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Biomedical subjects

Gerhard Rechkemmer

Publications and source records attributed to Gerhard Rechkemmer.

At least 19 recordsLinked to original sources
PubMed2006

Cellular uptake of carotenoid-loaded oil-in-water emulsions in colon carcinoma cells in vitro.

Oil-in-water emulsions allow the preparation of lipophilic compounds such as carotenoids in the liquid form. Here, the effect of a combination of some emulsifiers, such as two whey protein isolates (BiPro and BioZate), sucrose laurate (L-1695), and polyoxyethylene-20-sorbitan-monolaurate (Tween 20), on the stability of lycopene and astaxanthin in emulsions, droplet size, and cellular uptake of these carotenoids has been investigated. The degradation of lycopene was slightly more pronounced than that of astaxanthin in all emulsions. The concentration of lycopene and astaxanthin decreased by about 30% and 20%, respectively, in all emulsions after 3 weeks of storage in the dark at 4 degrees C. The kind of emulsifiers or their combinations have played an important role in the cellular uptake by the colon carcinoma cells line HT-29 and Caco-2.

Caco-2 Cells↗
PubMed2006

Intervention with polyphenol-rich fruit juices results in an elevation of glutathione S-transferase P1 (hGSTP1) protein expression in human leucocytes of healthy volunteers.

Polyphenols are probably antigenotoxic on account of their antioxidant activities and might alter phase I and II enzymes in a way that results in chemoprotection. We investigated the hypothesis that polyphenols enhance expression of glutathione S-transferases (GSTs), which increases carcinogen detoxification and thereby provides protection against oxidative stress. HGSTP1 protein expression and GST polymorphisms were determined in leucocytes obtained during an intervention study with healthy subjects consuming two fruit juices in an 8 wk trial (polyphenol-free run in phase, juice intervention phase, washout phase, second juice intervention phase, each treatment regime lasted for 2 wk). The study had originally shown that juice intervention significantly reduced oxidative DNA damage in leucocytes at week 8 (Bub, A., Watzl, B., Blockhaus, M., Briviba, K. et al., J. Nutr. Biochem. 2003, 14, 90-98). We reanalysed the levels of DNA damage based on GST genotypes. We also treated leucocytes in vitro with mixtures of polyphenols and determined cytotoxicity and expression of 96 genes related to drug metabolism. Key results with leucocytes of the intervention study were that the initial content of hGSTP1 protein was first suppressed at weeks 4 and 6. At week 8, however, hGSTP1 protein expression was significantly increased. HGSTP1 protein levels and DNA damage were inversely correlated (p = 0.005), but there was no difference for cells obtained from subjects with hGSTM1*1 and hGSTM1*0 genotypes, nor was there any difference between cells from subjects consuming the two different juices. The treatment of leucocytes with polyphenol mixtures in vitro did not result in modulated GST gene expression or total GST activity, but in an up-regulation of other biotransformation enzymes (e. g., members of the cytochrome P450 and the sulphotransferase family). In conclusion, in vitro treatment of leucocytes led to a modulated mRNA expression of selected genes, not directly related to oxidative defence systems. In vivo, however, we observed a delayed enhancement of hGSTP1, which could be associated with an initial repression of oxidative DNA damage in leucocytes from human subjects, consuming juices with high levels of polyphenols.

Adult↗
PubMed2005

Basal colon crypt cells are more sensitive than surface cells toward hydrogen peroxide, a factor of oxidative stress.

