torsdag 5 december 2019

D-talitoli

https://www.ncbi.nlm.nih.gov/pubmed/?term=D-talitol

2013 Nov 12;9:2434-45. doi: 10.3762/bjoc.9.281.

Biosynthesis of rare hexoses using microorganisms and related enzymes.

Li Z¹, Gao Y², Nakanishi H¹, Gao X¹, Cai L³.

1: The Key Laboratory of Carbohydrate Chemistry and Biotechnology, Ministry of Education, School of Biotechnology, Jiangnan University, Wuxi, 214122, China.
2: School of Food Science and Technology, Jiangnan University, Wuxi, 214122, China.
3: Division of Mathematics and Science, University of South Carolina Salkehatchie, Walterboro, South Carolina, 29488, USA.Abstract

Rare sugars, referred to as monosaccharides and their derivatives that rarely exist in nature, can be applied in many areas ranging from foodstuffs to pharmaceutical and nutrition industry, or as starting materials for various natural products and drug candidates. Unfortunately, an important factor restricting the utilization of rare sugars is their limited availability, resulting from limited synthetic methods. Nowadays, microbial and enzymatic transformations have become a very powerful tool in this field. This article reviews the biosynthesis and enzymatic production of rare ketohexoses, aldohexoses and sugar alcohols (hexitols), including D-tagatose, D-psicose, D-sorbose, L-tagatose, L-fructose, 1-deoxy-L-fructose, D-allose, L-glucose, L-talose, D-gulose, L-galactose, L-fucose, allitol, D-talitol, and L-sorbitol. New systems and robust catalysts resulting from advancements in genomics and bioengineering are also discussed. KEYWORDS:

biosynthesis; enzyme; hexose; microorganism; rare sugars

Seleno-D- talitolista hyviä sanoja:

https://www.ncbi.nlm.nih.gov/pubmed/31494145

Mucoraceae sienet hyödyntävät D- talitolia.

https://www.sciencedirect.com/science/article/pii/S1389172306705692?via%3Dihub

D-Tagatoosi ja sen kaupallinen käyttö. Näkymätöntä sokerilajia!

https://en.wikipedia.org/wiki/Tagatose
vain pelkkää puhdasta etua ja hyötyyäkö?

Tagatoosi on luonnostaan esiintyvä monosakkaridi, tarkemmin heksoosi. Sitä tavataan usein meijerituotteissa ja puhdistettuna se on valkoista kiteistä jauhetta, ominaisuuksiltaan hyvin samanlaista kuin sakkaroosi (tavallinen sokeri), vastaten 92 % sen makeudesta mutta vain 38 % sen kaloreista. D-tagatoosi on hyväksytty EU-markkinoille.^[1]

Lähteet

Makeutusaine tagatoosi hyväksyttiin EU:n markkinoille 23.1.2006. Finnfood. Viitattu 22.4.2013.

Siis jos ihmiselle tagatoosista on hyötyä siksi että se ei vaiuta verensokeria ja insuliinin kohonnutta tarvetta, niin mitä haitaa sen liika käytöstä voisi olla?
Mikäs sitä sitten hyödyntää? Eräät sienet, joten ihminen alkaa olla niille suotuisaa kasvualustaa. Arvelen.

Kts. lähde:
https://www.sciencedirect.com/science/article/pii/S1389172306705692?via%3Dihub
MUCORACEAE fungi

YoshihiroShinohara^a TakahiroHirotsu^a KenIzumori^b

https://doi.org/10.1263/jbb.101.219 Get rights and content

Rhizopus oryzae MYA-2483, which cannot utilize D-psicose as a sole source of carbon, converted D-psicose to two other compounds. These compounds were identified by NMR and IR as D-tagatose and D-talitol. In this study, we describe for the first time the bioconversion of D-psicose to D-tagatose. Various strains of Mucoraceae fungi, to which R. oryzae MYA-2483 belongs, exhibited conversion activity similar to that of R. oryzae MYA-2483. There is the possibility that a considerable number of fungi belonging to Mucoraceae possess such D-psicose conversion activity.

