory peptides. Regul Pept ; Obes Surg ; J Pediatr Endocrinol Metab ; The biology of incretin hormones.
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Genetic deletion or pharmacological inhibition of dipeptidyl peptidase-4 improves cardiovascular outcomes after myocardial infarction in mice. In this Issue July , 60 7. Search for this keyword.
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