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  • 1
    Electronic Resource
    Electronic Resource
    Microdialysis methodology for the measurement of dermal interstitial fluid in humans (1996)
    Oxford, UK : Blackwell Publishing Ltd
    British journal of dermatology 134 (1996), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In this study we aimed to validate the microdialysis technique for metabolic measurements in the dermal interstitial fluid. The abdominal and forearm skin was used for microdialysis in 15 healthy normal weight volunteers. The depth of the microdialysis catheter was assessed by ultrasound measurement. Structural impairment and blood flow were judged from biopsies and from laser Doppler measurements taken adjacent to the catheters. Dermal interstitial lactate and pyruvate concentrations were measured, under steady stale fasting conditions, after equilibrium calibration of each catheter in situ. The dermal Interstitial glucose concentration was estimated by means of the retrodialysis calibration method, which has previously not been evaluated for skin microdialysis. The mean catheter depth (± standard deviation) was 0.8 ± 0.3 mm. Small areas of localized bleeding, but no inflammatory reaction, was found surrounding the catheters. The perfusion in the microdialysis region was slightly increased (15–25%1. The lactate/pyruvate ratio (12 ±0.7) showed non–ischaemic values. The dermal interstitial lactate concentration was significantly higher (1171 ± 228μmol/l) than the plasma lactate (781 ± 180μmol/l), indicating an ongoing nonoxidative glucose metabolism. Retrodialysis calibration correctly estimated the dermal glucose level to be similar to that in plasma, which may indicate the usefulness of this calibration method for microdialysis studies of endogenous substrates in the dermal interstitial fluid.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2133.1996.d01-893.x
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  • 2
    Electronic Resource
    Electronic Resource
    Glycogen: its mode of formation and contribution to hepatic glucose output in postabsorptive humans (1994)
    Springer
    Diabetologia 37 (1994), S. 697-702 
    Details
    ISSN: 1432-0428
    Keywords: Glycogen ; gluconeogenesis ; glycogenolysis ; hepatic glucose output
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To assess the relative contributions of gluconeogenesis and glycogenolysis to overall hepatic glucose output in postabsorptive normal humans and those of the indirect and direct pathways for glycogen synthesis, we studied six normal volunteers, who had been fasted for 16 h to reduce their hepatic glycogen stores, and then ingested glucose (250 g over 10 h) enriched with [6-3H] glucose to replenish and label their hepatic glycogen. After a 10-h overnight fast, release of the [6-3H] glucose into the circulation was traced with [2-3H] glucose to estimate breakdown of glycogen that had been formed via the direct pathway while gluconeogenesis was simultaneously estimated by incorporation of infused [14C] lactate into plasma glucose. We found that release of [6-3H] glucose into plasma (6.79±0.69 μmol · kg−1 · min−1) accounted for 46±5% of hepatic glucose output (15.0±0.7 μmol · kg−1· min−1) while glucose formed from lactate (2.71±0.28 μmol · kg−1 · min−1) accounted for 19±2% of hepatic glucose output. Since these determinations underestimate direct pathway glycogenolysis and overall gluconeogenesis, a maximal estimate for the contribution of indirect pathway glycogenolysis to hepatic glucose output is obtained by subtracting the sum of direct pathway glycogenolysis and lactate gluconeogenesis from hepatic glucose output. This amounted to a maximum of 36±5 % of hepatic glucose output and 44±6% of overall glycogenolysis. Assuming that the relative proportions of direct and indirect pathway glycogen breakdown would reflect the relative contributions of these pathways to glycogen formation, we conclude that under our experimental conditions the direct pathway is the predominant route for glycogen formation in man and that in overnight fasted humans, hepatic glucose output is mainly the result of glycogenolysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417694
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  • 3
    Electronic Resource
    Electronic Resource
    Peroxovanadate and insulin action in adipocytes from NIDDM patients. Evidence against a primary defect in tyrosine phosphorylation (1997)
    Springer
    Diabetologia 40 (1997), S. 1197-1203 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Peroxovanadate ; insulin ; isoprenaline ; cAMP ; lipolysis ; glucose uptake ; tyrosine phosphorylation ; NIDDM ; adipocyte ; in vitro.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We studied the effects of insulin and the stable peroxovanadate compound potassium bisperoxopicolinatooxovanadate (bpV(pic)), a potent inhibitor of phosphotyrosine phosphatases, on lipolysis and glucose uptake in subcutaneous adipocytes from 10 male patients with non-insulin-dependent diabetes mellitus (NIDDM) and 10 matched non-diabetic control subjects. Lipolysis stimulated by isoprenaline or the cAMP analogue, 8-bromo-cyclic AMP (8-br-cAMP), was reduced by approximately 40 % in NIDDM compared to control subjects. In both groups bpV(pic) exerted an antilipolytic effect that was similar to insulin (∼ 50 % inhibition). 14C-U-glucose uptake was dose-dependently increased by bpV(pic) treatment, but this effect and also that of insulin were impaired in NIDDM compared to control (bpV(pic) 1.6-fold vs 2.4-fold and insulin 2.2-fold vs 3.4-fold). Furthermore, low concentrations of bpV(pic) did not affect insulin-stimulated glucose uptake, although tyrosine phosphorylation of the insulin receptor β-subunit was clearly increased by bpV(pic). In conclusion, 1) β-adrenergic stimulation of lipolysis in vitro is attenuated in NIDDM adipocytes due to post-receptor mechanisms. 2) Both insulin and bpV(pic) decrease lipolysis and enhance glucose uptake in control as well as NIDDM adipocytes. The effect on glucose uptake, but not that on lipolysis, is impaired in NIDDM cells. 3) Peroxovanadate does not improve sensitivity and responsiveness to insulin in NIDDM adipocytes, showing that insulin-resistant glucose uptake in NIDDM is not overcome by phosphotyrosine-phosphatase inhibition and, thus, probably is not caused by impaired tyrosine phosphorylation events alone. [Diabetologia (1997) 40: 1197–1203]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050807