Mitä mucoraceae si8enet voivat ihmisessä aiheuttaa?

2019 Nov;71(Suppl 3):1962-1971. doi: 10.1007/s12070-018-1384-6. Epub 2018 May 4.

Sinonasal Mucormycosis: A to Z.

Singh VP¹, Bansal C¹, Kaintura M¹.

1: Department of ENT, Shri Mahant Indiresh Hospital, Shri Guru Ram Rai Institute of Medical Sciences, Dehradun, Uttarakhand India.

Abstract

Mucormycosis caused by one of the members of Mucoraceae family, is one of the most rapidly spreading and fatal fungal infection occurring mostly in Diabetic or Immunocompromised patients especially in developing countries. 26 patients suffering from sinonasal mucormycosis admitted in SGRRIM&HS, Dehradun from January 2013 to January 2017 are discussed. Diagnosis of mucormycosis was established on strong clinical suspicion with presence of grayish black crusting on nasal endoscopy which is confirmed by histopathology examination. Immediate correction of underlying immunocompromised status with debridement with intravenous liposomal amphotericin B was done in all the 26 cases out of which 10 patients were cured. Early detection and aggressive multidisciplinary management is must for the successful treatment of mucormycosis.

Amphotericin; Invasive fungal sinusitis; Rhinocerebral mucormycosis; Rhizopus oryzae

PMID:: 31763277
PMCID:: PMC6848679; [Available on 2020-11-01]
DOI:: 10.1007/s12070-018-1384-6

2011;7(3):189-93.

Rhinocerebral mucormycosis: five cases and a literature review.

Mbarek C¹, Zribi S, Khamassi K, Hariga I, Ouni H, Ben Amor M, Ben Gamra O, El Khedim A.

1: Department of Otorhinolaryngology-Head and Neck Surgery, Habib Thameur Hospital, Tunis, Tunisia.

Abstract

OBJECTIVE:

In this retrospective study, we describe our experience in the diagnosis and management of rhinocerebral mucormycosis (RCM), a rapidly lethal fungal infection.

METHODOLOGY:

Between 1997 and 2007, five patients hospitalized for suspicion of RCM. Computed tomography was performed in all cases, and diagnosis was confirmed after anatomopathological or mycological examination. All patients underwent medical and surgical treatment. Follow-up was clinical and radiological with a mean period of 17 months.

RESULTS:

All patients were diabetic. Exophthalmia, rhinorrhea, and ophthalmoplegia were the most frequent symptoms observed. One patient had loss of visual acuity and another exhibited peripheral facial palsy. One patient had extensive hemifacial cutaneous necrosis. Nasal endoscopy revealed black necrotic lesions in one case, and another patient had a tumefaction localised in the left middle meatus. Necrotic lesions were most often found in the orbit, the maxillary and the ethmoidal sinuses on computed tomography (four cases for each site). One patient had thrombophlebitis of the cavernous sinus, and another had an intracranial extension. All patients were administered ordinary insulin and intravenous amphotericin B. Surgical debridement of the nasal cavity and the involved sinuses was performed through lateral rhinotomy (four cases) or endoscopy (one case). Unilateral orbital exenteration was associated in two cases. Progression was favourable in four cases; one patient died from sepsis despite aggressive treatment.

....

TAGATOOSIN osuus ravinnossa. Se on ruokaa mucormykoosisienille kehossa, vaikka ei näy verensokeriarvoissa.

SIIS: pitäisi maitoruoissa välttää liika tagatoosilisää. Myös galaktoosista muodostuu teknisesti tagatoosia, mutta tokko ihmisessä . Sellainen reitti ei kai ole ihmisen sokeriaineenvaihduntakaavoissa. Tagatoosin valmistuksen galaktoosista keksi G. Levin vuonna 1988.