Products of oxidative stress are possibly important risk factors for colon cancer. It is necessary to assess their toxicity in tumour target cells, which include the stem cells and dividing daughter cells located in the bottom of the colon crypts. Here, we investigated the sensitivity of crypt cells towards hydrogen peroxide (H(2)O(2)), a key genotoxin associated with oxidative stress. Primary rat colonocytes, were isolated from different regions of the crypts by fractionated digestion. Differentiation was determined by measuring the alkaline phosphatase activity. Deoxyribonucleic acid (DNA) damage and oxidised DNA bases were determined using the modified version Comet assay with endonuclease III. Major findings were that rat colonocytes had high levels of endogenous DNA single strand breaks, with no significant difference from basal crypt cells to surface cells. However, cells of the basal crypt had more oxidised DNA pyrimidines, which were probably a reflection of preceding in vivo exposure. An in vitro treatment with H(2)O(2) significantly increased DNA strand breaks in all fractions of rat colonocytes, but again cells of the basal crypt were more sensitive than cells of the surface epithelium. We conclude that cells from lower crypt sections are more sensitive towards H(2)O(2) than differentiated cells at the surface of the crypt.

Animals↗
PubMed2005

Stability and biotransformation of various dietary anthocyanins in vitro.

BACKGROUND: Anthocyanins, which are found in high concentrations in fruit and vegetable, may play a beneficial role in retarding or reversing the course of chronic degenerative diseases. However, little is known about the biotransformation and the metabolism of anthocyanins so far. AIM OF THE STUDY: The aim of the study was to investigate possible transformation pathways of anthocyanins by human faecal microflora and by rat liver microsomes as a source of cytochrome P450 enzymes as well as of glucuronyltransferases. METHODS: Pure anthocyanins, an aqueous extract of red radish as well as the assumed degradation products were incubated with human faecal suspension. The incubation mixtures were purified by solid-phase extraction and analysed by HPLC/DAD/MS and GC/MS. Quantification was done by the external standard method. Furthermore the biotransformation of anthocyanins by incubation with rat liver microsomes in the presence of the cofactor NADPH (as a model for the phase I oxidation) and in the presence of activated glucuronic acid (as a model for the phase II glucuronidation) was investigated. RESULTS: Glycosylated and acylated anthocyanins were rapidly degraded by the intestinal microflora after anaerobic incubation with a human faecal suspension. The major stable products of anthocyanin degradation are the corresponding phenolic acids derived from the B-ring of the anthocyanin skeleton. Anthocyanins were not metabolised by cytochrome P450 enzymes, neither hydroxylated nor demethylated. However they were glucuronidated by rat liver microsomes to several products. CONCLUSIONS: The gut microflora seem to play an important role in the biotransformation of anthocyanins. A rapid degradation could be one major reason for the poor bioavailability of anthocyanins in pharmacokinetic studies described so far in the literature. The formation of phenolic acids as the major stable degradation products gives an important hint to the fate of anthocyanins in vivo.

Animals↗
PubMed2005

Paraoxonase 1 Q192R (PON1-192) polymorphism is associated with reduced lipid peroxidation in healthy young men on a low-carotenoid diet supplemented with tomato juice.

The HDL-bound enzyme paraoxonase (PON) protects LDL from oxidation and may therefore attenuate the development of atherosclerosis. We examined the effect of tomato and carrot juice consumption on PON1 activity and lipid peroxidation in healthy young volunteers with different PON1-192 genotypes (Q/R substitution at position 192). In this randomized cross-over study twenty-two healthy, non-smoking men on a low-carotenoid diet received 330 ml/d tomato juice (37.0 mg lycopene, 1.6 mg beta-carotene) or carrot juice (27.1 mg beta-carotene, 13.1 mg alpha-carotene) for 2 weeks. Intervention periods were preceded by 2-week low-carotenoid intake. We determined the PON1-192 genotype by restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR) and measured ex vivo LDL oxidation (lag time), plasma malondialdehyde and PON1 activity at the beginning and end of each intervention period. At baseline, lag time was higher (P<0.05) in QQ (111 (sd 9) min) than in QR/RR subjects (101 (sd 8) min). Neither tomato nor carrot juice consumption had significant effects on PON1 activity. However, tomato juice consumption reduced (P<0.05) plasma malondialdehyde in QR/RR (Delta: -0.073 (sd 0.11) micromol/l) as compared to QQ subjects (Delta:+0.047 (sd 0.13) micromol/l). Carrot juice had no significant effect on malondialdehyde irrespective of the PON1-192 genotype. Male volunteers with the QR/RR genotype showed an increased lipid peroxidation at baseline. Although tomato and carrot juice fail to affect PON1 activity, tomato juice intake reduced lipid peroxidation in healthy volunteers carrying the R-allele of the PON1-192 genotype and could thus contribute to CVD risk reduction in these individuals.

