Andreas Peter

Helmholtz Zentrum München, München, Bavaria, Germany

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Publications (67)244.46 Total impact

  • PLoS ONE 05/2015; 10(5):e0127368. DOI:10.1371/journal.pone.0127368 · 3.53 Impact Factor
  • Blood Purification 05/2015; 39(4):331-332. DOI:10.1159/000381666 · 1.92 Impact Factor
  • PLoS ONE 05/2015; 10(5):e0126804. DOI:10.1371/journal.pone.0126804 · 3.53 Impact Factor
  • Diabetologie und Stoffwechsel 04/2015; 10(S 01). DOI:10.1055/s-0035-1549694 · 0.31 Impact Factor
  • Diabetologie und Stoffwechsel 04/2015; 10(S 01). DOI:10.1055/s-0035-1549702 · 0.31 Impact Factor
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    ABSTRACT: Conjugated linoleic acids (CLAs) affect body fat distribution, induce insulin resistance and stimulate insulin secretion. The latter effect is mediated through the free fatty acid receptor-1 (GPR40/FFAR1). This study examines whether GPR40/FFAR1 interacts with tissue specific metabolic changes induced by CLAs. After chronic application of CLAs C57BL/6J wild type (WT) and GPR40/FFAR1 (Ffar1(-/-)) knockout mice developed insulin resistance. Although CLAs accumulated in liver up to 46-fold genotype-independently, hepatic triglycerides augmented only in WT mice. This triglyceride deposition was not associated with increased inflammation. In contrast, in brain of CLA fed Ffar1(-/-) mice mRNA levels of TNF-α were 2-fold higher than in brain of WT mice although CLAs accumulated genotype-independently in brain up to 4-fold. Concomitantly, Ffar1(-/-) mice did not respond to intracerebroventricular (i.c.v.) insulin injection with an increase in cortical activity while WT mice reacted as assessed by radiotelemetric electrocorticography (ECoG) measurements. In vitro incubation of primary murine astrocytes confirmed that CLAs stimulate neuronal inflammation independent of GPR40/FFAR1. This study discloses that GPR40/FFAR1 indirectly modulates organ-specific effects of CLAs: the expression of functional GPR40/FFAR1 counteracts CLA-induced inflammation and insulin resistance in the brain, but favors the development of fatty liver. © 2015 S. Karger AG, Basel.
    Cellular Physiology and Biochemistry 04/2015; 35(6):2272-2284. DOI:10.1159/000374031 · 3.55 Impact Factor
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    ABSTRACT: Background/Aims: Determination of peptide biomarkers such as troponins, natriuretic peptides or the recently reported FGF23 can be useful to identify hemodialysis patients with a high risk of mortality. However, it is desirable to focus on few robust parameters to warrant their routine application. Methods: In a prospective cohort study with 239 prevalent hemodialysis patients we studied the prognostic significance of 10 simultaneously determined modern peptide biomarkers (high sensitive troponin I and T, NT-pro-BNP, BNP, MR-pro-ANP, MR-pro-ADM, CT-pro-ET1, copeptin, FGF23 and a-Klotho) and compared them with parameters traditionally associated with mortality (PTH, Ca, Pi, albumin, CRP, cholesterol, AP). Results: After a follow-up of 4 years, plasma concentration of troponins, natriuretic peptides, MR-pro-ADM, FGF23 as well as PTH, CRP, AP were significantly higher in deceased patients (n=95). Hazard ratios from cox regression on a continuous scale (doubling of plasma concentration) or relative in tertiles were highest for high sensitive troponins, followed by natriuretic peptides and MR-pro-ADM (1.6-2.0 and 2.3-5.5, resp.). C-indices were also highest for troponins (0.708-0.746), followed by natriuretic peptides (0.706-0.731). Traditional parameters had low c-indices (0.598-0.655). Stepwise cox regression revealed that among all parameters troponin I, NT-pro-BNP, PTH and CRP remained independent predictors of mortality and a composite score had the highest c-index (0.799 [0.740-0.849]). Conclusions: Among peptide biomarkers high sensitive troponins and to a lesser extent natriuretic peptides are strong predictors of mortality in asymptomatic hemodialysis patients, followed by markers of mineral-bone disease and inflammation. © 2014 S. Karger AG, Basel.