Keittämällä maitoa yli 61 asteen C saadaan tagatoosia hajoamaan. Siä on pidetty hyödyllisenä prebioottina.
https://www.ncbi.nlm.nih.gov/pubmed/22260107

söndag 10 november 2019

"Diabetes 3", aivon insuliiniresistenssi

http://jem.rupress.org/content/214/8/2171

DOI: 10.1084/jem.20170979 | Published June 26, 2017

In this issue of JEM, Marciniak et al. (https://doi.org/10.1084/jem.20161731) identify a putative novel function of tau protein as a regulator of insulin signaling in the brain. They find that tau deletion impairs hippocampal response to insulin through IRS-1 and PTEN dysregulation and suggest that, in Alzheimer’s disease, impairment of brain insulin signaling might occur via tau loss of function.

Alzheimer’s disease (AD) is the leading form of dementia worldwide. The two major histopathological hallmarks of AD are senile plaques composed of amyloid-β (Aβ) peptide and neurofibrillary tangles made of abnormally hyperphosphorylated tau protein. Tau pathology is important because it correlates with the degree of cognitive impairment in AD patients. The majority of AD cases are late onset and sporadic, and many environmental, biological, and genetic factors are thought to contribute to the disease. Epidemiological studies particularly suggest that metabolic disorders such as type 2 diabetes (T2D) could be such factors, as they are associated with a higher risk of AD later in life.

Brain insulin resistance appears to be an early and common feature of AD (for review see Stanley et al., 2016), and AD has been proposed as a “type 3 diabetes” representing a form of diabetes that selectively involves the brain (de la Monte and Wands, 2008). Our current knowledge on how AD pathologies may alter brain insulin signaling relies on evidence showing the development of brain insulin resistance after oligomeric Aβ exposure, thus implicating amyloid pathology as a major mediator of brain insulin resistance in AD (Bomfim et al., 2012). However, although the impact of insulin dysfunction on tau pathogenesis has been extensively studied (for review see El Khoury et al., 2014), the effects of tau pathology on insulin signaling has never been assessed before.

Tau is a microtubule binding protein whose most well-known function is to bind and stabilize microtubules. But it has also been suggested to have many other functions such as regulation of cell signaling, synaptic plasticity, and genomic stability (Guo et al., 2017). Tau pathology in AD is thought to exert its detrimental effects through a toxic gain of function, but a potential loss of physiological function might also contribute to some phenotype of the disease. In this issue, Marciniak et al. hypothesized that in AD, tau loss of function could alter brain insulin signaling and partly explain the cognitive and metabolic impairments observed in AD.

Using mice depleted for MAPT, the tau gene (tau KO mice), initially identified a reduction of hippocampal long-term depression of extracellular field excitatory postsynaptic potentials in brain slices from tau KO mice compared with littermate controls after insulin treatments. Altered response to insulin was confirmed in the same mice model ex vivo and in vivo with decreased activation of IRS-1 and AKT (both implicated in insulin signaling), suggesting brain insulin resistance in tau KO mice. By taking advantage of coimmunoprecipitation experiments and bimolecular fluorescence complementation assay, the authors further evaluated whether tau directly interacts with key insulin signaling molecules in neuroblastoma cells expressing non-mutated human tau protein. Unexpectedly, tau did not seem to interact with either the insulin receptor IRS-1 or with PI3K (p85). However, tau was found to interact with PTEN, a phosphatase known to inhibit insulin signaling through the PI3K-Akt pathway. Moreover, demonstrated that human tau is able to reduce PTEN activity and thus promote PIP3 production alone or by potentiating the effect of insulin (see figure).http://jem.rupress.org/content/jem/214/8/2171/F2.medium.jpg

Next, assessed whether tau deletion alters brain insulin functions. Interestingly, absence of tau reduced the anorexigenic effect of intracerebroventricular injection of insulin in tau KO mice. These mice also developed peripheral hyperinsulinemia and glucose intolerance. These data confirmed an important role of tau in the regulation of energy metabolism. Finally, the authors noticed an effect of tau haplotype on glucose tolerance in published genome-wide association study (GWAS) data. H1 haplotype is associated with higher risk of tauopathies (Pittman et al., 2005), and in the study by Marciniak et al. (2017), patients with H1 haplotype exhibited higher circulating glucose levels and lower insulin levels during an oral glucose tolerance test, suggesting that tau impacts peripheral metabolism in humans. Overall, the in vivo and in vitro results dovetail nicely together and with the GWAS data to provide compelling evidence that tau can regulate both brain insulin signaling and peripheral glucose metabolism.