Adult↗
PubMed2005

Novel lycopene metabolites are detectable in plasma of preruminant calves after lycopene supplementation.

Appropriate animal models such as preruminant calves are necessary to study the complex physiological functions of carotenoids and to relate them to possible health effects in humans. In this study, the bioavailability and metabolism of lycopene from 2 dietary supplements were compared. LycoVit containing synthetic lycopene and Lyc-O-Mato containing natural tomato oleoresin were administered to 2 groups of preruminant calves (each n = 8) for 14 d in daily doses of 15 mg of lycopene. Plasma was analyzed for carotenoids before the intervention period, directly after, and each day for 5 d after the end of the intervention. All-trans and 5-cis lycopene, and 3 lycopene metabolites not previously found in calf plasma were detected. These metabolites contributed 52% of the total lycopene content measured at the end of the intervention period. Based on spectroscopic data, they might be hydrogenation products, which are formed from all-trans and/or 5-cis lycopene. In the LycoVit group, total lycopene concentrations were approximately 300% higher (286 +/- 89 nmol/L) than in the Lyc-O-Mato group (72 +/- 33 nmol/L) (P < 0.001). This indicates that, unlike in humans, lycopene from LycoVit and Lyc-O-Mato does not have equal bioavailabilities in preruminant calves. Therefore, the preruminant calf may not be a suitable animal model with which to study the biological and physiological effects of lycopene.

Animals↗
PubMed2005

A half-marathon and a marathon run induce oxidative DNA damage, reduce antioxidant capacity to protect DNA against damage and modify immune function in hobby runners.

This study investigated whether a 21.1 km (half-marathon) or a 42.195 km (marathon) run modulates DNA damage, antioxidant capacity in lymphocytes and plasma, and the immune system in healthy hobby runners. Ten and 12 volunteers who completed the Baden-Marathon race in Karlsruhe with a running distance of 21.1 km and 41.195 km, respectively, were assessed 10 days before and immediately after the finish. There was no increase in the levels of endogenous DNA strand breaks immediately after half-marathon or marathon races. A statistically significant increase in the levels of oxidative DNA damage in lymphocytes was found using endonuclease III but not formamidopyrimidine glycolase (Fpg). The resistance of DNA to oxidative damage induced by hydrogen peroxide in isolated lymphocytes was significantly decreased after both races. The levels of plasma antioxidants such as alpha-tocopherol, beta-carotene and lycopene were close to, or higher than, those considered optimal for reducing the risk of cardiovascular diseases and there were no significant changes after the races in antioxidant capacity of LDL (lag-time test) or plasma in ORAC, TEAC or paraoxonase assays. The number and percentage of granulocytes and monocytes able to generate oxidative burst were significantly increased after both races, but the lytic activity of NK cells was significantly increased at the end of the half-marathon; no effect was observed in the marathon runners. Thus, oxidative DNA damage in lymphocytes, decreased the antioxidant capacity to protect lymphocytes against DNA strand breaks and increased the formation of reactive species by phagocytes in well-nourished hobby runners indicating moderate oxidative damage during such high-intensity exercise.

Adult↗
PubMed2004

Effects of supplementing a low-carotenoid diet with a tomato extract for 2 weeks on endogenous levels of DNA single strand breaks and immune functions in healthy non-smokers and smokers.