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  • 4
    Electronic Resource
    Electronic Resource
    Glycogen: its mode of formation and contribution to hepatic glucose output in postabsorptive humans (1994)
    Springer
    Diabetologia 37 (1994), S. 697-702 
    Details
    ISSN: 1432-0428
    Keywords: Key words Glycogen, gluconeogenesis, glycogenolysis, hepatic glucose output.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To assess the relative contributions of gluconeogenesis and glycogenolysis to overall hepatic glucose output in postabsorptive normal humans and those of the indirect and direct pathways for glycogen synthesis, we studied six normal volunteers, who had been fasted for 16 h to reduce their hepatic glycogen stores, and then ingested glucose (250 g over 10 h) enriched with [6-3H] glucose to replenish and label their hepatic glycogen. After a 10-h overnight fast, release of the [6-3H] glucose into the circulation was traced with [2-3H] glucose to estimate breakdown of glycogen that had been formed via the direct pathway while gluconeogenesis was simultaneously estimated by incorporation of infused [14C] lactate into plasma glucose. We found that release of [6-3H] glucose into plasma (6.79±0.69 µmol·kg−1·min−1) accounted for 46±5 % of hepatic glucose output (15.0±0.7 µmol·kg−1· min−1) while glucose formed from lactate (2.71± 0.28 µmol·kg−1·min−1) accounted for 19±2 % of hepatic glucose output. Since these determinations underestimate direct pathway glycogenolysis and overall gluconeogenesis, a maximal estimate for the contribution of indirect pathway glycogenolysis to hepatic glucose output is obtained by subtracting the sum of direct pathway glycogenolysis and lactate gluconeogenesis from hepatic glucose output. This amounted to a maximum of 36±5 % of hepatic glucose output and 44±6 % of overall glycogenolysis. Assuming that the relative proportions of direct and indirect pathway glycogen breakdown would reflect the relative contributions of these pathways to glycogen formation, we conclude that under our experimental conditions the direct pathway is the predominant route for glycogen formation in man and that in overnight fasted humans, hepatic glucose output is mainly the result of glycogenolysis. [Diabetologia (1994) 37: 697–702]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00417694
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  • 5
    Electronic Resource
    Electronic Resource
    Evidence for lactate production by human adipose tissue in vivo (1990)
    Springer
    Diabetologia 33 (1990), S. 253-256 
    Details
    ISSN: 1432-0428
    Keywords: Adipose tissue ; lactate ; glucose metabolism ; microdialysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Microdialysis of the abdominal subcutaneous tissue was performed in seven healthy normal weight subjects after an overnight fast and also after oral ingestion of 100 g glucose. The lactate concentration in the interstitial water was compared with that in the venous and arterialized plasma from the cubital veins. In the postabsorptive state the lactate concentration in the subcutaneous tissue (1128±72 μmol/l, mean±SEM) was significantly higher (p〈0.01) than that in both arterialized (722±72 μmol/l) and venous plasma (798±41 μmol/l). The oral glucose load further increased the lactate level in the subcutaneous tissue throughout the observation period of 2 h. The kinetics for the increase in the lactate concentration was not apparently different in blood or tissue. The highest lactate levels were 1798±173 umol/l in the subcutaneous tissue and 1199±150 μmol/l and 1275±123 μmol/l in arterialized and venous plasma, respectively. It is concluded that abdominal adipose tissue produces lactate both in the fasting state and after an oral glucose load. The data emphasize the importance of the adipose tissue as a significant source of lactate production in the body.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404805
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  • 6
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    Impact of age, BMI and HbA1c levels on the genome-wide DNA methylation and mRNA expression patterns in human adipose tissue and identification of epigenetic biomarkers in blood (2015)
    Oxford University Press
    Details
    Publication Date: 2015-06-09
    Description: Increased age, BMI and HbA1c levels are risk factors for several non-communicable diseases. However, the impact of these factors on the genome-wide DNA methylation pattern in human adipose tissue remains unknown. We analyzed the DNA methylation of ~480 000 sites in human adipose tissue from 96 males and 94 females and related methylation to age, BMI and HbA1c. We also compared epigenetic signatures in adipose tissue and blood. Age was significantly associated with both altered DNA methylation and expression of 1050 genes (e.g. FHL2 , NOX4 and PLG ). Interestingly, many reported epigenetic biomarkers of aging in blood, including ELOVL2 , FHL2 , KLF14 and GLRA1 , also showed significant correlations between adipose tissue DNA methylation and age in our study. The most significant association between age and adipose tissue DNA methylation was found upstream of ELOVL2 . We identified 2825 genes (e.g. FTO , ITIH5 , CCL18 , MTCH2 , IRS1 and SPP1 ) where both DNA methylation and expression correlated with BMI. Methylation at previously reported HIF3A sites correlated significantly with BMI in females only. HbA1c (range 28–46 mmol/mol) correlated significantly with the methylation of 711 sites, annotated to, for example, RAB37 , TICAM1 and HLA-DPB1 . Pathway analyses demonstrated that methylation levels associated with age and BMI are overrepresented among genes involved in cancer, type 2 diabetes and cardiovascular disease. Our results highlight the impact of age, BMI and HbA1c on epigenetic variation of candidate genes for obesity, type 2 diabetes and cancer in human adipose tissue. Importantly, we demonstrate that epigenetic biomarkers in blood can mirror age-related epigenetic signatures in target tissues for metabolic diseases such as adipose tissue.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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