The study by Marciniak et al. (2017) further addresses a question that has emerged over the last few years as to whether AD is a cause or consequence of insulin signaling impairment (Stanley et al., 2016). Epidemiological studies supported by in vivo and in vitro experiments establish metabolic problems as risks for AD. However, the study by is the first assessing whether tau pathology affects brain insulin signaling in AD. Interestingly, metabolic changes and central insulin resistance have been reported in other tauopathies such as progressive supranuclear palsy or corticobasal degeneration (Ahmed et al., 2014; ). This suggests that the alteration of insulin signaling resulting from the loss of tau function upon tau pathology may explain metabolic changes in many tauopathies. At the same time, raise new questions regarding mechanisms underlying the role of tau protein as a regulator of brain insulin signaling that need clarification. For instance, the two molecular events suggested to explain this novel function of tau involved IRS-1 and/or PTEN. Early studies have in fact reported that total IRS-1 but also IRS-2 are decreased in the brain of AD patients along with increased phosphorylated IRS-1 on Ser^636/639 and Ser⁶¹⁶, which colocalizes and correlates with neurofibrillary tangle deposition and inversely correlates with cognitive score (Ma et al., 2009; Moloney et al., 2010; Talbot et al., 2012). This is consistent with altered IRS-1 activity in tau KO mice reported in this issue, whereas the authors could not establish a direct interaction between tau and IRS-1. Another explanation lies in the direct interaction between PTEN and tau, which can modulate the PTEN activity and thus explain decreased responsiveness to insulin in tau KO mice. Although at the current stage it is still impossible to determine which of IRS-1 or PTEN is the instrument of tau to regulate brain insulin signaling, the intervention of these two proteins together in this process is not to be neglected, especially considering that PTEN has been shown to act as tyrosine phosphatase for IRS-1 in vitro (). Nonetheless, the finding by Marciniak et al. (2017) that tau has insulin signaling regulator functions in the brain is remarkable, as it further expands the knowledge about AD and brain insulin resistance.

However, some of the results of this study need independent confirmation in other tau KO models. Indeed, the tau KO model used here is not a true KO, as it was produced by insertion of EGFP in exon 1 of MAPT, and a fusion protein with the first 31 amino acids of tau followed by EGFP is expressed (Tucker et al., 2001). Whether some of the results might stem from the production of this fragment in the absence of functional murine tau will need to be clarified. This also raises the question as to which region of tau is mediating the effects observed. The repeat region is involved in microtubules binding and stability, whereas the projection domain mediates some of tau signaling functions (Guo et al., 2017). The region or regions where PTEN binds and the region or regions important for the regulation of brain insulin sensitivity might be the same or might be different.

Similarly, and as mentioned by Marciniak et al. (2017), it would be important to address the sensitivity of central and peripheral insulin in a conditional KO mice model because tau is present in the pancreas and could even modulate the secretion and the transcription of insulin (Neuville et al., 1995; Maj et al., 2016). Peripheral injections of insulin in tau KO mice could provide important elements for the understanding of this new function of tau outside of the brain. Finally, the confirmation of these results in a mouse model that exhibits tau pathology will be necessary to support the hypothesis of tau loss of function involvement in brain insulin signaling impairment in AD, although it is not clear whether the mouse models of tauopathies available have prominent tau loss of function.

To conclude, the study by Marciniak et al. (2017) not only identifies a new function of tau protein as a modulator of brain insulin signaling, but also highlights potential mechanistic explanation whereby alteration of insulin signaling would occur in AD via tau loss of function.

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torsdag 2 januari 2020

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torsdag 5 december 2019

Biosynthesis of rare hexoses using microorganisms and related enzymes.

Lähteet

Sinonasal Mucormycosis: A to Z.

Abstract

Rhinocerebral mucormycosis: five cases and a literature review.

Abstract

OBJECTIVE:

METHODOLOGY:

RESULTS:

söndag 10 november 2019

fredag 8 november 2019

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