Increased consumption of tomato products is associated with a decreased risk of cancer. The present study was performed to investigate whether consumption of a tomato oleoresin extract for 2 weeks can affect endogenous levels of DNA single strand breaks in peripheral blood lymphocytes in healthy non-smokers and smokers. We also assessed, the effect of the tomato oleoresin extract on various immunological functions of peripheral blood mononuclear cells. A double-blinded, randomized, placebo-controlled study design was used. Over a period of 2 weeks 15 non-smokers and 12 smokers were given three tomato oleoresin extract capsules daily (each containing 4.88 mg lycopene, 0.48 mg phytoene, 0.44 mg phytofluene and 1.181 mg alpha-tocopherol). The control group received placebos. The baseline level of endogenous DNA damage for non-smokers was slightly (13%) and non-significantly (P = 0.44) lower than that of smokers. Placebo supplementation of non-smokers and smokers for 2 weeks did not significantly affect lycopene plasma levels or DNA damage in either group. Intervention with tomato oleoresin extract resulted in significant increases in total plasma lycopene and resulted in decreased levels of DNA strand breaks of approximately 32 (non-smokers) and 39% (smokers). However, this effect was not statistically significant in either group (P = 0.09 for non-smokers and P = 0.12 for smokers). Analysis of the distribution pattern of DNA strand breaks showed a statistically significant (P < 0.05) increase in the number of comets in class 0 (undamaged) and a decrease in classes 1 and 2 (damaged) after the tomato oleoresin extract intervention in non-smokers. The changes in the smoker group were not statistically significant. Treatment with the tomato extract had no effect on lymphocyte proliferation, NK cell activity, interleukin (IL)-2 production and tumor necrosis factor (TNF)alpha production, but it significantly reduced IL-4 production in smokers (P = 0.009).

Adult↗
PubMed2004

Peripheral amylin activates circumventricular organs expressing calcitonin receptor a/b subtypes and receptor-activity modifying proteins in the rat.

The pancreatic hormone amylin (AMY) and the AMY-receptor-agonist salmon-calcitonin (sCT) reduce short-term food-intake after binding to the area postrema (AP), a circumventricular organ (CVO) lacking blood-brain-barrier characteristics. AMY has also been proposed to induce drinking via another CVO, the subfornical organ (SFO). In cellular systems, AMY-binding is generated by interaction of calcitonin-receptor a/b (CT((a))/CT((b))) with receptor-activity modifying proteins (RAMPs). By using in situ hybridization, the codistribution of CT((a))/CT((b)) with RAMP1-3 and c-fos was mapped in CVOs of rats. AMY and sCT induced c-fos within the SFO which contained CT((a)) and/or CT((b)) and RAMP1/2 mRNA. AMY and sCT also activated AP neurons, which express the CT((a)), but not the CT((b)), receptor and RAMP2/3 mRNA. These data emphasize the important role of these structures as primary targets for circulating AMY.

Amyloid↗
PubMed2004

PASSCLAIM--diet-related cancer.

BACKGROUND: The role of dietary factors in the aetiology of human cancer is an area, which has attracted intense interest in recent years. The suggestion that approximately one third of all cancers may be caused by an 'inappropriate' balance of food components has led to the attractive contention that we can significantly decrease cancer incidence through dietary recommendations and a change in dietary habits in populations. Thus, a key issue must be to establish clear criteria, which must be met in order to be able to make 'cancer risk reduction' claims for food components. In this area, the one true marker is the malignant human tumour, which for practical reasons is usually not accessible to claims. In its absence, we must rely on alternative markers--biomarkers/surrogate endpoints. This paper mainly deals with the link of these biomarkers to the endpoint tumour and their usefulness for making claims. Some claims have been made based on epidemiological studies. AIM: Can we identify targets/ biomarkers in the chain of events from initial 'exposure' to overt malignant tumour, whose modification can be used to make 'anticancer' claims for food components? RESULTS: We identified 18 targets/markers in the above chain of events whose modification 'have the potential' to be used for 'reduction of cancer risk' claims for food components. These targets/markers fall under 5 broad headings: tumours and preneoplastic changes; cellular targets/markers; gut luminal markers; angiogenesis and metastasis; carcinogen metabolising enzymes; genetic events. CONCLUSIONS: The strongest markers presently available are precancerous lesions (e. g. polyps or aberrant crypt foci) in humans and precancerous lesions and tumours in animal models. The only marker that presently can be used for a 'reduction of disease risk' claim (type B) for food components is 'polyp recurrence'. Type B claims cannot be made on the basis of results in animal models. All of the other biomarkers examined presently lack validation against the 'true endpoint', the tumour, and thus cannot be used for type B claims. 'Reduction of disease risk' claims in the area of 'diet-related cancer' should be based primarily on human intervention studies using relevant/acceptable endpoints. An important area for future research will be the validation of these surrogate endpoints.