    Kidney and Blood Pressure Research 12/2014; 39(6):563-572. DOI:10.1159/000368468 · 1.82 Impact Factor
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    ABSTRACT: Background Besides its advantages, bariatric surgery implicates a risk of nutritional deficiencies, which might result in impaired bone metabolism. We assessed the effect of laparoscopic sleeve gastrectomy (LSG) on blood markers of bone metabolism in obese patients during a 3-year observation period. Methods In 39 obese patients (29 women, 10 men, mean BMI 51.8 ± 6.8 kg/m2) undergoing LSG, we measured blood concentrations of 25-hydroxyvitamin D (25(OH)D), calcium, parathyroid hormone (PTH), bone alkaline phosphatase (BAP), and N-telopeptides crosslinks (NTx) before LSG and up to 3 years postoperatively. Vitamin D and calcium supplementations were recorded. Results LSG caused an excess weight loss (EWL) of 54 ± 20 % after 3 years. Before surgery, we found decreased levels of 25(OH)D and calcium in 80 and 5 % of the subjects, respectively, while increased levels of PTH, BAP, and NTx were found in 39, 28, and 21 %, respectively. Mean levels of NTx and the prevalence of elevated levels of NTx increased within 2 years (p p Conclusions Morbid obesity is associated with pronounced changes of markers of bone metabolism; LSG did neither aggravate nor ameliorate vitamin D metabolism within a 3-year time period, but led to increased bone resorption 2 years postoperatively. Routine supplementation of calcium and vitamin D is not likely sufficient to compensate the obesity-associated deficiencies in bone metabolism.
    Obesity Surgery 12/2014; DOI:10.1007/s11695-014-1509-2 · 3.74 Impact Factor
  • Diabetes Care 12/2014; 37(12):e278-9. DOI:10.2337/dc14-1272 · 8.57 Impact Factor
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    ABSTRACT: Animal studies suggest that insulin action in the brain is involved in the regulation of peripheral insulin sensitivity. Whether this holds true in humans is unknown. Using intranasal application of insulin to the human brain, we studied impacts of brain insulin action on whole-body insulin sensitivity and mechanisms involved in this process.Insulin sensitivity was assessed by hyperinsulinemic euglycemic glucose clamp, before and after intranasal application of insulin and placebo in randomized order in lean and obese men. After insulin spray application in lean, higher glucose infusion rate was necessary to maintain euglycemia compared to placebo. Accordingly, clamp-derived insulin sensitivity index improved after insulin spray. In obese subjects, this insulin sensitizing effect could not be detected.Change in the high frequency band of heart rate variability, an estimate of parasympathetic output, correlated positively with change in whole-body insulin sensitivity after intranasal insulin. Improvement in whole-body insulin sensitivity correlated with the change in hypothalamic activity as assessed by functional magnetic resonance imaging.In summary, intranasal insulin improves peripheral insulin sensitivity in lean but not in obese men. Furthermore, brain-derived peripheral insulin sensitization is associated with hypothalamic activity and parasympathetic outputs. Thus, our findings provide novel insights into the regulation of insulin sensitivity and the pathogenesis of insulin resistance in humans.
    Diabetes 07/2014; 63(12). DOI:10.2337/db14-0477 · 8.47 Impact Factor
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    ABSTRACT: History and admission findings: A 90-year-old female patient treated with dabigatran for atrial fibrillation presented emergently with a spontaneous vaginal bleeding due to endometrium carcinoma. Investigations: Laboratory analysis revealed azotemia consistent with acute-on-chronic renal failure. Coagulation was deranged (prolongation of activated partial thromboplastin time (aPTT) by 3.5-fold, international normalized ratio (INR) 7.8) due to a massive accumulation of dabigatran (measured plasma concentration 2230 ng/ml). Diagnosis, treatment and course: Vaginal bleedings were treated with external tamponade. Hemodialysis treatment was commenced due to uremia and dabigatran accumulation. Over night, the patient was dialysed with a SLED (sustained low efficiency dialysis) regimen. After volume resuscitation renal function promptly ensued indicating prerenal azotemia as a cause of renal failure. After two more hemodialysis sessions dabigatran concentrations were no longer detecable and this was paralleled by normalization of coagulation tests. Conclusions: Dabigatran can accumulate massively during acute renal failure and evoke a life-threatening bleeding diathesis. Dabigatran can be removed with low efficient dialysis (such as SLED).
