bims-meglyc Biomed News
on Metabolic disorders affecting glycosylation
Issue of 2024‒01‒14
four papers selected by
Silvia Radenkovic



  1. Cardiovasc Res. 2024 Jan 09. pii: cvae006. [Epub ahead of print]
      AIMS: Heart failure with preserved ejection fraction (HFpEF) is a prevalent disease worldwide. While it is well established that alterations of cardiac energy metabolism contribute to cardiovascular pathology, the precise source of fuel used by the heart in HFpEF remain unclear.The objective of this study was to define the energy metabolic profile of the heart in HFpEF.METHODS AND RESULTS: 8-week-old C57BL/6 male mice were subjected to a '2-Hit' HFpEF protocol (60% high-fat diet (HFD) + 0.5 g/L of Nω-nitro-L-arginine methyl ester (L-NAME)). Echocardiography and pressure-volume loop analysis were used for assessing cardiac function and cardiac hemodynamics respectively. Isolated working hearts were perfused with radiolabeled energy substrates to directly measure rates of fatty acid oxidation, glucose oxidation, ketone oxidation, and glycolysis.HFpEF mice exhibited increased body weight, glucose intolerance, elevated blood pressure, diastolic dysfunction, and cardiac hypertrophy. In HFpEF hearts, insulin stimulation of glucose oxidation was significantly suppressed. This is paralleled with an increase in fatty acid oxidation rates, while cardiac ketone oxidation and glycolysis rates were comparable to healthy control hearts. The balance between glucose and fatty acid oxidation contributing to overall adenosine triphosphate (ATP) production was disrupted, where HFpEF hearts were more reliant on fatty acid as the major source of fuel for ATP production, compensating for the decrease of ATP originating from glucose oxidation. Additionally, p-PDH (pyruvate dehydrogenase) levels decreased in both HFpEF mice and human patients heart samples.
    CONCLUSIONS: In HFpEF, fatty acid oxidation dominates as the major source of cardiac ATP production at the expense of insulin stimulated glucose oxidation.
    Keywords:  cardiac energy metabolism; fatty acid oxidation; glucose oxidation; glycolysis; ketone oxidation
    DOI:  https://doi.org/10.1093/cvr/cvae006
  2. medRxiv. 2023 Dec 24. pii: 2023.12.21.23300393. [Epub ahead of print]
      It is estimated that as many as 1 in 16 people worldwide suffer from rare diseases. Rare disease patients face difficulty finding diagnosis and treatment for their conditions, including long diagnostic odysseys, multiple incorrect diagnoses, and unavailable or prohibitively expensive treatments. As a result, it is likely that large electronic health record (EHR) systems include high numbers of participants suffering from undiagnosed rare disease. While this has been shown in detail for specific diseases, these studies are expensive and time consuming and have only been feasible to perform for a handful of the thousands of known rare diseases. The bulk of these undiagnosed cases are effectively hidden, with no straightforward way to differentiate them from healthy controls. The ability to access them at scale would enormously expand our capacity to study and develop drugs for rare diseases, adding to tools aimed at increasing availability of study cohorts for rare disease. In this study, we train a deep learning transformer algorithm, RarePT (Rare-Phenotype Prediction Transformer), to impute undiagnosed rare disease from EHR diagnosis codes in 436,407 participants in the UK Biobank and validated on an independent cohort from 3,333,560 individuals from the Mount Sinai Health System. We applied our model to 155 rare diagnosis codes with fewer than 250 cases each in the UK Biobank and predicted participants with elevated risk for each diagnosis, with the number of participants predicted to be at risk ranging from 85 to 22,000 for different diagnoses. These risk predictions are significantly associated with increased mortality for 65% of diagnoses, with disease burden expressed as disability-adjusted life years (DALY) for 73% of diagnoses, and with 72% of available disease-specific diagnostic tests. They are also highly enriched for known rare diagnoses in patients not included in the training set, with an odds ratio (OR) of 48.0 in cross-validation cohorts of the UK Biobank and an OR of 30.6 in the independent Mount Sinai Health System cohort. Most importantly, RarePT successfully screens for undiagnosed patients in 32 rare diseases with available diagnostic tests in the UK Biobank. Using the trained model to estimate the prevalence of undiagnosed disease in the UK Biobank for these 32 rare phenotypes, we find that at least 50% of patients remain undiagnosed for 20 of 32 diseases. These estimates provide empirical evidence of a high prevalence of undiagnosed rare disease, as well as demonstrating the enormous potential benefit of using RarePT to screen for undiagnosed rare disease patients in large electronic health systems.
    DOI:  https://doi.org/10.1101/2023.12.21.23300393
  3. Chem Biol Interact. 2024 Jan 05. pii: S0009-2797(24)00002-4. [Epub ahead of print]389 110856
      Neurodegeneration is a complex process involving various inflammatory mediators and cellular responses. Aldose reductase (AR) is a key enzyme in the polyol pathway, which converts glucose to sorbitol. Beyond its metabolic role, AR has also been found to play a significant role in modulating neuroinflammation. This review aims to provide an overview of the current knowledge regarding the involvement of AR inhibition in attenuating neuroinflammation and complications from diabetic neuropathies. Here, we review the literature regarding AR and neuropathy/neurodegeneration. We discuss the mechanisms underlying the influence of AR inhibitors on ocular inflammation, beta-amyloid-induced neurodegeneration, and optic nerve degeneration. Furthermore, potential therapeutic strategies targeting AR in neurodegeneration are explored. The understanding of AR's role in neurodegeneration may lead to the development of novel therapeutic interventions for other neuroinflammatory disorders.
    Keywords:  Aldose reductase; Microglia; Neurodegeneration; Ocular inflammation
    DOI:  https://doi.org/10.1016/j.cbi.2024.110856
  4. Mol Genet Metab. 2024 Jan 04. pii: S1096-7192(24)00001-5. [Epub ahead of print] 108125
      
    DOI:  https://doi.org/10.1016/j.ymgme.2024.108125