Animals↗
PubMed2004

Dietary intervention with the probiotics Lactobacillus acidophilus 145 and Bifidobacterium longum 913 modulates the potential of human faecal water to induce damage in HT29clone19A cells.

Probiotics reduce the risk of colon cancer by inhibiting carcinogen-induced DNA damage in animals, but there are no analogous data in human subjects. To enhance knowledge of the effects of probiotics in human subjects, we have investigated the genotoxicity of faecal water after dietary intervention with standard yoghurt or with probiotic yoghurt, which included the strains Lactobacillus acidophilus 145 and Bifidobacterium longum 913. Faeces were collected from nine healthy volunteers after intervention with probiotic yoghurt or standard yoghurt. Faecal water was isolated and incubated with human colon tumour cells HT29clone19A. DNA strand breaks, oxidised DNA bases and damage after challenge with H2O2 were determined by micro-gel-electrophoresis. Faecal water was genotoxic in comparison with NaCl, but protected against H2O2-induced DNA strand breaks. The intervention with probiotic yoghurt significantly lowered faecal water genotoxicity compared with standard yoghurt. However, probiotic intervention also increased oxidative damage; this either reflected prooxidative activity or stimulation of endogenous defence systems. Altogether, the balance of effects favoured protection, since faecal water from the probiotic group reduced overall genetic damage. Thus, there was a reduction of strand break-inducing compounds in human faeces after dietary intervention with probiotic bacteria. This protection reflected results from previous studies in carcinogen-exposed animals where probiotics reduced DNA damage in colon cells.

Adult↗
PubMed2004

Intestinal immunity of rats with colon cancer is modulated by oligofructose-enriched inulin combined with Lactobacillus rhamnosus and Bifidobacterium lactis.

Probiotics (PRO) are known to modulate immunity in animals and human subjects and to inhibit colon carcinogenesis in experimental models, but the effects of synbiotics (SYN) are not well understood. Therefore, the effects of PRO (Lactobacillus rhamnosus GG and Bifidobacterium lactis Bb12), PRE (inulin-based enriched with oligofructose, 100 g/kg) and SYN (combination of PRO and PRE) on the immune system of rats were investigated in the azoxymethane (AOM)-induced colon cancer model. After 33 weeks, rats with and without AOM treatment were killed and immune cells were isolated from spleen, mesenterial lymph nodes (MLN) and Peyer's patches (PP). AOM treatment significantly reduced natural killer (NK) cell-like cytotoxicity in control rats and in PRO- and PRE-supplemented rats. SYN supplementation prevented the AOM-induced suppression of NK cell-like cytotoxicity in PP compared with control rats (P<0.01). SYN and PRE supplementation stimulated IL-10 production in PP in these rats (P<0.01) and in MLN of rats not treated with AOM (P<0.05). Interferon-gamma production in PP was decreased by PRO supplementation (PRO and SYN groups combined; P<0.05). Proliferative responsiveness of lymphocytes (PP) from AOM-treated rats was suppressed in SYN-supplemented rats (P<0.01). Overall, SYN supplementation in carcinogen-treated rats primarily modulated immune functions in the PP, coinciding with a reduced number of colon tumours. PRE and PRO provided in combination as SYN may contribute to the suppression of colon carcinogenesis by modulating the gut-associated lymphoid tissue.