    DMW - Deutsche Medizinische Wochenschrift 07/2014; 139(30):1539. DOI:10.1055/s-0034-1370191 · 0.55 Impact Factor
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    ABSTRACT: Aims/hypothesis The common sequence variant I148M of the patatin-like phospholipase domain-containing protein 3 gene (PNPLA3) is associated with increased hepatic triacylglycerol (TAG) content, but not with insulin resistance, in humans. The PNPLA3(I148M) variant was previously reported to alter the specificity of the encoded enzyme and subsequently affect lipid composition. Methods We analysed the fatty acid composition of five lipid fractions from liver tissue samples from 52 individuals, including 19 carriers of the minor PNPLA3(I148M) variant. Results PNPLA3(I148M) was associated with a strong increase (1.75-fold) in liver TAGs, but with no change in other lipid fractions. PNPLA3(I148M) minor allele carriers had an increased n-3 polyunsaturated fatty acid (PUFA) alpha-linolenic acid content and reductions in several n-6 PUFAs in the liver TAG fraction. Furthermore, there was a strong inverse correlation between n-6 PUFA and TAG content independent of PNPLA3 genotype. In a multivariate model including liver fat content, PNPLA3 genotype and fatty acid composition, two significant differences could be exclusively attributed to the PNPLA3(I148M) minor allele: reduced stearic acid and increased alpha-linolenic acid content in the hepatic TAG fraction. Conclusions These changes therefore suggest a mechanism to explain the PNPLA3(I148M)-dependent increase in liver fat content without causing insulin resistance. Stearic acid can induce insulin resistance, whereas alpha-linolenic acid may protect against it.
    Diabetologia 06/2014; 57(10). DOI:10.1007/s00125-014-3310-0 · 6.88 Impact Factor
  • Diabetologie und Stoffwechsel 05/2014; 9(S 01). DOI:10.1055/s-0034-1374867 · 0.31 Impact Factor
  • Diabetologie und Stoffwechsel 05/2014; 9(S 01). DOI:10.1055/s-0034-1374900 · 0.31 Impact Factor
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    ABSTRACT: Treatment of diabetic subjects with cinnamon demonstrated an improvement in blood glucose concentrations and insulin sensitivity but the underlying mechanisms remained unclear. This work intends to elucidate the impact of cinnamon effects on the brain by using isolated astrocytes, and an obese and diabetic mouse model. Cinnamon components (eugenol, cinnamaldehyde) were added to astrocytes and liver cells to measure insulin signaling and glycogen synthesis. Ob/ob mice were supplemented with extract from cinnamomum zeylanicum for 6 weeks and cortical brain activity, locomotion and energy expenditure were evaluated. Insulin action was determined in brain and liver tissues. Treatment of primary astrocytes with eugenol promoted glycogen synthesis, whereas the effect of cinnamaldehyde was attenuated. In terms of brain function in vivo, cinnamon extract improved insulin sensitivity and brain activity in ob/ob mice, and the insulin-stimulated locomotor activity was improved. In addition, fasting blood glucose levels and glucose tolerance were greatly improved in ob/ob mice due to cinnamon extracts, while insulin secretion was unaltered. This corresponded with lower triglyceride and increased liver glycogen content and improved insulin action in liver tissues. In vitro, Fao cells exposed to cinnamon exhibited no change in insulin action. Together, cinnamon extract improved insulin action in the brain as well as brain activity and locomotion. This specific effect may represent an important central feature of cinnamon in improving insulin action in the brain, and mediates metabolic alterations in the periphery to decrease liver fat and improve glucose homeostasis.