Animals↗
PubMed2004

Prebiotic inulin enriched with oligofructose in combination with the probiotics Lactobacillus rhamnosus and Bifidobacterium lactis modulates intestinal immune functions in rats.

Probiotics (PRO) modulate systemic immunity in animals and humans. In contrast, the effects of prebiotics (PRE) on systemic and intestinal immunity have not been investigated. Whether the combined application of PRO and PRE [synbiotics (SYN)] has synergistic or additive effects is presently unknown. Therefore, PRO (Lactobacillus rhamnosus GG and Bifidobacterium lactis Bb12), PRE (inulin enriched with oligofructose), and SYN (combination of PRO and PRE) were fed to F344 rats for 4 wk as supplements to a high fat diet. Functions of immune cells isolated from peripheral blood mononuclear cells (PBMC), spleen, mesenterial lymph nodes and Peyer's patches (PP) were investigated. The SYN supplement increased secretory immunoglobulin A (sIgA) production in the ileum compared with controls fed the high fat diet alone (P<0.05), and decreased the oxidative burst activity of blood neutrophils (P<0.05) compared with rats fed PRO. The PRE supplement enhanced the production of interleukin-10 (P<0.05) in PP as well as the production of sIgA in the cecum (P<0.05), compared with controls. The PRO supplement modestly affected immune functions, whereas systemic immunomodulatory effects were observed in rats fed SYN. The PRE supplement primarily acted at the level of the gut-associated lymphoid tissue. The combined application of PRO and PRE has different effects from those of the individual supplements, but does not simply result in additive or synergistic effects.

Animals↗
PubMed2004

Supplementation of a diet low in carotenoids with tomato or carrot juice does not affect lipid peroxidation in plasma and feces of healthy men.

Antioxidant properties of carotenoids are thought to be at least partly responsible for the protective effects of fruits and vegetables rich in carotenoids against colon cancer. There are large amounts of in vitro data supporting this hypothesis. But there is little known about the antioxidant effects of carotenoid-rich food in vivo particularly in the gastrointestinal tract. In a randomized, crossover trial, healthy men (n = 22) who were consuming a low-carotenoid diet drank 330 mL/d tomato juice or carrot juice for 2 wk. Antioxidant capacity was assessed by the "lag time" of ex vivo LDL oxidation induced by copper and lipid peroxidation as determined by measurements of malondialdehyde (MDA) in plasma and feces using HPLC with fluorescence detection. Although consumption of both carotenoid-rich juices for 2 wk increased the carotenoid level in plasma and feces (P < 0.001), the antioxidant capacity of LDL tended to be increased by only approximately 4.5% (P = 0.08), and lipid peroxidation in the men's plasma and feces was not affected. Thus, processes other than lipid peroxidation could be responsible for the preventive effects of tomatoes and carrots against colon cancer.

Antioxidants↗
PubMed2003

Phytoestrogens modulate binding response of estrogen receptors alpha and beta to the estrogen response element.

Binding of estrogen receptor (ER) to estrogen response element (ERE) induces gene activation and is an important step in estrogen-induced biological effects. Here, we investigated the effects of some dietary phytoestrogens such as the isoflavones genistein and daidzein, its metabolite equol, and the coumestane coumestrol on the binding rate of ERalpha and ERbeta to ERE by a nonradioactive real-time method, the Biacore Technology. ERalpha and ERbeta were able to bind to ERE immobilized on the surface of a sensor chip even in the absence of estrogens. 17beta-Estradiol and phytoestrogens induced an increase in ER binding to ERE in a concentration-dependent manner. 17beta-Estradiol was a more potent activator of binding than the phytoestrogens studied. The concentrations of 17beta-estradiol inducing an increase in the binding response of ERalpha and ERbeta to ERE by 50% (EC(50)) as compared to unliganded ER were 0.03 and 0.01 microM, respectively. Regarding the efficacy of activation of ERalpha, from the most to the least effective compound, the sequence and the EC(50) were as follows: 17beta-estradiol (0.03 microM) > coumestrol (0.2 microM) > equol (3.5 microM) > genistein (15 microM) > daidzein (>300 microM) and for ERbeta 17beta-estradiol (0.01 microM) > coumestrol (0.025 microM) > genistein (0.03 microM) > daidzein (0.35 microM) > equol (0.4 microM). The ratios EC(50)alpha/EC(50)beta were calculated to be for 17beta-estradiol, 3; coumestrol, 8; equol, 8.8; genistein, 500; daidzein > 850. These ratios indicate that genistein and daidzein preferentially activate the binding of ERbeta to ERE. The endogenous hormone 17beta-estradiol as well as coumestrol and daidzein metabolite equol activate the binding of ERbeta to ERE only slightly more effectively than the binding of ERalpha to ERE. Thus, the effect of daidzein can be changed from a specific activator of ERbeta to an activator of both ER isotypes alpha and beta in humans who are able to convert daidzein to equol. While the results of the measurements with ERalpha were in line with the binding affinities of compounds tested for ER, there was a distinct difference between our results and the binding affinities of phytoestrogens for the ERbeta. This leads to the conclusion that phytoestrogens differ not only in their binding affinities for the ER, but also in their potential to increase the rate of receptor binding to the ERE.

DNA↗
PubMed2003

Differential effects of amylin and salmon calcitonin on neuropeptide gene expression in the lateral hypothalamic area and the arcuate nucleus of the rat.

The pancreatic peptide hormone amylin (AMY) and the AMY receptor agonist salmon calcitonin (sCT) reduce short-term food intake in rats primarily by activating neurons located in the circumventricular area postrema. In the present study we analyzed the involvement of (an)orexigenic neuropeptides expressed in the lateral hypothalamic area (LHA) and in the arcuate nucleus in mediating the AMY and sCT-induced suppression of food intake. By using semiquantitative in situ hybridization 120 min after intraperitoneal injection of AMY or sCT (50 microgram/kg), orexin mRNA levels were decreased in LHA by AMY or sCT treatment. Moreover, sCT significantly suppressed the orexigenic melanin concentrating hormone in LHA, whereas mRNA levels of neuropeptide Y, cocaine and amphetamine regulated transcript, agouti-gene-related protein and proopiomelanocortin were unaffected by either treatment. In conclusion, the anorexigenic effect of AMY/sCT might be mediated by the observed reduced expression of orexigenic neuropeptides in the LHA.

Agouti-Related Protein↗
PubMed2003

Micronutrient deficiencies. Hohenheim Consensus Conference.

OBJECTIVE: The aim of this study was to consider the risk of micronutrient deficiencies and approaches for intervention, and to summarize existing knowledge and identify areas of ignorance. DESIGN: Experts from a range of relevant disciplines received and considered a series of questions related to aspects of the topic. INTERVENTION: The experts met and discussed the questions and arrived at a consensus. CONCLUSION: Though healthy balanced diet is available for the general European population, a few defined groups are at risk of micronutrient deficiencies. In addition, the intake of specific micronutrients such as iron, folic acid, vitamin D and vitamin B12 are often marginal. To overcome these deficiencies, either selected micronutrients or a mixture of different micronutrients might be recommended. However, to define and detect micronutrient deficiencies, specific biomarkers are only available for a few micronutrients (e. g. vitamin D, folic acid, vitamin C, iron). The definition of a risk group, based on scientific data, might be an appropriate way to justify intervention with supplements.

Aging↗