    PLoS ONE 03/2014; 9(3):e92358. DOI:10.1371/journal.pone.0092358 · 3.53 Impact Factor
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    ABSTRACT: The factor V Leiden (FVL) mutation is the most frequent genetic cause of venous thrombosis in Caucasians. However, protective effects have been suggested to balance the disadvantages. We have recently observed protective effects of FVL mutation on experimental diabetic nephropathy in mice as well as an association with reduced albuminuria in two human cohorts of diabetic patients. In the present study we aimed to reevaluate these findings in an independent, larger cohort of 1905 Caucasians at risk of developing type 2 diabetes and extend possible associations to earlier disease stages of nephropathy. Carriers of FVL mutation had a significantly lower urine albumin excretion (P = 0.03) and tended to have lower plasma creatinine concentrations (P = 0.07). The difference in plasma creatinine concentrations was significant after adjustment for the influencing factors: age, gender, and lean body mass (P = 0.048). These observations at a very early "disease" stage are an important extension of previous findings and suggest that modification of glomerular dysfunction by FVL mutation is relevant during very early stages of diabetic nephropathy. This makes the underlying mechanism an interesting therapeutic target and raises the question whether FVL mutation may also exert protective effects in other glomerulopathies.
    03/2014; 2014:530830. DOI:10.1155/2014/530830
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    ABSTRACT: Vasopressin, endothelin and adrenomedullin are vasoactive peptides that regulate vascular tone and might play a role in hypertensive diseases. Recently, laboratory assays have been developed to measure stable fragments of vasopressin, endothelin and adrenomedullin. Little is known about their diagnostic and prognostic value in hemodialysis patients. In this study, we measured the plasma concentration of copeptin, mid-regional-pro-adrenomedullin (MR-pro-ADM) and C-terminal pro-endothelin 1 (CT-pro-ET1) in stable ambulatory hemodialysis patients (n = 239) and investigated their associations with clinical factors and mortality. In all patients enrolled, the plasma concentrations of copeptin, MR-pro-ADM and CT-pro-ET1 were largely elevated with a median concentration of 132 pmol/L (interquartile range [IQR] 78-192) for copeptin, 1.26 nmol/L (IQR 1.02-1.80) for MR-pro-ADM and 149 pmol/L (IQR 121-181) for CT-pro-ET1. The plasma concentrations of all vasoactive peptide fragments correlated with time on dialysis and plasma β2-microglobulin concentration and were negatively correlated to residual diuresis. The plasma concentration of MR-pro-ADM was a strong predictor of all-cause (univariate hazard ratio for a 10-fold increase 9.94 [3.14;32], p<0.0001) and cardiovascular mortality (hazard ratio 34.87 [5.58;217], p = 0.0001) within a 3.8-year follow-up. The associations remained stable in models adjusted for dialysis specific factors and were attenuated in a full model adjusted for all prognostic factors. Plasma copeptin concentration was weakly associated with cardiovascular mortality (only in univariate analysis) and CT-pro-ET1 was not associated with mortality at all. In conclusion, vasoactive peptide fragments are elevated in hemodialysis patients because of accumulation and, most likely, increased release. Increased concentrations of MR-pro-ADM are predictive of mortality.
    PLoS ONE 01/2014; 9(1):e86148. DOI:10.1371/journal.pone.0086148 · 3.53 Impact Factor
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    ABSTRACT: Background: Oxidative stress (OS) represents an important pathogenetic factor of acute liver failure and chronic liver diseases. To elucidate whether the liver itself is a major source of OS, the present study was performed to assess OS and antioxidant status in an anhepatic porcine model. Methods: Six pigs underwent a total hepatectomy, five pigs were sham operated. OS and antioxidant status were evaluated by measuring plasma concentrations of malondialdehyde (MDA), xanthine oxidase (XO), superoxide dismutase (SOD) and the ferric reducing ability of plasma (FRAP). They were sampled at the start of the experiment, immediately after surgery, and then at 8 and 16 hours post hepatectomy. Results: Increased concentrations of MDA were observed in anhepatic pigs postoperatively (p < 0.02) and 8 hours after hepatectomy (p < 0.003) compared to controls. XO activity increased soon after hepatectomy (22.6 ± 5.4 mU/L versus 3.3 ± 2.1 mU/L in sham animals, p < 0.03) but returned to normal values in the further course. SOD levels did not change during the observational period in both groups. FRAP values rose significantly in the anhepatic animals compared to control (p < 0.015). A significant positive correlation was observed between MDA levels and FRAP levels (Spearman's ρ = 0.62; p < 0.0001). Conclusions: These findings show that hepatectomy does not completely prevent the occurrence of OS because the production and regulation of OS are also located outside the liver.
    Zeitschrift für Gastroenterologie 01/2014; 52(1):43-49. DOI:10.1055/s-0033-1356362 · 1.67 Impact Factor
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    ABSTRACT: Purpose Over 90 % of fatal mushroom poisoning occurs after ingestion of amanitin-containing species. This study aimed to investigate markers indicating spontaneous liver regeneration in a porcine acute liver failure (ALF) model after α-amanitin intoxication. Methods German landrace pigs received either 0.15 mg/kg (n = 5) α-amanitin intravenously or 0.35 mg/kg (n = 5) intraportally. Pigs were invasively monitored and kept under general anesthesia throughout the experiment. Laboratory parameters were analyzed every 8 h. Results ALF occurred in all animals (10/10) 41 ± 3 h after intoxication. All pigs receiving 0.35 mg/kg α-amanitin and one pig receiving 0.15 mg/kg α-amanitin died 57 ± 16 h after the primary onset of ALF. Four pigs of the 0.15 mg/kg intoxication group recovered spontaneously from ALF after 56 ± 6 h. Starting at 32 h after intoxication, significantly higher values of albumin and total plasma protein could be measured in surviving animals (p < 0.05). A significant temporary increase in the tumor necrosis factor alpha (TNF-α) plasma concentration was detected 40–80 h after intoxication in recovering animals (p < 0.05). Conclusions This porcine model represents a novel tool to analyse multiple aspects of liver regeneration following α-amanitin poisoning to allow early discrimination between a fatal course and survivors. Decreased albumin and total plasma protein concentrations in the early intoxication phase indicated a lethal outcome, while an increase in the TNF-α plasma concentration was identified as the earliest prognostic plasma marker detecting liver regeneration a long time before liver function was biochemically and clinically impaired.
    Hepatology International 01/2014; 8(1). DOI:10.1007/s12072-013-9491-7 · 2.47 Impact Factor
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    ABSTRACT: Currently available assays for the widely used marker for neuroendocrine tumors chromogranin A have a weak comparability, involve manual work, and require batch processing of the samples. In this study, we evaluated the automated chromogranin A KRYPTOR assay compared with the widely used DAKO ELISA. 83 samples were measured with the DAKO ELISA (EDTA plasma) and the KRYPTOR assay (serum), since different sample materials are recommended. Furthermore, different sample materials were compared. The results between the two assays were highly correlated (KRYPTOR serum (ng/mL) = 2.887 ELISA EDTA (U/L) + 5.028; r = 0.99). The inter-assay variation for the KRYPTOR assay was determined as 5.56% at low (95 ng/mL; n = 34) and 6.21% at high (530 ng/mL; n = 33) chromogranin A concentrations. EDTA plasma samples revealed significantly lower results than serum in the KRYPTOR assays and could not be used. In conclusion, the new chromogranin A KRYPTOR assay is fast, reliable, and compares well to an established test after adaptation of sample material and reported units.

Publication Stats

922 Citations
244.46 Total Impact Points

Institutions

  • 2014
    • Helmholtz Zentrum München
      München, Bavaria, Germany
  • 2009–2014
    • Universitätsklinikum Tübingen
      • Department of General, Visceral and Transplant Surgery
      Tübingen, Baden-Württemberg, Germany
  • 2008–2014
    • University of Tuebingen
      • Department of Internal Medicine
      Tübingen, Baden-Württemberg, Germany